Surgical Oncology 1

Breast
▪ Authors

Prof. Dr. Sameh Roshdy Prof. Dr. Islam Hany

Dr. Ahmed Hassan

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 Index
1 Introduction.

2 Anatomy.

8 Benign breast diseases;

o Congenital.
o Traumatic.
o Inflammatory.
o ANDI.
o Neoplastic;
- Fibroadenoma.
- Phyllodes.

37 Breast cancer;
o Non-infiltrating carcinoma;
- LCIS.
- DCIS.
- Paget disease of breast.
o Infiltrating carcinoma.
o TTT of breast cancer.
o Breast reconstruction.
o Metastatic breast cancer.
o SLNB = Sentinel Lymph node biopsy.
o Locally recurrent BC.

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120 Miscellaneous topics in breast;
o Gynaecomastia.
o Galactorrhea.
o Zuska's disease.
o Mastalgia.
o Breast swellings.
o Nipple discharge.
o Breast screening.
o Breast cancer with pregnancy.
o Breast sarcoma.
o Lymphoma.
o Melanoma.
o Metastasis to breast.
o Male breast cancer.
o BIA-ALCL.
o TNBC.
o TAD.
o Goldilocks mastectomy.

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 Introduction
❖ The commonest cancers in Egypt according to national cancer registry →
1. Male in this order:
• HCC.
• UB.
• Lung.
• NHL.
• CNS.
• Prostate.
2. Female in this order:
• Breast.
• HCC.
• CNS.
• Ovary.
• NHL.

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 Anatomy
❖ Embryology:
➢ 2 ectodermal ridges (Milk lines):
o 6th week: extend from anterior axially fold to groin.
o 9th week: disappear completely except front of chest (middle part of upper 1/3 of line).
o 15-20 solid columns of cells arise on each side → canalized → alveoli & milk ducts.
➢ Supporting vascularized CT derived from mesenchyme.
❖ Lie:
➢ Whole breast: integrates into superficial fascia of anterior chest wall.
➢ Superficial fascia: encases glandular tissue with its anterior & posterior lamella:
o Anterior lamella: superficial to gland at varying distances from dermis & has clinical significance
during SSM.
o Posterior lamella: covers undersurface of gland + continues as Scarpa’s fascia inferiorly.
o Anterior lamella connects to Posterior lamella at level of 5th rib.
➢ Axillary tail of Spence: lies deep to axillary fascia & pass through opening in deep fascia called
foramen of langer.
❖ Extent:

➢ In non-lactating:
o From 2nd to 6th rib.
o From lateral sternal border to midaxillary line.
➢ In lactating:
o From clavicle to 8th rib.
o From midline to anterior border of LD muscle.
❖ Retromammary space = Chassaignac’s bursa:
➢ Between posterior lamella & pectoral fascia.
➢ Loose areolar CT allowing mobility of breast on chest wall.
➢ Can be dissected bluntly & serves as pocket during sub-glandular breast augmentation.

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❖ Cooper’s ligament:
➢ Fibrous thickening of supportive CT containing bl.v. & lymphatics.
➢ Course from pectoral fascia through glandular tissue to skin.
➢ 3 distinct segments: deep & middle & superficial created by anterior & posterior lamella of superficial
fascia.
o Deep segment: between pectoral fascia & posterior lamella.
o Middle segment: between posterior & anterior lamella.
o Superficial segment: between anterior lamella & skin.
➢ The surgical importance:
o Responsible for skin dimpling in carcinoma due to involvement of lymphatics in it.
o In virgin: attach breast to chest wall → providing structural support & breast contour (pendular
after pregnancy & lactation due to stretch of ligament).

❖ Septum Fibrosum:
➢ Located horizontally at level of the 5th rib towards nipple.
➢ It divides glandular tissue into upper & lower part.
➢ It is reinforced medially & laterally by vertical horns:
o Medial horn attaches parasternally between 2nd & 5th rib.
o Lateral horn attaches to lateral margin of pectoralis major muscle.
➢ It contains neurovascular structures supplying NAC & gland.
➢ The thoracoacromial & deep branches of lateral thoracic artery travel on cranial side of septum.
➢ The 4th – rarely the 5th and 6th – intercostal artery perforators travel on caudal side of septum.
➢ The lateral cutaneous branches of 4th intercostal nerve travel along septum.
➢ The breast can be dissected bluntly along septum from posterior side ,so blood supply is preserved to
NAC during surgery.

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❖ Areola: 3 types of glands:
➢ Sebaceous glands → for lubrication of nipple during lactation.
➢ Sweat glands.
➢ Accessory mammary glands = Accessory gland of montogomry.
❖ Nipple:
➢ lies at midclavicular line in 4th IC space.
➢ Orifices of lactiferous ducts lie near its apex.
➢ Points forward & outwards & downwards.

❖ Underlying muscles:
➢ Upper 2/3 lies on pectoralis major.
➢ Infrolateral 1/3 lies on serratus anterior & external oblique.
➢ Lower medial part lies over upper part of anterior rectus sheath.

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❖ Histology:
➢ Lobes: 15-20 lobes of tubuloalveolar glandular tissue separated by cooper's ligaments → subdivided
into lobules.
➢ Duct system: Each lobe drain in separate main lactefrous duct → form lactefrous sinus under areola
→ open separately on nipple.
➢ TDLU: responsible for all breast diseases (affected by hormones) except duct papilloma & duct
ectazia.
❖ Supply:
➢ Arterial supply:
1. Internal mammary artery:
• Origin: 1st part of subclavian artery.
• Course: parallel to lateral sternal border.
• Branches: anterior perforating arteries in 2nd & 3rd & 4th IC spaces.
2. Axially artery:
• From 1st part: Superior thoracic artery.
• From 2nd part:
o Lateral thoracic artery.
o Acromiothoracic artery.

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 3. Posterior intercostal arteries:
• lateral perforating arteries to lateral portion of breast.
➢ Venous drainage:
• Perforating branches of internal mammary vein.
• Axillary vein tributaries.
• Perforating branches of posterior intercostal veins.
➢ Nerve supply:
• Lateral & anterior cutaneous branches of 2-6 intercostal nerves (T2-T6).
• Intercosto-brachial nerve:
o origin: 2nd intercostal nerve.
o traverse axilla.
o supply sensation to upper medial aspect of arm & axilla.
➢ Lymphatic drainage:
A. Lymphatic plexus within breast:
• Superficial or Subareolar lymphatic plexus.
• Interlobular or Parenchymatous lymphatic plexus.
• Submammary or Deep lymphatic plexus → drain deep parenchyma.

B. Lymphatic drainage of breast:

• 75% into axillary LNs:
o Step ladder manner: Level I → Level II → Level III → subclavian lymph trunk → on Lt side: ends
into thoracic duct & on Rt side: ends into Rt lymphatic duct → to junction between Subclavian vein
& IJV.
o If thoracic duct or Right lymphatic duct obliterated by mg cells spread to → supraclavicular LNs.
• 25% drains into:
o From medial part of breast into → internal mammary LNs.

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 o From upper part of breast into → interpectoral LNs of Rotter.
o Some lymphatics drain into → opposite breast in advanced tumor.
o Some lymphatics drain into → posterior intercostal LNs near head of ribs.
o From LIQ of breast into → lymphatics along medial rectus ms → subperitoneal lymphatics → liver
retrograde lymphatics → falciform ligament → umbilicus → Sister Jossef nodules → cancer cells
may drop by gravity → mets in pelvis.
A. LNs:
❖ Axillary LN levels:
➢ Level I → below & lateral to pectoralis minor = lateral & anterior & posterior.
➢ Level II → behind pectoralis minor = central & interpectoral.
➢ Level III → above & medial to pectoralis minor = apical.
❖ Axillary LN groups:
➢ Anterior = Pectoral group:
• at lateral edge of pectoralis major.
• along course of lateral thoracic vessels on chest wall.
➢ Posterior = Scapular group: on subscapular vessels & their thoracodorsal branches.
➢ Lateral = Humeral group: on lateral part of axillary vein.
➢ Central = Medial group:
• embedded in fat in center of axilla.
• along intercosto-brachial nerve.
• afferent: from lateral & anterior & posterior groups.
• efferent: to apical group.
➢ Subclavicular = Apical group:
• on medial part of axillary vein.
• Afferent: from all other groups & direct from upper part of breast.
• Efferent: to subclavian lymph trunk → on Lt side: ends into thoracic duct + on Rt side: ends into Rt
lymphatic duct.

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 Benign breast diseases (CTIN + ANDI)
Congenital breast anomalies
❖ Amazia: aplasia of one or both breasts.
❖ Polymazia: accessory breast along milk line.
➢ The commonest site: lower axilla.
❖ Micromazia: small breasts.
❖ Diffuse hypertrophy: huge breasts.
❖ Athelia: absence of nipple.
➢ Commonly associated with amazia.
❖ Polythelia: accessory nipple along milk line.
➢ The commonest site: just below normal breast.
❖ Poland syndrome:
➢ Breast hypoplasia or aplasia +
➢ Absence of ipsilateral pectoralis M & m +
➢ Costal and rib defects +
➢ Ipsilateral UL malformation.
❖ Fleischer syndrome:
➢ Lateral nipple displacement +
➢ Bilateral renal hypoplasia.
❖ Congenital nipple inversion:
➢ Failure of nipple to follow growth spurt.
➢ Appears at puberty.
➢ Bilateral: > 50% of cases.
➢ Not surrounded by groove.
➢ Difficult suckling.
Nipple retraction Congenital Acquired

Onset During puberty Recent

Side Bilateral 25% Unilateral
Suckling Difficult Not difficult
Groove around retracted nipple No Yes

❖ Causes of acquired nipple retraction:

➢ Traumatic fat necrosis. ➢ Chronic breast abscess.
➢ Mammary duct ectazia.
➢ BC.

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❖ Grading of nipple inversion:
➢ G1:
• Easy pulling out of nipple by gentle areola squeezing.
• Nipple projection maintained for several minutes → ,then nipple reinverted.
➢ G2:
• The majority.
• Pulling out of nipple by forceful manipulation → reinverted quickly.
➢ G3:
• Invaginated.
• No nipple projection.
• Nipple buried below skin.
• Not pulled out despite maximal manipulation.
❖ TTT:
➢ Purse string around neck of nipple.
➢ Selective ductal division.
➢ Triangular skin flaps mobilized to add bulk to base of nipple.
➢ Percutaneous release:
- wire subcision.
- Needle tip lysis.

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 Traumatic breast diseases
1. Cracked nipple:
➢ Etiology:
o Bad breast hygiene during lactation.
o Trauma by baby teeth.
➢ C/P:
o Fissure: pain & bleeding during suckling.
o If neglected → acute mastitis.
➢ TTT:
o Stop lactation from diseased side for 48h + evacuating it with breast pump.
o Wash nipple + antiseptic cream.
o If soreness disappears → resume lactation.
2. Hematoma:
➢ The commonest.
➢ Etiology:
o Trauma: surgical or non-surgical.
o may occur spontaneous.
➢ C/P: Calcified haematoma → Hard mass may be mistaken for carcinoma.
➢ TTT:
o small: support + analgesia + antibiotic + observation.
o large: evacuation.
3. Traumatic fat necrosis:
➢ Etiology: usually minor direct trauma.
➢ Pathology:
o Trauma hydrolysis of necrotic fat → liberation of FA which combine with Ca of local tissue fluid → Ca
soaps.
o Affected area becomes surrounded with phagocytes & fibroblasts & giant cells → Hard & Chalky & White
mass.
o DD: differs from cancer as no yellow specks & no gritty sensation.
➢ C/P:
o Common in middle aged obese & pendulous breast.
o Occurs in superficial breast tissue.
o History of trauma in 50% of cases.
o Painless & Firm & Poorly defined mass.
o Nipple retraction + skin dimpling.

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➢ Investigations:
o BBMM: Speculated mass + microcalcification + architectural distortion.
o US: oily cyst + circumscribed mass of mixed soft tissue density & fat with calcified rim.
o Biopsy: FNAC or CNB.
➢ TTT: Excision biopsy to exclude malignancy.
4. Mammary duct Fistula:
➢ Etiology:
o Rupture of subareolar abscess: the commonest cause.
o Incision or injury of lactating breast.
➢ C/P: discharging fistula at areolar margin + nipple retraction.
➢ TTT:
o In lactating: Stop lactation → If discharge continues → Excision of fistula & affected breast sector +
Bromocriptine.
o In nonlactating:
- Local periductal sepsis: Fistulectomy.
- Diffuse periductal sepsis: Total duct excision + close wound primarily under antibiotic cover.
5. Traumatic mastitis: ill fitted brassier → local irritation.
6. Open wounds: during repair → attention:
➢ not to injure much milk ducts +
➢ to close dead spaces +
➢ to preserve cosmetic appearance.

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 Inflammatory breast diseases:
1. Acute mastitis
A. Neonatal mastitis:
➢ Etiology:
• Maternal galactagogue act on baby’s breast after labour → stimulate milk secretion.
• Withdrawal of maternal estrogen from baby after labour → stimulates newborn pituitary to produce
prolactin → stimulates milk secretion (Witch’s milk).
➢ C/P: swollen breasts & few milk drops
• appears on 3rd & 4th day.
• disappears on 3rd W.
➢ TTT: assurance.
B. Mastitis of mumps:
➢ Usually unilateral.
➢ Common in females.
C. Mastitis of puberty:
➢ Usually unilateral.
➢ Common in males during puberty.
➢ Etiology: Hormonal imbalance at age of puberty.
➢ C/P:
• Enlarged & tender & indurated.
• Never suppurates.
• Subsides spontaneously within weeks.
➢ TTT: assurance.
D. Milk engorgement mastitis:
➢ Other name: Milk congestion mastitis.
➢ Etiology: Duct obstruction by dry milk or epithelial debris during lactation.
➢ C/P: as cellulitis ,but
o No redness.
o No axillary lymphadenopathy.
o If neglected → breast cellulitis ,then abscess.
➢ TTT: as cellulitis.
E. Acute breast abscess:
❖ Other name: Acute bacterial mastitis.
❖ The commonest.

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❖ Etiology: (Risk factors & Organisms & Route of infection)
Risk factors:
• In lactating: usually in 1st month of 1st lactation or during weaning (incisors are developed):
➢ Milk congestion due to duct obstruction.
➢ Lack of hygiene.
➢ Cracked nipple.
➢ Cleaning baby’s mouth with swab → excoriation of its epithelium & staph infection transmitted to
nipple.
• In non-lactating:
➢ Degenerated tumor.
➢ Infected hematoma.
➢ Immunosuppression: DM & RA & Steroid therapy.
Organisms:
➢ Staph aureus: the commonest.
➢ Streptococci.
Route of infection:
➢ Direct through milk duct or fissured nipple: the commonest.
➢ Blood born: rare.
❖ Sites:
➢ Supramammary:
• Occurs in SC tissue in front of breast substance.
• Should be dealt with as common SC abscess & furuncle.
➢ Retromammary:
• Occurs behind breast tissue in front or behind pectoral fascia.
• Extremely rare.
➢ Intramammary:
• The commonest.
• Occurs in breast parenchyma.
• Starts in one lobe → bursts into other lobes.
• Classified into Peripheral abscess & Subareolar abscess.

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 Peripheral abscess Subareolar abscess
Breast periphery
Site Subareolar or Periareolar
Not related to major duct system
Usually Unilocular
Locularity Always Multilocular
may be Multilocular
Organism Common gram +ve staph Combined aerobic & anaerobic
Predisposing Breast milk engorgement Severe form of duct ectasia
Breast feeding
+ve -ve
association
Smoking
-ve +ve
association
Complete aspiration + culture + Open drainage + combination antibiotic
TTT Amox-Clav empirical till culture If failed → definitive ttt is Hadfield
result operation

Hadfield’s operation = Total duct excision:

➢ Incision: circumareolar.
➢ Excision of all major ducts + breast tissue core till pectoralis major muscle.
➢ Indications:
o Duct ectasia.
o Definitive ttt of subareolar abscess.

Adair's operation = Major duct excision alone:

➢ leaving remnant of ducts
➢ Disadvantage: recurrence.
➢ Complications of breast abscess:
o Destruction of breast tissue.
o Ulcer & Sinus & Fistula formation.
o Spread: septicemia & pyemia.
o Chronic abscess formation = antibioma if badly treated.
➢ Stages:
➢ Stage of cellulitis.
➢ Stage of acute abscess formation.
➢ C/P:
1) Stage of cellulitis:
➢ General constitutional manifestations: FAHM.

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 ➢ Local:
o Pain: mild → increases gradually.
o Skin: hot & red with dilated veins.
o Swelling: indurated & & ill defined & tender.
o Axillary LNs: large & firm & tender.
2) Stage of abscess formation (After localization):
➢ Fever: hectic. ➢ Pain: throbbing.
➢ Toxaemia: severe. ➢ Pitting skin edema: 1st sign.
➢ Fluctuation: late & the surest sign.
➢ Investigation:
➢ CBC: Leucocytosis.
➢ US.
➢ TTT:
1) Stage of cellulitis:
➢ General:
o Antibiotics: Cloxacillin for penicillinase resistant staph (Tetracycline & Chloramphenicol &
Quinolones avoided as they are secreted in milk).
o Analgesic. o Antipyretic.
➢ Local:
o Elevate breast (rest).
o Hot application.
o Weaning: not advised.
o Stop suckling from diseased side.
o Evacuate it with breast pump to facilitate drainage of engorged segment.
o Use healthy side for feeding.
o Some advocate if baby > 9 M → Stop lactation & suppress milk secretion with Bromocriptine.
2) Stage of abscess formation → incision & not wait for fluctuation:
➢ Supramammary abscess: incision where it points.
➢ Intramammary abscess:
o Radial incision: to avoid injury to many milk ducts.
o Circumareolar incision in skin only → then Radial in breast tissue.
o After incision → finger passed in cavity to break all septa.
o Wound packing for 48h as haemostatic & allow granulation tissue to fill cavity from below.
➢ Retromammary abscess: incision in submammary fold.

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 2. Chronic mastitis
A. Non-specific:
1. Chronic breast abscess (Antibioma):
❖ Etiology:
➢ Insufficient antibiotics in cellulitis stage.
➢ Treating acute abscess with antibiotics alone without drainage.
➢ Insufficient drainage: Independent incision or incomplete opening of all loculi.
❖ Pathology:
➢ Cavity: contain pus ,but sometimes in long standing cases, organisms die & contents become sterile.
➢ Wall: thick fibrous wall lined by pyogenic membrane surrounded by zone of breast tissue with evidence of
chronic inflammation.
❖ Complications:
➢ Damage to the breast tissue.
➢ Toxaemia
➢ Fistula formation.
➢ Recurrent acute exacerbation.
❖ C/P:
➢ Toxaemia.
➢ Recurrent acute exacerbation.
➢ Hx of acute abscess usually with abs therapy.
➢ Mass: difficult to be differentiated from carcinoma.
❖ Investigations:
➢ Lab: CBC → leucocytosis in acute exacerbation.
➢ Rad: BBMM → Coarse calcification.
➢ Biopsy: FNAC or CNB.

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❖ DD:

Breast cancer Chronic breast abscess

Hx of acute mastitis -ve +ve
Episodes of acute
exacerbations -ve +ve

Pain & Tenderness No except if T4d No except in exacerbation

Consistency Hard Hard due to fibrosis

Posterior surface Flat Rounded

+ve due to cutaneous lymphatic

+ve due to cutaneous lymphatic
obstruction by mg cells.
Pea d’ orange obstruction by fibrosis.

Nipple retraction &

May be +ve due to fibrosis.
Skin dimpling
Adherent to skin &
May be +ve
deep fascia
Firm & Tender
Axillary LNs: Hard painless

❖ TTT:
➢ Excision biopsy to exclude malignancy.

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 B. Specific: ‫قراءة‬
1. TB:
❖ Etiology:
➢ Lymphatic spread: from cervical & axillary & mediastinal LNs.
➢ Blood spread: less common.
➢ Along nipple.
➢ Retromammary cold abscess may be due to T.B rib.
❖ C/P:
➢ Multiple abscesses +
➢ Multiple axillary or breast sinus (50% of cases) discharging caseous material.
❖ TTT:
➢ Anti TB drug therapy +
➢ Mastectomy: rarely needed.

2. Syphilis:
❖ Incidence: Uncommon.
❖ Types:
➢ 1ry: May affect nipple or areola from kissing or nursing syphilitic child who can infect healthy wet nurse
,but not his mother (Colle’s law) because syphilitic mother is immune against reinfection from her baby.
appears as indurated ulcer + enlarged axillary LNs.
➢ 2ry: Mucous patches (Condylomata lata) in submammary fold due to wet surface + painful swollen breast.
➢ 3ry: Gumma of breast is very rare.

3. Actinomycosis:
❖ Incidence: Very rare.
❖ C/P: sinuses discharging sulphur granules.
❖ TTT: mastectomy.

4. Mondor’s disease:
❖ Etiology:
➢ Thrombophlebitis of superficial veins of breast & anterior chest wall (lateral thoracic vein &
thoracoepigastric vein): unknown etiology.
➢ 2ry to breast trauma & surgery & irradiation & non-palpable cancer.
❖ C/P:
➢ Acute pain in lateral half of breast or anterior chest wall.
➢ Thrombosed vein presents with firm tender cord like structure (string phlebitis).

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 ➢ Can be misdiagnosed with lymphatic permeation from occult breast cancer.
❖ TTT:
➢ Restriction of movement of ipsilateral arm & shoulder.
➢ Hot fomentation along distribution of symptomatic vein.
➢ Liberal use of salicylates.
➢ Usually resolves within 2-6 W.
➢ If persist → division of vein above & below involved area.

5.Diabetic mastopathy:
➢ Lymphocytic mastitis or lymphocytic mastopathy.
➢ Type of patients: premenopausal women with longstanding IDDM.
➢ Pathogenesis: unknown & may autoimmune reaction.
➢ Pathology: dense keloid-like fibrosis & Periductal, lobular infiltration & Perivascular lymphocytic
infiltration.
➢ Mg risk: No.
➢ C/P: suspicious like breast mass.
➢ BBMM: dense pattern.
➢ CNB: for diagnostic confirmation.
➢ TTT: Excision not necessary.

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 ANDI (Aberrations of Normal Development & Involution):
➢ During development:
▪ Fibroadenoma.
▪ Nipple retraction.
▪ Juvenile hypertrophy.
➢ During cyclic changes:
▪ Fibroadenosis.
➢ During involution:
▪ Duct ectasia.
▪ Macrocyst.
▪ Sclerosing adenosis.

Fibroadenosis
❖ Incidence: the commonest breast disease.
❖ Etiology: (4H3S)
1. Hormonal imbalance:
▪ High Estrogen/Progesterone.
▪ High FSH & LH/Androgen.
▪ High prolactin or prolactin receptor sensitivity.
2. High fat intake:
▪ Fat increases estrogen production.
▪ Abnormal FA metabolism: lacking essential FA (linolenic acid) → Precursor to PGE1 → Bind to ER →
competing with circulating estrogen.
3. High caffeine → High catecholamine → High cAMP → High cellular proliferation.
4. High nicotine & tyramine.
5. Salt & Water retention.
6. Stress: physical & emotional.
7. SHBG: abnormal level.

❖ Pathology:
➢ N/E:
▪ Side: common bilateral & may be unilateral.
▪ Site: common UOQ & may affect whole breast.
▪ Thick & Tough & Rubbery.
▪ C/S:
o Consistency: Soft (Cancer is gritty).

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 o Color: White or Yellow (Cancer is grey).
o Capsule: No.
o Cystic areas: dominant large one (Blue-domed cyst of Bloodgood)
➢ M/E:
▪ Panplasia: Hyperplasia of all elements.
▪ Fibrosis: fibrous tissue replaces fat & elastic tissue.
▪ Adenosis: High number of acini & ductules.
▪ Epitheliosis or Epithelial hyperplasia: High number of layers of epithelial cells lining lobules & ducts
(> 2 cell layer).
▪ Papillomatous projections.
▪ Sclerosing adenosis: High fibrosis & acini & clinically = scirrhous carcinoma.
▪ Radial Scar: as sclerosing adenosis ,but < 1 cm.
▪ Cyst Formation contains dark mucoid:
▪ Microcyst: Degeneration cysts of acini.
▪ Macrocyst: Retention cyst due to duct obstruction by fibrosis or epitheliosis.
▪ Round cell infiltration: Plasma cells & Lymphocytes in interstitial tissue.
❖ Complications:
➢ Hge in cysts.
➢ Infection.
➢ Carcinoma (controversial)
❖ Mg risk:
➢ Fibroadenosis is not precancerous ,but may coexist with BC in 3%.
➢ Precancerous lesions: (FAM & RS)
o Florid epithelial hyperplasia: acini & ductules lined by > 4 layers of epithelial cells & without cellular
atypia.
o Atypical epithelial hyperplasia.
o Macrocyst.
o Radial scar.
o Sclerosing adenosis.

❖ C/P:
➢ Type of patients:
▪ Age: CBP & never before puberty or after menopause.
▪ Risk: common in unmarried & nullipara & non-lactating (breasts denied of natural function)
➢ Symptoms:
1) Pain:

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 Nipple discharge
o Nature: Dull aching.
o Site: localized to breast or shooting to arm.
o Rhythm: common cyclic. Pain Lump
o Start before menses (congestion) & last for 2-3 days & gradually disappear partially or completely.
o Relieved by pregnancy.
o Severity: may be marked (Mastodynia).
2) Nipple discharge: serous & green & dark brown & black (never bloody).
3) Lump: painful either single or multiple. (painless lump is suspicious)
➢ Signs:
1) Breast nodules:
o Fine or Coarse.
o Tender & Mobile.
o Better felt with tips of fingers.
o Milking of breast → nipple discharge.
2) Ax LNs:
o May be enlarged & tender & firm (never hard).
o Due to chemical irritation by hypersecretion from hyperplastic epithelium.
❖ Investigations:
➢ Rad: BBMM → focal or diffuse breast masses.
➢ Pathological:
▪ Cytological exam of nipple discharge.
▪ Biopsy of breast lump.
❖ DD:
➢ Mass: from other causes of breast mass.
➢ Nipple discharge: from other causes of nipple discharge.
➢ Pain: from other causes of mastalgia.
❖ TTT:
1) Assurance.
2) Non hormonal:
➢ Change lifestyle:
▪ Stop Smoking.
▪ Stress management.
▪ Support breast by suitable bra.
▪ Shift from estrogen containing OCs to progestrone containing OCs.
➢ Nutritional: Avoid →

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 ▪ Methyl xanthine: coffee & tea & chocolate & cola.
▪ Tyramine: cheese & wine & beer & spices & nuts & mushrooms & bananas.
▪ High fat diet.
▪ High salt diet.
➢ Drugs:
▪ Analgesic to relieve pain.
▪ GLA: evening primrose oil: 500 mg & 3-6 tab/day.
3) Hormonal:
➢ Long acting dopaminergic drugs (Bromocriptine): decreases prolactin →
▪ Lactodil or Parlodil: 2.5mg tab.
▪ Lisuride (Dopergin): 0.2 mg tab.
▪ Cabergoline (Dostinex or Elonda): 1/2 tab/3 days.
➢ Danazol (attenuated androgen): decrease pituitary GTH → decrease ovarian function → decrease
estrogen.
➢ Tamoxifen:
▪ 10mg daily.
▪ From 5-25 day of cycle or continuous for 3 months.
▪ Exclude previous TE disease.
▪ Inform to stop if suspected pregnancy
▪ Council for possible mens irregularities.
➢ Progestin cream or oral progesterone.
➢ LHRH (Zoladex):
▪ Increase hypothalamic GTRH → initial increase of pituitary GTH followed by persistent suppression
of GTH.
4) Surgical:
➢ Excision of:
▪ Localized mass with suspicion of malignancy.
▪ Atypical hyperplasia.
▪ Recurrent cyst
➢ Aspiration of cysts.

23
 Mammary duct ectasia
❖ Other name: Plasma cell mastitis.
❖ Definition: Bg dilatation & shortening of terminal ducts within 3 cm of nipple.
❖ Etiology: 2 processes occur together →
➢ 1ry process: stagnation of secretion → epithelial ulceration → leak of irritant FA in periductal tissue →
plasma cell infiltration (autoimmune disease) & anaerobic infection (some cases) → periductal fibrosis →
nipple retraction & dilatation of ducts.
➢ Periductal mastitis (mainly in cigarette smokers) → weakening of ducts → 2ry duct dilatation.
➢ Cigarette smoking can cause periductal mastitis through:
• Higher Conc of substances of cigarette smoke as cotinine & nicotine derivatives in subareolar ducts than
in plasma → ductal epithelial damage.
• Microvascular damage by lipid peroxidase → local ischemia.
• Altered bacteria flora: overgrowth of gram -ve due to inhibition of gram +ve bacteria.
❖ Pathology:
➢ Ducts dilate → contain inspissated material with minimal surrounding inflammation (lymphocytes & plasma
cells).
❖ Complications:
➢ Abscess.
➢ Mammary duct fistula.
❖ C/P:
➢ Type of patient: common in middle age women.
➢ Symptoms & Signs:
• Stage of acute inflammation: pain & fever.
• Usually passes unnoticed.
• Subareolar hard mass simulating carcinoma.
• Transverse slit-like nipple retraction may be the only presenting feature.
• Nipple discharge: cheesy (creamy) toothpaste like.
❖ Investigations:
➢ BBMM.
➢ Biopsy from mass or
➢ cytology from nipple discharge.
❖ DD:
➢ Mass: from other causes of hard masses of breast.
➢ Nipple retraction: from other causes of acquired nipple retraction.

24
 ➢ Nipple discharge: from other causes of nipple discharge.
❖ TTT:
➢ Assurance.
➢ Antibiotic therapy (Flucloxacillin & Metronidazole).
➢ Steroids.
➢ Nipple discharge: Hadfield’s operation.

25
 GM (Granulomatous mastitis)
❖ Etiology:
➢ 1ry = idiopathic = IGM: autoimmune reaction to extravasated secretions from lobules.
➢ 2ry GM:
• sarcoidosis.
• TB.
• Nocardia asteroids: fungal infection.
• Diroflaria tenuis: parasite infection.
• FB (silicone gel).
❖ Pathology:
➢ Non caseating granulomatous lesion + giant cells + chronic inflammation + microabscess + necrosis.
❖ Complications:
➢ Abscess.
➢ Duct fistula.
➢ Recurrence: common.
❖ C/P:
➢ Type of patient: common in 3rd & 4th decades.
➢ S & S:
• Hard tender breast mass + inflammation of overlying skin.
• Recurrent or Multiple abscesses.
• May be bilateral.
• Difficult to differentiate from cancer.
❖ Investigations:
➢ Lab: Serum prolactin.
➢ Rad:
• BBMM: nodular opacities.
• BBUS: hypoechoic nodules.
➢ Biopsy:
• CNB or incisional biopsy.
• FNAC: useless.
• Tissue should be sent for acid-fast bacillus & fungal stains to rule out TB or nocardia.
❖ DD:
➢ Non puerperal mastitis.
➢ Breast abscess. ➢ Breast cancer.

26
❖ TTT:
➢ IGM:
• No specific ttt.
• Self-limiting inflammation: Complete resolution in 5-20 M.
• Not recommend surgical ttt due to slow wound healing.
• If asymptomatic & uncertain diagnosis: close FU.
• If 2ry infection or abscess → antibiotics according to C/S & drainage.
• If mass painful & enlarging or diagnosis uncertain: excision biopsy followed by prednisolone 60 mg/day
for 6 W.
• Preoperative ttt with Steroids & NSAIDs or Colchicine → more conservative surgery.
➢ If Only Corynebacterium recovered:
• Optimal ttt is uncertain because of multiple species of Corynebacterium & lack of predictable
susceptibility patterns.
• Doxycycline:100 mg BID If fails → Linezolid 600 mg BID.
➢ Localized pain: NSAIDs.
➢ Recurrent mass: Surgery not recommended.
➢ If prolactin elevated → Antiprolactin ttt.
➢ Steroids & Methotrexate:
• Routine use: not warranted.
• Remission occurs within 12-24 M course of low dose of Methotrexate & Prednisone.
• reduce swelling.
• not alter natural history ,especially in small localized lesions.
• Discontinuation → rebound inflammation.
➢ Persistent or refractory symptoms:
• Steroid therapy: Prednisolone 0.5-1 mg/kg/d for 4 W till erythema & pain → improve → tapering over
8-12 W +/-
• Methotrexate: 10-15 mg/W +
• Daily folic acid supplementation.
• Reduced /M over 12 M.

27
 Neoplastic breast diseases
Benign breast tumors:
❖ Epithelial:
➢ Duct papilloma.
➢ Adenoma: tubular or lactating.
❖ CT:
➢ Neurofibroma.
➢ Lipoma.
❖ Mixed:
➢ Fibroadenoma.
➢ Adenolipoma (hamartoma).
➢ Papillary cystadenoma.

Duct papilloma
❖ Pathological types:
➢ 1. Solitary
• The commonest.
• Origin: columnar cells lining major lactiferous ducts within 5 cm from nipple.
• N/E: Small & Soft & Pedunculated mass with finger like processes.
• M/E: Vascular CT core covered with columnar epithelium.
➢ 2. Multiple:
• Minimum of 5 clearly separate papillomas within localized segment of breast tissue usually in peripheral
location.
➢ 3. Juvenile papillomatosis (Swiss Cheese disease):
• Marked multiple ductal papillomas.
❖ Complications:
➢ Mg transformation.
➢ Can harbor areas of atypia or DCIS.
➢ Bleeding per nipple: due to kink of pedicle with venous obstruction → rupture of capillaries.
• Spontaneous & Fresh.
• Profuse: more than duct carcinoma in which excess fibrosis entangles blood vessels & obstructs duct.
➢ Retention cyst full of blood due to duct obstruction.

28
❖ C/P:
➢ Type of patients:
• Solitary: usually between 30-50y.
• Multiple & juvenile: < 30y.
➢ Symptoms:
• Solitary papilloma:
▪ Bleeding per nipple: common.
▪ Mass: retention cyst.
• Multiple papillomas:
▪ Nipple discharge: rare.
▪ Palpable lump.
• Juvenile papillomatosis: painless mobile mass like fibroadenoma.
➢ Signs:
• RA mass (retention cyst): papilloma itself is not palpable.
• Differential pressure: squeeze blood from affected duct.
❖ Investigations:
➢ Rad: Galactography (Ductography): cannulation of affected duct & lipidol injection → filling defect.
➢ Endoscopy: Ductoscopy + biopsy.
➢ Biopsy: Cytology of discharge.
❖ DD:
➢ RA mass (retention cyst): differentiated clinically from cyst of fibroadenosis by being beneath areola & in
fibroadenosis → away from areola.
❖ TTT:
➢ Solitary papilloma (localized to 1 duct): Microdochectomy & Biopsy.
• fine sewing needle with blunt end inserted into duct using magnification.
• Incision: radial or better circumareolar.
• Excision of wedge of breast tissue around cannulated duct of at least 2-3 cm.
➢ Multiple papillomas (not localized): Removal by vacum assisted core biopsy device.
➢ Juvenile papillomatosis: excision.

29
 Adenoma
❖ Types:
➢ Tubular adenoma: glands + very little stroma.
➢ Lactating adenoma: like tubular adenoma in pregnant or lactating & often multiple & clinically like
fibroadenoma.
❖ BBMM: diffuse punctuate microcalcification within acini.
❖ TTT:
➢ Tubular adenoma: excision.
➢ Lactating adenoma: conservative through lactation as tend to regress after cessation of lactation.

Adenolipoma = Hamartoma:
❖ = adipose + glandular + fibrous tissues.
❖ C/P: usually asymptomatic & may be palpable in women > 35 y.
❖ BBMM: circumscribed area consisting of soft tissue + lipomatous elements surrounded by thin radiolucent zone.
❖ TTT: excision.

30
 Fibroadenoma:
❖ Def: Mixed Bg tumor of epithelial & fibrous tissue origins.
❖ Incidence:
➢ The commonest benign tumor in breast.
➢ 50% of all breast biopsies.
➢ 20% multiple.
➢ Age: Common in women 15-35 y.
❖ Etiology: Evidence of hormonal relationship:
➢ Persist during CBP.
➢ Increase in size during pregnancy or with estrogen ttt.
➢ Usually regress after menopause.
❖ Classifications:
A. Old classification:
➢ Hard: Pericanalicular.
➢ Soft: Intracanalicular.
Recently pathologic differentiation of both types of limited value as management is similar with negligible mg
risk.

HARD (Pericanalicular) SOFT (Intracanalicular)

Small & firm & well capsulated mass Large & soft & well capsulated mass.
N/E
C/S: bulges on cutting C/S: cystic areas
Ducts are patent & surrounded by dense Loose CT presses on ducts & transforms
M/E
fibrous CT them into slits
Cystadenoma
Complications Rarely turns mg = 1 / 1000 → lobular CIS Phylloides
Sarcomatous changes

B. Recent classification:
➢ Simple fibroadenoma.
➢ Complex fibroadenoma:
• Contains other proliferative changes as sclerosing adenosis & duct epithelial hyperplasia & calcification
& papillary apocrine changes.
• Slight high risk of cancer if multicentric proliferative changes in surrounding glandular tissue.
➢ Giant fibroadenoma:

31
 • > 10 cm.
• Should be differentiated from phyllodes.
➢ Juvenile fibroadenoma: in young women 10-18 y.

❖ C/P: (Mass)
➢ Painless. ➢ Firm & Well defined.
➢ Small & Slow growing, ➢ No LNs.
➢ Highly mobile within breast (mouse of breast)
❖ Investigations: BBMM & Biopsy.
❖ TTT:
➢ Excision biopsy if:
• Painful.
• Symptomatic.
• Atypical.
• Giant.
• Rate of growth: >15% in 1 y.
• Cosmetic.
• Patient wish.
• Associated with contralateral breast cancer.
• Patient with high risk of breast cancer.
• American Society of Breast Surgeons recommends excision in:
- suspicious of either phyllodes or future malignancy.
- stromal activity.
- stromal overgrowth.
- stromal mitosis.
- nuclear pleomorphism.
- adipose tissue infiltration.
➢ Cryoablation or percutaneous vacuum assited US guided excision for:
• Simple fibroadenoma confirmed by CNB.
• Less effective if > 2 cm.

32
 Phyllodes tumors
❖ Definition: fibroepithelial breast tumors = Group of lesions of varying mg potential ranging from completely
Bg tumor to sarcoma.
❖ Other names: Serocystic disease of Brodie or cystosarcoma.
❖ Epidemiology:
➢ <1% of all breast tumors.
➢ Median age of presentation: 42-45 y.
➢ High grade tumors: common in old.
❖ Etiology:
➢ Unknown.
➢ Association with Li-Fraumeni syndrome.
➢ Association with Gynecomastia in men.
❖ Classification:
➢ Based on 4 features:
• Stromal overgrowth.
• Stromal cellular atypia.
• Mitosis.
• Infiltrative or circumscribed tumour margins.
➢ Into:
• Bg: 60%.
• Borderline: 15%.
• Mg: 25% & most clinically mg/metastatic phyllodes tumors are with overgrowth of 1 or several
sarcomatous elements as:
- Liposarcoma.
- Rhabdosarcoma.
- Chondrosarcoma.
- Undiff/unclassified sarcoma.
❖ Pathology:
➢ N/E:
• Size: Huge.
• Consistency: soft.
• Surface: lobulated or bosselated.
• Radial growth → pseudocapsule through which stroma may protrude into adjacent tissue.
• May ulcerate overlying skin through pressure necrosis (not infiltration).

33
 • C/S: cystic deg into which branching projections of tumor appear like leaves of lettuce.
➢ M/E: ‫مهم‬
• Have cystic components.
• Not true sarcoma by either cellular origin or biologic behavior.
• Resembles intracanalicular fibroadenoma + cystic deg + sarcomatous tissue like stroma.
• Histopathologic spectrum: from resembling Bg fibroadenoma to high-grade sarcoma.
• Stromal elements: key component in differentiating it from fibroadenoma & differentiating Bg from Mg.
• Characteristic leaf-like architecture = elongated cleft like spaces containing papillary projections of
epithelial-lined stroma + varying degrees of hyperplasia & atypia.
❖ Classification:
• Bg: 60% & that are capable of a diverse range of biologic behaviours. In their least aggressive form,
behave like benign fibroadenomas, although with a propensity to recur locally following excision without
wide margins. At the other end of the spectrum, it can metastasize distantly, sometimes degenerating
histologically into sarcomatous lesions that lack an epithelial component.
• Borderline: 15%.
• Mg: 25%.
➢ Mg based on:
• High stromal cellularity.
• Cytologic atypia.
• Mitosis.
• Necrosis.
❖ Complications:
➢ Recurrence: Bg may recur or even spread (20%).
➢ Mg transformation: rare.
➢ Mets via blood (3-12%) → mainly to lung & bone.
❖ C/P:
➢ Type of patients: Common > 35y.
➢ S & S: Breast lump →
• Huge.
• Rapidly growing.
• Sudden increase in growth of long standing soft fibroadenoma like mass, involving whole breast.
• Rounded borders & lobulated or bosselated surface + soft consistency.
• Tear drop sign: mass may extend outside breast.
• Overlying skin stretched with dilated veins.

34
 • Ulceration & necrosis may occur.
• Axillary L.Ns. not enlarged unless infected or mets < 1%.
• Mets: <1%.
❖ Investigations:
➢ Rad:
• BBMM: round borders & lobulated or bosselated appearance.
• US: cystic area within solid mass.
➢ Biopsy:
• FNAC: less sensitive than CNB because of heterogenous lesion.
• High stromal cellularity + Indeterminate heterogenous features.
❖ DD: differentiated from sarcoma in:
➢ Skin: not infiltrated ,so probe can be put between skin and tumor.
➢ Ulcer edge: tender.
❖ TTT:
➢ Small: BCS with SM at least 1 cm. .
➢ Massive or Recurrent: Simple mastectomy.
➢ No ALND except for clinically suspicious LNs which is rare.
➢ Systemic therapy based on sarcoma guidelines rather than BC.
1. Adjuvant RT:
• Borderline & mg..
• Inadequate margins.
• Recurrent mg phyllodes tumors.
• >10cm.
• Mg AX LNs.
2. Adjuvant chemo:
• High-risk.
• >10 cm.
• Recurrent mg phyllodes tumors.
• Excellent functional status.
• Minimal comorbidities.
• Only after thorough discussion about risks & benefits of ttt.
3. Hormonal ttt:
• Not effective despite presence of HR in epithelial component as stromal component is the principle
neoplastic cell population responsible for metastatic behavior.

35
 • The stromal component primarily expresses ER beta instead of alpha that is expressed by BC.
❖ Recurrence:
➢ Recurrences typically have same grade as original tumors ,but several case reports → Bg tumors transforming
into Mg upon recurrence.
➢ If resectable recurrence: Re-excision with wide margins or Mastectomy → followed by RT.
➢ If unresectable recurrence: Palliative RT.
➢ If metastatic to lung: Resection of pulmonary mets if feasible.
❖ Prognosis: poor response to chemo & RT.

36
 Breast cancer
❖ Epidemiology: Incidence:
➢ The commonest female cancer.
➢ About 30% of female cancers.
➢ The leading cause of cancer death in world & Egypt.
➢ Age: common > 40 y.
➢ Sex: female to male 99:1.
➢ Side: Lt > Rt & Bilateral (Synchronous 1% & Metachronous 5%).
➢ Site: UOQ 60%.
➢ Geographic: West > East & Developed > Developing countries.

❖ Etiology:
Predisposing factors: (7)
1. Genetic: 5-10% (Hereditary & Familial).
A.Hereditary: All AD except ATM.
➢ High penetrance genes:
Hereditary breast ovarian cancer syndromes: (BRCA 1 & 2):
• Mutation in BRCA1 tumor suppressor gene on long arm of chromosome 17 →
▪ Breast: common medullary & TNBC.
▪ Ovary: common high grade serous.
▪ Colon cancer.
▪ Male: common castrate resistant prostate cancer.
• Mutation in BRCA2 tumor suppressor gene on long arm of chromosome 13 →
▪ Female: common high grade & ER +ve.
▪ Male: more common BC.
Li-fraumeni syndrome: Mutation in P53 tumor suppressor gene on chromosome 17 → (LABS)
▪ L: Lung & Laryngeal & Leukaemia.
▪ A: Adrenocortical.
▪ B: Breast & Brain.
▪ S: Soft tissue sarcoma.
Cowden syndrome: Mutation in PTEN tumor suppressor gene on chromosome 10 →
▪ Hamartomas: skin & oral mucosa & intestine.
▪ Breast.
▪ Thyroid.
Lynch II syndrome: Mutation in MMR tumor suppressor gene on chromosome 2 →

37
 ▪ Colon cancer +
▪ Extracolonic cancers: Endometrial & Ovary & Breast & Thyroid & Urothelial carcinoma.
Peutz-jeghers syndrome: Mutation in STK11/LKB tumor suppressor gene on chromosome 19 →
▪ GI hamartomatous polyps.
▪ Melanosis.
▪ Stomach & Duodenum & Pancreas & Colon & Breast.
Hereditary diffuse gastric cancer syndrome: Mutation in CDH1 E Cadherin tumor suppressor gene on
chromosome 16 →
▪ Diffuse gastric cancer at young age.
▪ 40% risk of breast ILC at advanced age.
➢ Moderate penetrance genes:
ATM (Ataxia Telangiectasia Mutation) →
▪ BC.
▪ Leukemia.
▪ Lymphoma.
▪ Cerebral ataxia.

NF1 mutation.
CHEK2 mutation.
PALB2 mutation.
Mouse mammary tumor Virus: transmitted via milk.
B.Familial:
➢ Greater risk if →
▪ 1st degree relative: mother 3 times & sister 2 times.
▪ 2nd degree relative.
➢ Due to either:
▪ Unknown gene mutation or
▪ Geographic factor.

38
 2. Geographic Factors:
▪ Common in Western Europe & USA.
▪ Uncommon in Asia & Japan.
3. Hormonal: High estrogen →
▪ Spinster.
▪ Nullipara.
▪ Early menarche.
▪ Non-lactating.
▪ Late menopause.

4. Radiation exposure:
▪ Nuclear war.
▪ Medicine.
5. Drugs:
▪ CPs > 10 y.
▪ Postmenopausal combined HRT.
6. Dietary factors:
▪ Obesity: fat metabolizes adrenal DHEA to E2 & E1.
▪ Diet rich in saturated FA.
▪ Alcohol & Smoking.
7. Diseases:
▪ Past history of breast cancer (6 times).
▪ Past history of Bg proliferative diseases.
➢ Precancerous lesions:
1. Slight high risk (< 2 folds):
▪ Flat epithelial atypia.
▪ Papillary breast lesions.
2. Slight high risk (2 folds): (MDH RCS)
• Macrocyst.
• Moderate & Florid hyperplasia • High density.
• Duct papilloma.
• Radial scar.
• Complex fibroadenoma.
• Sclerosing adenosis

39
 3. Moderate high risk (4-5 folds):
▪ ADH.
▪ ALH.
4. Marked high risk (10 folds):
▪ LCIS.
❖ Pathology:
➢ Site:
• UOQ: 60% due to high glandular tissue.
• RA 12%.
• LOQ 10%.
• UIQ 12%.
• LIQ 6%.
➢ Modified Foote & Stewart classification:
1) Ductal origin:
A. Non infiltrating: DCIS.
B. Infiltrating: IDC.
➢ NOS:
▪ Scirrhous.
▪ Atrophic scirrhous.
➢ Specified: (MMTP)
• Medullary (Encephaloid).
• Mucinous (Colloid).
• Tubular.
• Papillary.
2) Lobular origin:
A: Non infiltrating: LCIS.
B: Infiltrating: ILC.
3) Paget disease of breast: +/- mass.
4) Rare types: (NSMA)
➢ NET = Neuroendocrinal Tumor.
➢ Signet ring carcinoma.
➢ Sweat gland carcinoma.
➢ Metaplastic carcinoma = Glandular (IDC) + Non-glandular element that may be:
▪ Squamous element → Squamous metaplastic carcinoma like SCC.

40
 ▪ Spindle cell & Cartilage & Bone & Muscle & Fat & Vascular element → Heterologous metaplastic
carcinoma.
▪ Poorly differentiated element → Carcinosarcoma.
▪ Rapidly growing & Well circumscribed & Firm & Variable sizes & Central degeneration & necrosis.
➢ Adenoid cystic carcinoma:
▪ Perineural spread.
▪ Common TNBC.
▪ Good prognosis.
➢ Apocrine carcinoma.
❖ WHO classification 5th edition 2019:
A. Insitu carcinoma:
➢ DCIS (low & intermediate & high grade).
➢ Insitu papillary neoplasms:
• Papillary DCIS.
• Encapsulated papillary CIS.
• Solid papillary CIS
B. Invasive carcinoma: (ITC NSMA)
➢ IDC of NST = NOS.
➢ ILC.
➢ Invasive papillary carcinoma:
▪ Micropapillary.
▪ Encapsulated.
▪ Solid (low - intermediate grade).
➢ Tubular carcinoma.
➢ Tall cell carcinoma with reversed polarity.
➢ Cribriform carcinoma.
➢ NET & NEC.
➢ Salivary gland adenocarcinoma:
• Acinic cell.
• Adenoid cystic.
• Secretory.
• Mucoepidermoid.
➢ Microinvasive carcinoma.
➢ Mucinous:
▪ Mucinous carcinoma.

41
 ▪ Mucinous cystadenocarcinoma.
➢ Metaplastic carcinoma:
▪ Spindle cell.
▪ Squamous.
▪ Heterologous differentiation.
▪ Low grade adeno-squamous carcinoma.
▪ Low grade fibromatosis like.
▪ Mixed metaplastic.
❖ Papillary breast tumors:
▪ Intraductal papilloma.
▪ Atypical papilloma.
▪ Papilloma with DCIS.
▪ Insitu papillary tumors.
▪ Invasive papillary carcinoma.

❖ Micropapillary carcinoma:
▪ Poor prognosis.
▪ ER +ve.
▪ LVI +ve.
▪ LN metastasis.
▪ Extensive intraduct component
❖ The 5 favourable histologic types:
▪ Tubular carcinoma.
▪ Cribriform carcinoma.
▪ Mucinous carcinoma.
▪ low grade adeno-squamous carcinoma.
▪ low grade fibromatosis like.

42
 Non-infiltrating carcinoma
LCIS = Lobular carcinoma in situ
❖ Pathologic marker of high risk of BC:
➢ Either in ipsilateral or contralateral breast.
➢ Either ILC or IDC.
❖ Pleomorphic LCIS is more prone to progress to ILC in 30% of cases.
❖ Usually ER, PR +ve.
❖ Difference between DCIS & LCIS

DCIS LCIS
palpable mass & pain & nipple
Non palpable mass.
C/P:
discharge.

diffuse.
Distribution localized

Papillary growth within No

Yes
lumen of TDLU
Association with
inflammatory reaction
& stromal response & Yes No
lymphoid infiltration
surrounding TDLU
E-cadherin. +ve -ve

Multifocality Rare Common

43
 LIN= Lobular Intraepithelial Neoplasm.
❖ Tavassoli classification:
➢ LIN1: ALH = No complete replacement of lobular unit.
➢ LIN2: LCIS.
➢ LIN3:
▪ Pleomorphic LCIS.
▪ LCIS + necrosis.
❖ TTT:
➢ Surgical excision without safety margin.
➢ Value:
▪ to exclude occult invasive carcinoma.
▪ to decrease incidence of local recurrence in pleomorphic variant.
➢ Pleomorphic LCIS:
▪ Better removed with safety margin ,but unfortunately this may → high mastectomy rate (controversial).
▪ RT after CBS: not indicated.
➢ Risk reduction:
1. Change life style: ABC PEM
▪ Avoiding COCs.
▪ Avoiding HRT.
▪ Avoiding alcohol.
▪ Breast feeding.
▪ Ca & vitamin D.
▪ Consuming low-fat diet & dairy products.
▪ Consuming fruits & vegetables.
▪ Pregnancy before 25 y or multiple pregnancies.
▪ Exercise.
▪ Maintaining healthy body weight
2. Close BB FU by triple assessment.
3. Chemoprevention:
➢ Indications:
▪ LCIS & ALH & ADH.
▪ Strong FH of BC even without BRCA1 or BRCA2 mutation.
▪ BRCA1 or BRCA2 mutation.
➢ Effect: not as effective as risk reducing surgery.
➢ Lines:

44
 ▪ If HR +ve:
- Premenopausal: Tamoxifen.
- Postmenopausal: Tamoxifen or Raloxifene or AIs.
▪ If ER -ve: Retinoids & PARP inhibitors & TKIs.
4. Prophylactic Surgery:
➢ Bilateral mastectomy:
▪ Types: Simple & SSM & ASM.
▪ Indication: only if life expectancy > 10 y.
▪ Value: decreases risk of BC by 90%.
➢ Bilateral RRSOP:
▪ Limited to those with BRCA 1/2 + should be sent to pathology.
▪ Decreases risk of breast cancer by 50% & ovarian cancer by 85%.
▪ Can be delayed for BRCA2 because of delayed onset of ovarian cancer.
▪ Salpingectomy + delayed oophorectomy may be considered, but not standard.

45
 DCIS = Ductal Carcinoma Insitu
❖ Incidence:
➢ Widespread use of screening mammography → 10-fold increase in incidence of DCIS since 1980s.
➢ > 25 % of all new cases of breast cancer.
➢ Diagnosis of DCIS peaks between 60 & 74 y earlier than for IDC.
➢ Diagnosis of which peaks between 75 & 79 y.
❖ Risk factors:
➢ As IDC, but OCPs do not appear to increase risk of DCIS.
❖ Difference between DCIS & LCIS: see table.
❖ M/E:
➢ Classification:
1) Comedo (more anaplastic):
▪ Ducts are expanded by malignant cells, which undergo central necrosis leading to extrusion of sebaceous-
like material from cut surface of tumor (cancer juice).
2) Non-comedo:
▪ Solid.
▪ Cribriform.
▪ Micropapillary.
▪ Papillary
❖ Classification based on nuclear grade:
➢ High.
➢ Intermediate.
➢ Low.
❖ Van Nuys classification (most useful):
➢ Grade I: Non-High grade + No Comedo.
➢ Grade II: Non-High grade + Comedo.
➢ Grade III: High grade +/- Comedo.
❖ Van Nuys/USC scoring system for recurrence risk = Age + Size + Grade + Margin = 4-12
Age score Size score Grade score Margin score

1 > 60 < 15 mm I 1 cm
2 40-60 16 – 40 mm II 1 mm – 9 mm
3 < 40 > 40 mm III < 1 mm

46
❖ C/P:
➢ Palpable mass: the most commonly found.
➢ Accidentally discovered on routine screening mammography.
➢ May be found incidentally in otherwise Bg breast biopsy specimen.
➢ Paget disease of nipple.
➢ Nipple thickening.
➢ Nipple discharge.
➢ Clinically occult DCIS is more likely diagnosed With screening mammography.
❖ Investigations:
1. Rad:
A. BBMM:
➢ The gold standard for radiographic evaluation of DCIS.
➢ Findings:
• Microcalcification: the commonest mammographic finding in DCIS.
• Soft tissue density/asymmetry.
• Both.
➢ Microcalcifications are divided into 2 classes in case of architectural type of DCIS:
- Linear branching type: more with high grade comedo type.
- Fine granular type: more with micropapillary & cribriform & low grade without necrosis.
➢ Disadvantages:
• It can significantly underestimate pathological extent of disease in micropapillary DCIS.
• Pathologic lesions > 2 cm than by Mammographic estimation occurs in about 40 % of micropapillary DCIS
& 10% of pure comedo DCIS.
Microcalcifications:
➢ Incidence:
• More in older patients: the number of microcalcification clusters increases with age increases.
• Affected by epithelial-mesenchymal transition cell necrosis and debris.
➢ Risk:
• There is association between microcalcifications found during mammographic screening and risk of breast
cancer → 3 folds increased risk of breast cancer regardless of menopausal status and breast density.
• Risk increases when combined with breast density
• Although breast density and breast microcalcification are independently associated with breast cancer, the
relationship between these two factors and age is the opposite. Both microcalcification and higher breast
density categories increased breast cancer risk.

47
 • Potential surrogate for breast cancer recurrence.
• Prognostic marker for residual disease after excision.
• Women with microcalcification and BIRADS 4 had an approximately 6 folds higher risk of breast cancer.
• As number of microcalcification clusters increases → Risk of invasive BC & DCIS likewise increases.
• 3 or more microcalcification clusters → higher premenopausal breast cancer risk than postmenopausal
with similar HRs.
• A recent Swedish population study indicated that microcalcification clusters can be observed as a
complementary risk indicator of breast cancer.
➢ Risk factors for microcalcification clusters:
• Older age.
• Breast density.
• Genetic predictors of breast cancer.
• > 2 children.
• Long breastfeeding periods.
➢ Protection = -ve association with microcalcification clusters:
• BMI.
• Smoking.
• Alcohol consumption.
• Protective effect of estrogen.
➢ Precautions:
• Breast density & presence of microcalcification & BI-RADS classification should be read by single
radiologist at each center.
• Age-dependent prevalence of microcalcification clusters could be explained by effect of normal aging
due to epithelial-mesenchymal transition over age.
• It is unclear whether microcalcification is a risk factor for benign breast diseases, breast cancer or an
early detection marker for these diseases.

Calcifications seen in DCIS

48
 B. MRI:
➢ Not routinely done in preoperative evaluation of DCIS.
➢ Indications:
• High risk DCIS as high grade or comedo.
• High dense breast in aim for BCS.
➢ Disadvantages:
• Breast MRI likely leads to overtreatment.
• Cost & limited accessibility → less feasible as screening method.
2. Biopsy:
➢ DCIS diagnosed in screening programs are usually impalpable.
➢ Methods of biopsy: ‫مهم‬
• Mammographic stereotactic guided needle biopsy with self retaining hook wire localization.
• US guided needle biopsy with wire localization or radioactive seeds insertion.
• Charcoal localization followed by excision biopsy.
• VABB = Vacuum assisted breast biopsy: systems as Mammotome are the method of choice according to
European guidelines.
• BLES = Breast lesion excision system: Recent & completely excise subcentimetric lesions.
➢ Percutaneous image guided breast biopsy specimens represent only sample of abnormality observed on
mammography: may be with sampling error.
➢ Invasive carcinoma is detected upon lumpectomy in 10–20 % of cases in whom DCIS diagnosed by stereotactic
biopsy.
➢ DCIS is diagnosed upon excision biopsy in 10–30% of cases with ADH or Radial scar on stereotactic biopsy.
➢ If CNB results discordant with Rad findings → Repeat image guided biopsy.
➢ HR status testing:
• Knowing HER 2 status in DCIS not alter management plan + not needed.
❖ TTT:
1. Surgery:
A. CBS:
➢ Indications: as invasive BC.
➢ Contraindications: as invasive BC.
➢ WLE with SM at least 2 mm.
• Margins < 1 mm may be accepted in selected cases if R.th is planned.
• Preoperative image-guided localization either wire or radioactive seeds as it is usually nonpalpable.

49
 • If extensive calcifications → Bracketing with 2 or more wires or seeds to assist excision of all suspicious
microcalcifications.
➢ Specimen radiography: to confirm removal of both marking clip & all suspicious microcalcifications.
C. Mastectomy +/- immediate reconstruction.

2. Adjuvant ttt:
A. RT:
➢ Indications: only in BCS.
➢ WBRT = Whole breast RT: reduce risk of ipsilateral recurrence risk 50-70%.
➢ APBI = Accelerated Partial breast irradiation in cases fulfilling RTOG 9804 trial criteria:
• Screening detected DCIS.
• Low to intermediate nuclear grade.
• Tumor size <2.5 cm.
• Surgical resection free margin >3 mm.
➢ RT can be omitted in selected low-risk cases:
• Small <1 cm tumor size.
• Low-grade tumors excised with margins of at least 5 mm.
• ER+ve tumors that can be observed diligently for recurrence.
B. Endocrine ttt:
➢ Indications: ER +ve tumors underwent BCS as risk reducing therapy for ipsilateral & contralateral breast.
➢ Duration: 5 y.
➢ Drugs:
• Tamoxifen: the Main.
• AIs considered in postmenopausal <60 y old ,especially if at risk of embolism.
➢ Efficacy: No evidence of improved survival.
3. Axillary management:
A. No axillary staging:
➢ if microinvasion or frank invasion identified on final pathology after BCS → return to OT for SLNB or
B. SLNB:
➢ Indications:
• If treated with mastectomy.
• If excision in anatomic sites compromising performance of future SLNB.
➢ Results:
• +ve in about 12% of high risk DCIS.
• +ve in about 10% of DCIS with microinvasion.

50
❖ FU: NCCN ttt guidelines recommend →
➢ Annual BBMM after BCS +/- R.th +/- endocrine ttt.
➢ Annual physical exam after mastectomy.
➢ Monitoring for development of new 1ry cancers in contralateral breast.
❖ Microinvasive DCIS (DCISM):
➢ 5–10% of DCIS.
➢ Higher incidence if:
• Size: >2.5 cm (29%). • DCIS presents as palpable mass or nipple
• Grade: High. discharge.
• Type: Comedo.
➢ Can metastasize to Ax LNs or distant sites.
➢ Axillary staging is indicated in multifocal microinvasion.
❖ Local relapse:
➢ Predictors of local relapse (not contraindications for BCS): ‫مهم‬
▪ Size: >3 cm. ▪ Age < 50 y.
▪ Grade: High. ▪ FH of BC.
▪ Type: Comedo. ▪ Past history of BC
▪ Margins: +ve.
➢ Management depends on ttt that patient received for 1ry cancer.
• If BCS without RT → Re-excision to -ve margins + PORT.
• If BCS with RT → Mastectomy.
• If local recurrence after mastectomy → WLE + RT.
• If tissue coverage is a concern → tissue transfer techniques as LDF

51
 Paget disease of breast
❖ Theories:
➢ Epidermotropic theory: Breast DCIS in which mg cells migrate →
• towards skin: NAC erosion.
• towards breast parenchyma: mass simulating scirrhous carcinoma.
➢ In situ transformation theory:
• Paget cell is transformed Mg keratinocyte.
• Paget disease is independent skin CIS.
❖ Paget cell: large cell with clear cytoplasm (clear halo) & eccentric hyperchromic nuclei found throughout the
epidermis.
❖ DD: Paget disease (Mg eczema) should be differentiated from ordinary eczema (dermatitis).

Mg eczema Ordinary eczema

Age Old Young

Side Unilateral Bilateral
Itching & Vesicles & Oozing No Yes
Edge Well defined Ill defined
Erosion of NAC Yes No
Palpable mass +/- No
Response to steroids No Yes

❖ TTT of Paget disease without mass:

➢ Surgical:
• NACectomy with 2 mm SM or
• Simple mastectomy +/- SLNB.
➢ PORT after WLE.
➢ Tamoxifen if ER +ve.

52
 Infiltrating carcinoma
❖ Pathology
IDC NOS Medullary Mucinous &Tubular Papillary ILC

Age 40-60 y < 40 y Elderly elderly elderly

Small & hard &

irregular & flat
undersurface & fixed.
➢ C/S: large & soft & irregular.
- Gritty & ➢ C/S: if lactiferous duct is
ill defined
- Chalky white & - Soft (brain like) opened → pedicle
difficult to recognize
yellow streaks & arising from duct wall &
clinically &
N/E extending into - Greyish & soft & well-defined small finger like
mammographically as it
surrounding - Non-capsulated processes passing to
grows as Indian file
parenchyma. - Bulge (convex) smaller ducts which are
pattern.
- Non-capsulated & areas of Hge dilated
- Retract & necrosis .
(concave) due to
pull of fibrous
tissue.

53
 Classical pattern: grows
as single linear file of
small mg cells that are
Large masses of highly * Mucinous: lakes of
arranged
Small masses of mg mg spheroidal cells mucin extracellular:
Fibrovascular CT core circumferentially around
spheroidal cells arranged arranged in pseudo- intra-acinar & between
with finger like ducts & lobules (Indian
in irregular groups acinus form separated acini & intracellular.
M/E processes covered by Files pattern)
separated by dense by scanty stroma & * Tubular: well- diff
several layers of mg Variants: small mg cells
fibrous tissue & Hge & minimal vascularity & tubules in > 75% of
columnar cells. arranged in solid &
necrosis. lymphocytic infiltration. tumor lined with mg
alveolar & tubular &
cells.
mixed pattern.
IHC: loss of E-cadherin
adhesive molecule.
HR Usually TNBC Usually TNBC Usually ER +ve
The best due to early Good due to
presentation & late Better prognosis than early presentation by Better prognosis than
Bad
Prognosis spread & lymphocytic NOS Bleeding & slow growth NOS
infiltration & young age & late spread

54
❖ Molecular types:
➢ Luminal A:
• ER & PR +ve and
• HER2neu -ve and
• Ki67 < 14%.
➢ Luminal B:
• ER +/- PR +ve and
• HER2neu +ve or
• Ki67 > 14%.
➢ HER2 enriched:
• ER & PR -ve.
• HER2neu +ve.
➢ TNBC:
• ER & PR & HER2neu -ve.
➢ Basal like BC:
• Carries molecular features like basal/myoepithelial cells of breast.
• TNBC may be basal like.
• Classification: Basal A & Basal B.
• = Most BRCA1 or claudin low variant.
• Not all TNBC is basal like BC.
➢ Quadruple -ve BC:
• TNBC + -ve Androgen Receptor (AR -ve).
• Worse prognosis as AR play synergistic action with ER/PR.
• AR acts as possible target for hormonal ttt.

55
 ❖ Spread:
1) Direct:
➢ Intrinsic: to surrounding breast tissue
▪ Infiltration of Cooper ligament: skin tethering & fixation.
▪ Infiltration of ducts with fibrosis: nipple retraction & deviation.
➢ Extrinsic:
▪ To skin → ulceration & fungation (late).
▪ To deep structures: pectoral fascia & muscles & serratus anterior.
2) Lymphatic: by embolization & permeation.
3) Blood:
➢ Bone:
▪ The commonest.
▪ Esp Luminal.
▪ 90% osteolytic.
▪ Lumbar vertebrae > neck of femur > thoracic vertebrae > skull.
▪ Lumbar vertebrae common due to free communication between posterior intercostal veins + Vertebral
Batson venous plexus.
➢ Lung & Liver: Esp HER2 +ve.
➢ Brain: Esp TNBC.
4) Transperitoneal:
➢ More with ILC.
➢ PONA:
▪ Peritoneal nodules.
▪ Ovarian deposits.
▪ Nodules in DP = Rectal Plummer shelf.
▪ Ascites.
➢ Krukenberg tumour is term originally designed for ovarian mets from GIT malignancies.
❖ Staging:
1. Prognostic staging = TNM + Grade + Molecular type.
2. Anatomical staging:
A. TNM Staging:
➢ T:
▪ TX: 1ry tumor can’t be assessed (previously removed).
▪ T0: No evidence of 1ry tumor.

56
 ▪ TIS: CIS = DCIS + Paget disease without mass. (Paget disease with mass is classified according to mass
size)
▪ T1: < 2cm.
o T1mic: < ,1 cm. (Micro invasive BC)
o T1a: ,1 - ,5 cm.
o T1b: .5 - 1 cm.
o T1c: 1 - 2 cm.
▪ T2: 2 - 5 cm.
▪ T3: > 5 cm.
▪ T4:
o T4a: Chest wall involvement not including pectoralis ms.
o T4b: Skin involvement (Ulceration & Peau d’ orange >1/3 of breast & Satellite nodules).
o T4c: a + b.
o T4d: Inflammatory BC.
➢ N:
▪ Nx: Regional LNs can’t be assessed (previously removed).
▪ N0: No regional LNs mets.
▪ N1: Mobile ipsilat Ax LNs.
▪ N2:
o a: Fixed ipsilat Ax LNs.
o b: Clinically apparent internal mammary LNs without Ax LNs.
▪ N3:
o a: Ipsilat infraclavic LNs.
o b: Clinically apparent internal mammary LNs with Ax LNs.
o c: Ipsilat supraclavic LNs
➢ M:
▪ M0: No evidence of Mets.
▪ M1: Distant Mets.
B. Pathological nodal staging (pN):
➢ pNx: Regional LNs can’t be assessed.
➢ pN0: No regional LNs mets histologically.
➢ pN1: +ve 1-3 Ax LNs.
➢ pN2: +ve 4-9 Ax LNs.
➢ pN3: +ve > 10 Ax LNs or ipsilateral infraclavicular or supraclavicular LNs.
C. Manchester staging system:

57
➢ Stage 1: Tumor confined to breast.
➢ Stage 2: Tumor confined to breast + palpable & mobile Ax LNs.
➢ Stage 3: Tumor extends beyond breast:
• 3a: skin invasion or ulceration or fixation over area large in relation to breast size.
• 3b: tumor fixation to underlying muscle or fascia + mobile Ax LNs.
➢ Stage 4: Tumor extends beyond breast:
• fixed or matted of Ax LNs.
• fixation of tumor to chest wall.
• supraclavicular LN mets.
• opposite breast deposits.
• distant mets.
D. Stages:
➢ Stage 0: CIS.
➢ Stage I,II: Early BC.
➢ Stage III: Locally advanced BC.
➢ Stage IV: Metastatic BC.
Stage 0 Tis

Stage I T1N0 M0
T0N1M0
IIA T1N1M0
Stage II T2N0M0
T2N1M0
IIB
T3N0M0
Stage III IIA T0 N2 M0

T1 N2 M0
T2 N2 M0
IIIB
T3 N1-2 M0
Stage IV
T4 N0-2 M0
IIIC Any T N3 M0
Any T any N and M1

58
59
❖ Complications:
➢ Skin ulceration & fungation.
➢ Infection & Hge.
➢ Lymphedema of arm (brawny arm):
o Extensive lymphatic infiltration of Ax LNs.
o Surgical Ax clearance.
➢ Infiltration of surroundings:
o Intercostal muscles & serratus anterior.
o Intercostal nerves → pain.
o Intercostal veins to vertebral Batson plexus → vertebral mets.
o Pleura: Mg effusion.
➢ Distant mets. (BLBL)
o Bone: pain & pathological fracture.
o Lung: pain & cough & hemoptysis.
o Brain: manifestations of high ICT.
o Liver: pain & mass & jaundice.
❖ C/P (symptoms & signs)
➢ Symptoms:
▪ Asymptomatic: detected by screening.
▪ Painless breast mass:
- The commonest presentation.
- commonly discovered accidentally.
▪ Ax mass either from:
- Axillary tail of spense.
- Accessory breast.
- Heterotopic breast tissue in axillary LNs.
▪ Pain:
- Rare 10%.
- Late.
- Due to nerve infiltration or mastitis carcinomatosis.
▪ Nipple discharge:
- Bloody in duct carcinoma.
- Pasty like in comedo carcinoma.
- Necrotic in degenerating carcinoma.
▪ * Skin & Nipple manifestations.

60
 ▪ Occult carcinoma: Enlarged Ax LNs without breast mass.
▪ Complications.
➢ Signs:
▪ General: (ABC)
o Anaemia.
o Bone:
- Tender on percussion &
- Swelling &
- Pathological fracture.
o Cachexia.
o Chest: pleural effusion.
▪ Abdominal:
o Periumbilical Sister-Josef nodules.
o Hepatomegaly & ascites.
▪ Local:
o Breast compared to healthy side:
- Smaller & Higher.
- Protrude to lesser extent on leaning forward.
- Ascend to higher level on raising arm up.
o Nipple & areola: (7D)
- Deviation.
- Displacement.
- Depression.
- Destruction.
- Discharge.
- Discoloration.
- Dermatitis.
o Mass: (S CTEM)
- Surface: Irregular & Flat posterior surface due to easy anterior invasion.
- Consistency: Hard.
- Tenderness: No.
- Edge: iIl defined late.
- Mobility: Fixed late.
o Ax LNs:
- Hard

61
 - Fixed late.
- May be associated with Supraclav LNs.
o Skin manifestations:
I. Due to direct infiltration:
a) Skin Dimpling & Tethering & Puckering:
• Earliest sign.
• Not pathognomonic.
- Dimpling: pulling of skin at 1 point due to complete infiltration of single Cooper ligament.
- Tethering: Induced dimpling if leaning forward or arm elevation due to partial infiltration of
single Cooper ligament.
- Puckering (Marked dimpling) Pulling of skin at > 1 point due to complete infiltration of multiple
Cooper ligaments.
b) Skin fixation: The mass can’t be moved without moving skin due to direct skin infiltration.
c) Skin ulceration & fungation.
d) Nipple retraction: Due to infiltration & duct.
e) Paget disease of breast.

II. Due to lymphatic involvement:

a) Peau d’orange:
▪ Not pathognomonic.
▪ Non pitting edema pitted at sites of hair follicles due to skin lymphatic tumor compression (not
permeation).
b) Satellite nodules:
▪ Late sign.
▪ Pathognomonic.
▪ Appear away from mother carcinoma.
▪ Separated from each other by healthy skin.
▪ Due to skin lymphatic tumor permeation.
c) Cancer en cuirasse:
▪ Very late sign.
▪ Pathognomonic.
▪ Skin: very thick & hard & stretched & leathery & indurated & metallic & brownish simulating
shield of wars.
▪ Involve breast + chest wall + back.
▪ Due to extensive skin lymphatic tumor permeation.

62
 d) Mastitis carcinomatosis: Due to dermal lymphatic tumor embolization.
e) UL: Mg edema (Brawny arm).

III. Due to venous involvement:

a) Dilated veins: Due to venous obstruction.
❖ Investigations:
A. For diagnosis: (Triple assessment)
❖ Clinical.
❖ Rad:
1. Soft tissue mammography:
➢ Nature: low voltage high amplitude X-ray.
➢ Views: Craniocaudal & Mediolateral & Oblique.
➢ Dose: 0.1 cGy (1cGy = 1 rad) (Normal CXR deliver 25% of this dose).
➢ Value:
o Screening.
o Detection of small subclinical tumor esp in large breast.
o Detection of occult BC.
o Detection of tumor size which is < clinical size due to immune reaction (lymphocytic infiltration) Le
Borgne’s law.
o Detection of Multiplicity:
- Multicentric: > 1 tumor in separate quadrants or > 5 cm away from each others.
- Multifocal: > 1 tumor in same quadrant.
- Tumor is staged by largest mass ,not by total tumor volume.
o Detection of Bilaterality:
- Synchronous Bilat BC: 1%
- Metachronous Bilat BC: 5% & in ILC: 30-50%.
o Diff between Bg & Mg masses.
o Preoperative localization of impalpable mass with stereotaxis.
o Postoperative BB FU in BCS cases.
➢ Disadvantages of Mammogram:
• Can’t differentiate fibrosis from recurrence ,especially if reconstructed breast.
• Can’t be done during pregnancy.
• Can’t be done < 30 y & Less accurate in young patients.
• Less accurate in dense breasts.

63
➢ New Mammography modalities:
• Digital mammography: has replaced conventional one.
• DBT = Tomosynthesis Mammography: more used now & higher radiation dose.
• Contrast enhanced Mammography.
• PEM = FDG PET Mammography: may replace the need for SLNB in LN -ve BC.

64
65
 ➢ Mammographic features of:
• DCIS: Microcalcification is the commonest mammographic feature:
- Linear branching in comedo lesions.
- Fine granular in non-comedo lesions.
• LCIS: area of parenchymal distortion.
• IBC:

Mg Bg

Irregular speculated
Smooth border.
Heterogenous.
Homogenous.
Opaque.
Macro or
Microcalcifications:
microcalcifications.
Clustered.
Scattered (punctuate).
1ry signs More in centre & periphery.
Widespread.
Unequal size.
Pleomorphic
Uniform size.
Linear, branching in duct carcinoma.
Monomorphic:
Coarse granular type & regular outline in
Rounded or crescentic (tea-cupping)
medullary carcinoma.
Disturbed architecture. Preserved.
Prominent vascular system. Normal.
Prominent duct system. Normal.
2ry signs
Perifocal haziness. Rare.
Nipple retraction. No.
Skin thickened due to edema. No.

2. US:
➢ 5-20 MHz.
➢ Values:
• Localizes masses in dense & pregnant breasts.
• Differentiates between solid & cystic swellings.
• Detects enlarged Ax LNs.
• US guided CNB.
• US Complementary to BBMM.

66
➢ Sonomammography: BIRADs = Breast imaging reporting and data system:

➢ BIRADS classification of mammography abnormalities:

• I. Normal: continue routine screening.
• II. Bg: continue routine screening.
• III: Probably benign: FU/6 M imaging.
• IV: Suspicious: biopsy.
• V: Highly suggestive of Mg: biopsy
• VI: pathologically proven BC.
➢ US varieties:
• Elastography: delineate BIRADS 3 lesions.
• Automated Breast US: decrease operator dependent errors.
• 3D US: accurate tumor dimensions.
3. MRI:
➢ Good data.
➢ Expensive.
➢ Types:
• Contrast enhanced. • Diffusion weighed.
• MRI spectroscopy.
➢ Indications: (OIL & FS & 2E)
• Occult BC. • Implant imaging.
• ILC to detect occult focus up to 7%.
• FU of BCS or reconstruction to differentiate fibrosis from recurrence.
• Screening in known gene mutations at early age and in extremely dense breasts.
• Evaluating tumor response to NAT in selected cases.

67
❖ Pathological: (The most important single diagnostic tool)
A. Cytology:
▪ Exfoliative cytology for nipple discharge: low yield.
▪ Scrape cytology: rapid & non-invasive & reliable for Paget’s disease.
B. Biopsy:
➢ For impalpable lesions: see DCIS.
➢ For palpable lesions:
• Surgical biopsy:
o Incisional or Piece meal for: incompletely resectable tumor.
o Wedge: areolar skin in suspicious Paget disease.
o Excisional for: small suspicious mass either:
- Intraoperative Frozen section or touch imprint.
- PO Paraffin section.
• Needle biopsy:
o FNAC:
- Sizes: 21 gauge (green) or 23 gauge (blue) & syringes at least 10 ml (for adequate suction).
- Use either too & fro technique from 2 sites or fan shape method.
o CNB: sizes range from 14-18 gauge & NB: gauge number increase → diameter decrease.

FNAC CNB Surgical biopsy

simple & rapid & moderate & rapid &

Technique complex
outpatient clinic outpatient clinic
Cost cheap expensive more expensive
False +ve No No No
False –ve Yes rare very rare
Complications No some high
needs expert
Interpretation needs routine pathology
pathologist
IHC Difficult Easy Easier
Diff of CIS from IC
No Yes
& HR status test

68
❖ Hormonal receptor (HR) status:
➢ ER & PR.
➢ 70% of female BC are HR +ve.
➢ 80% of male BC are HR +ve.
➢ Occult BC: Examination of nodal tissue for HR to confirm breast 1ry tumor & BC can’t be excluded if nodal
tissue is HR-ve.
❖ Her2neu testing.
❖ Ki67 testing if adjuvant Abemaciclib.
❖ BRCA gene testing indications:
➢ FH of male BC.
➢ 1st degree relative with bilateral BC.
➢ 1st or 2nd degree relative with both BC & ovarian cancer at any age.
➢ 1st and 2nd degree relatives with BC and ovarian cancer.
➢ 2 1st degree relatives with BC & one diagnosed < 50 y.
➢ > 2 relatives (1st or 2nd) with ovarian cancer regardless of age.
➢ > 3 relatives (1st or 2nd) with BC regardless of age.
➢ Ashkenazi Jewish descent with 1 1st degree or 2 2nd degree relatives with BC or ovarian cancer.
➢ If patient has TNBC at any age or candidate for Olaparib.
B. Investigations for mets:
❖ Lab:
➢ Serum ALK phosphatase: routinely done.
➢ Tumor markers:
o CA 15-3 & CA 27-29 & CEA. o Prognostic rather than Diagnostic.
❖ Rad:
➢ Indications:
o S & S of mets disease.
o ALK phosphatase significantly elevated.
o > 4 +ve AX LNs. o Known metastatic BC.
➢ Include:
o Bone survey (plain X-ray): more specific in detecting bone mets.
o Bone scan (99T pyrophosphate): more sensitive in detecting bone mets.
o CT chest & abdomen & pelvis +/- MRI brain guided by symptoms.
o PET-CT scan
o 18f-fluroestradiol-PET/CT: new tracer for detecting mets in ER +ve BC (in trial).

69
❖ Testing for biomarkers associated with FDA approved target therapy:
➢ Only in recurrent unresectable or mets disease.
➢ For HR +ve & HER2 -ve BC:
o BRCA 1 & 2.
o NTRK fusion.
o MSI/dMMR.
o TMB-H.
o PIK3CA.
• For TNBC: PD-L1 expression.
C. Gene signatures for BC:
❖ Indicated for:
➢ LN -ve & luminal A & non-favourable histology >0.5 cm to determine candidates for adjuvant chemo.
➢ Only 3-5% are benefiting from chemo & the rest are overtreated.
❖ Examples;
➢ Oncotype DX: analyses panel of 21 gene assay within tumor to determine recurrence score (0-100) =
likelihood of BC recurrence within 10 y of initial diagnosis.
➢ MammaPrint test: analyses panel of 70 gene assay & alternative to Oncotype DX.
➢ ProSigna (PAM50).
➢ Rotterdam (76 genes).
➢ Genomic Grade Index.
➢ Breast Cancer Index.
➢ Endopredict & NanoString nCounter Dx.

70
❖ DD:
➢ Mass: from other causes of hard breast mass.
➢ Nipple discharge: from other causes of nipple discharge.
➢ Nipple retraction: from other causes of nipple retraction.
➢ Mastitis carcinomatosis from acute breast abscess:

Mastitis carcinomatosis Acute breast abscess

History
Onset Gradual Acute
Course Slowly progressive Rapidly progressive
Fever Low grade High grade
Examination:
Inspection
> 1/3 of breast. Sector of breast
Edema
Dusky red & dilated veins Firely red
Skin over
Mild Marked
Palpation
Non pitting Pitting
Tenderness
Not tender & Hard Tender & Firm
Edema
Axillary LNs
leukocytosis No Yes
No response to antibiotic during
Cured or
TTT 1st W +
Form abscess.
Biopsy should be done

71
 TTT of breast cancer:
Non-metastatic BC (Stage I-III) = (NAT & Locoregional ttt)
1) NAT:
➢ = Primary systemic ttt (PST).
➢ Today is established ttt strategy in early BC in up to 20% of patients.
➢ Rationale:
• Early BC:
o Decreasing tumor size → increasing BCT rates.
o PST can reduce the extent of surgery and improve quality of life due to higher rates of breast- and axilla-
conserving surgeries.
o Decreasing micro-metastasis & altering tumor kinetics, but trials failed to demonstrate survival superiority
in comparison to adjuvant ttt.
o Nodal downstaging → reduce extent of axillary surgery.
o Important prognostic factor and a surrogate marker for OS at least for some intrinsic subtypes.
o In vivo evaluation of tumor resistance or sensitivity → provide opportunity to modify ttt if no response or
progression.
o May improve surgical decision making in suspected BRCA mutation carriage where delaying definitive
surgery during PST permits time for gene testing.
o The ability to assess efficacy of new chemo agents in clinical trials.
• LABC:
o Converting cases planned for MRM to cases who can undergo BCS (T3 & all T4).
o Rendering inoperable breast cancer (T4 & IBC) into operable.
➢ Disadvantages:
• Tumor downstaging may be inadequate to achieve preferred surgical therapy.
• Chemo-resistant tumors progress → rendering patients inoperable.
• Undertreatment locoregionally with RT if clinical stage is underestimated.
• Overtreatment locoregionally with RT if clinical stage is overestimated.
➢ Initial evaluation before NAT:
• Lab: Alk phosphatase.
• Rad: BBMM or BB MRI.
• Pathological: CNB.
• Staging & Mets work up.
• Biochemical markers: ER & PR & HER2 & Ki67%.
• Post-biopsy localization clip that can be detected post chemo & its location should be confirmed prior to
initiation of ttt.

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➢ Indications:
• Large tumor to breast size if desire BCS.
• cN+ve likely to become cN0 with NAT.
• Preferred for cT >2 cN >1 HER2 enriched & TNBC
• Considered for cT1 N0 HER2 enriched & TNBC.
• Cases in whom definitive surgery may be delayed.
➢ Candidates for NAT:
• IBC.
• Inoperable breast cancer.
• cT4 tumors.
• Bulky or matted cN2.
• cN3.
➢ Non candidates:
• Extensive insitu disease when extent of invasive carcinoma is not well defined.
• Non-palpable tumors.
➢ Therapeutic implications of breast surgery after PST:
• Randomized trials have shown equivalency between adjuvant and NAT in terms of DFS & OS.
• NSABP-B 18 trial: significantly higher rate of BCT was achieved for patients who underwent PST without
jeopardizing DFS or OS at FU of 15 y.
• Downstaging of axillary LNs status can be achieved in > 20% of patients according to early randomized trials
and may spare these women from full ALND; Today even higher rates of axillary downstaging are expected.
• Clinical response rates are achieved in up to 80% of patients treated with NACT.
➢ PCR
• = Absence of any residual cancer on evaluation of the breast specimen and all sampled ipsilateral LNs
following completion of PST.
• Associated with improved DFS & OS in some intrinsic subtypes of BC.
• New prognostic surrogate marker with high potential to tailor future loco-regional and systemic ttt decisions.
• The US FDA recently recommended PCR as an endpoint for accelerated approval of new drugs in NAT setting.
• Tumor biology is highly indicative of the response to PST:
o TNBC >> PCR rates up to 64%.
o ER-negative/HER2 +ve BC >> up to 76%.
o Luminal BC >> much lower response rates, even in +ve HER2 receptors.
o Add use of carboplatin or pertuzumab + transtuzumab in TNBC and HER2+ve BC >> improved PCR
compared to the standard regimen.

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➢ Lines of NAT:
1. NA hormonal therapy:
• Rationale:
o Decreasing tumor size to facilitate BCS in postmenopausal with HR +ve BC.
o As effective as NACT in downstaging tumors & increasing BCS rates in postmenopausal women.
o Relative lack of S/E & high potential for excellent tumor response.
o 1ry endocrine blockade acts as chemo-sparing ttt strategy.
• 3 M course in Luminal A.
• AIs superior to tamoxifen as regard tumor response & BCS rates: NA hormonal ttt with Anastrozole &
Letrozole for > 4 M → clinical response rates 55-98% & BCS rates 43-86%.
Fulvestrant = Pure estrogen antagonist as effective as Anastrazole in postmenopausal women with advanced
BC progressing after prior endocrine ttt.
2. NACT:
• 1st line ttt.
• Combination chemo.
• Preferred to complete the standard 6-8 cycles.
• If progressing after 3 cycles of 1st line (anthracycline based) → 2nd line (Taxane based) is used & surgery is
an option.
3. NA Trastuzumab with chemo in HER2 +ve → higher CPR rates as compared to
chemo alone.
4. NA Pembrolizumab with chemo in >T2N1 → high risk TNBC → higher CPR rates as
compared to chemo alone.

➢ Evaluation of response to NACT:

A. Clinical response:
• Detected with physical exam & imaging as physical exam alone is inaccurate.
• BBMM & BBUS & BB MRI used as adjuncts to increase accuracy.
• MRI is better for evaluating NACT response → detect angiogenic changes observed before reduction in tumor
size.
• CCR: complete resolution of all detectable disease.
• Clinical partial response: > 50% reduction in tumor size.
• Clinical progressive disease: > 50 % increase in tumor size.
B. Pathological response:
• Detected by surgical pathology.

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 • CPR: lack of invasive tumor in breast or LNs whereas residual in situ disease is allowed.
• Early response of 1ry tumor after 2 or 3 cycles of chemo is predictor of CPR.
➢ Discrepancy between clinical & pathologic responses:
• CCR: 36% & CPR: 26%.
• Breast tumors responses exhibit 2 patterns to NCT: Concentric decrease & Patchy regression.
• Intraductal tumors not responding to chemo
• Multiple microscopic residue areas can’t be observed via Rad assessment.
➢ Predictors of pattern of shrinkage (suggestive of scattering):
• Tumor >4 cm.
• Skin edema.
• LVI.
➢ Pathologic prognostic tools for evaluation:
• yP stage.
• Residual Cancer Burden (RCB).
• Miller Payne system.
• Neobioscore: nomogram incorporates clinical grade + pathologic grade + stage + HR status. in pre- and post-
neoadjuvant setting
➢ Shifting non-responders into responders:
• Degree of response; complete, partial or none; strongly related to OS & DFS & recurrence-free survival.
• 1ry tumor response has better prognosis than pathological LNs status.
• Clinically non-responders on 1st line chemo rendered responders by: increasing cycles +/- dose & shifting to
2nd line chemo & addition of Trastuzumab.

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76
 Locoregional ttt = (Surgical ttt + PORT + Systemic ttt)
❖ Surgical ttt:
1ry tumor:

BCS
➢ Indications:
• Single or multiple tumors in same quadrant.
• Tumor/breast size allowing acceptable cosmetic outcome.
• Large tumors after NAT.
➢ Contraindications: (if BCS → increase risk of LRR)

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• Absolute:
o IBC.
o Persistent +ve margins after reasonable surgical attempts.
o Diffuse microcalcifications on BBMM.
o Extensive associated DCIS.
o Pregnancy in 1st & early 2nd trimester as RT can’t be delivered.
o Homozygous for ATM mutation.
o Patient prefering mastectomy.
• Relative:
o Multicentric disease.
o Prior therapeutic chest RT as ttt of lymphoma due to high risk of RT related cancer after 2-3 decades.
o Hereditary BC due to mutation in BRCA1 & BRCA2 genes due to high risk of RT related cancer &
development of 2nd 1ry cancers.
o Collagen vascular diseases as scleroderma due to high RT toxicity.
o Li-Fraumeni syndrome.
o Extensive intraductal component: > 25% tumor is DCIS + additional separate focus DCIS due to
false -ve SM. (not considered as contraindication now).

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➢ Techniques:

Traditional approaches:
• WLE with pathological -ve SMs.
• Negative margin = No ink on tumor.
• Classification of margins:
o Negative: ≥2 mm width.
o Close: <2 mm width.
o Focally +ve: ≤4 mm length of tumor touching inked margin.
o Extensively +ve: >4 mm length.
• Incidence of residual disease after:
o Focally +ve SM not different from close margins.

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 o Extensively +ve SM: significantly higher.
• Quantifying extent of margin involvement in all pathology reports is recommended.
• No evidence indicates that more widely clear SMs reduce LRR in young or in unfavourable ILC with
extensive intraductal component.
• Safety margins:
o DCIS or DCIS with invasive focus < 1 mm → SM > 2 mm.
o If DCIS with invasive focus > 1 mm → SM width evaluated according to invasive focus.

OPS approaches:
❖ Definition: WLE of cancer + partial reconstruction of defect to maintain breast's shape & appearance.
❖ Techniques = Volume displacement + Volume replacement
5. Volume displacement:
Criteria Level I Level II

Maximum excision volume ratio 20% 20-50%

Requirement of skin excision for reshaping No Yes
Specific training in reduction mammoplasty
No Yes
techniques
Glandular characteristics Dense Dense or Fatty

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❖ Level I OPS
➢ Steps:
• Incision.
• Skin undermining
• NAC undermining
• Full thickness excision from SC fat down to pectoral fascia.
• Before closing defect → metal clips placed on edges of defect to guide PORT.
• Re-approximation of glandular defect.
• Crescent-shaped de-epithelization opposite tumor bed.
• NAC repositioning.
➢ OPS choice depends on:
• Tumor/Breast size ratio.
• Degree of ptosis: (modified Regnault ptosis scale)
o Grade I (mild ptosis): nipple is at level of IMF & higher than most of lower breast tissue.
o Grade II (moderate ptosis): nipple is located below IMF & higher than most of lower breast tissue.
o Grade III (advanced ptosis): nipple is below IMF & at level of maximum breast projection.
o Grade IV (severe ptosis): nipple is far below IMF & points toward floor.
o Pseudoptosis: nipple is either at or above IMF & lower 1/2 of breast sagging below IMF & Often seen
when stop nursing as milk glands atrophy → breast tissue sagging below IMF.

❖ OPS techniques according to tumor site:

➢ Lower pole location (5-7 O'clock):
• Superior pedicle reduction mammoplasty.
• Inferior crescentic mammoplasty.
➢ LIQ:
• Superior pedicle reduction mammoplasty.
• V-type mammoplasty.
• Thoraco-epigastric flap.
➢ UIQ:
• Medial mammopasty.
• Inferior pedicle reduction mammoplasty.
➢ Upper pole location (11-1 O'clock):

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 • Inferior pedicle reduction mammoplasty.
• Round block mammoplasty (Dounut mastopexy): for any periareolar tumors & mainly for upper pole
tumors.
• Horizontal mammoplasty (Batwing excision mastopexy).
➢ UOQ:
• Fusiform mammoplasty (Lateral mastoplasty).
• Matrix rotation flap.
• Inferior pedicle reduction mammoplasty.
➢ LOQ:
• Superior pedicle reduction mammoplasty.
• J-type (comma shape) mammoplasty.
➢ RA location:
• Modified inverted mammoplasty + NACectomy: similar to superior pedicle mammoplasty. The only
modification is the 2 vertical incisions encompass NAC removal together with tumor.
• Modified Lejour + NACectomy.
• J-type mammoplasty + NACectomy.
• Grisotti advancement rotation flap + NACectomy.
❖ Reduction mammoplasty:
➢ Types according to tumor site:
• Inferior pedicle.
• Superior pedicle.
• Medial pedicle.
• Lateral pedicles (Snowman technique). ‫خد بالك‬
• Bipedicled or Amputation mammoplasty + NAC grafting in huge breasts if distance from present to future
nipple position > 12 cm.
➢ Methods:
• Standard wise pattern (inverted T) or
• Vertical mammoplasty (Lejour/Lassus): avoid sub-mammary scar.
➢ General Rules for Pedicles mammoplasty:
• Base: 8-10 cm with length to base ratio 3 :1.
• Future areola marked by semi-circle with diameter up to 5 cm.
• Each pillar extending from future areola is at least 5 cm.
• Length of each of 2 arcs extending from pillars should be just > 1/2 of IMF (which is usually 20-24 cm).
• Nipple sensation is derived from anterior & lateral branches of 4th intercostal nerve.

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 6. Volume replacement = level III oncoplasty:
➢ Indications:
• Defect size: > 50% of breast volume.
• Defect site: central zone & lower pole & medial quadrants.
➢ Timing:
• Immediate.
• Delayed.
• Delayed immediate.
➢ Techniques:
A. Autologous tissue reconstruction:

1. Local flaps:
• Adipofascial flap.
• Breast sharing (myomammary flap from healthy side).
• Thoracic advancement flap.
2. MCFs = Myocutaneous flaps:
➢ LDF:
• Conventional.
• Mini LDF.
➢ TRAM:
• Bipedicled.
• Unipedicled.
• Supercharged. • Turbo.
• Free TRAM.
• DIEP.
• SIEP
3. Pedicled perforator flaps:
• TDAP flap.
• LICAP flap.
• LTAP flap.
• AICAP flap.
• SAAP flap.
• IMAP flap.
4. Free flaps transfers with microvascular anastomosis:
• Free gluteal flaps: superior & inferior gluteal artery free flap.
• ALT flap.
• Transverse rectus abdominis free flap.
• Latissmus dorsi free flap.

B. Prosthetic implants:

• Simple placement of sub-muscular gel implants

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 • Initial placement of sub-muscular expander followed at 2nd stage with permanent gel.
• Placement of permanent expansible implant.
C. Lipomodelling (NICE guidelines 2012):

• Use patient's own fat cells to replace volume after breast reconstruction or to fill defects after BCS.
• Used on its own or as adjunct to other reconstruction techniques.
• Source: commonly from abdomen & outer thigh & flank.
• Aim: restore breast volume & contour without morbidity of other reconstruction techniques.
• Procedure:
o Under general or local anaesthesia.
o Fat harvested by aspiration with syringe & cannula.
o Fat washed & centrifuged before injected into breast.
o 2-4 sessions.
• S/E:
o Up to 70% fat resorption common in 1st 6 M.
o May make future mammographic images difficult to interpret.
o Adipose tissue may be carcinogenic.
o Donor site morbidity as peritoneal perforation & bleeding).
o Recipient site morbidity: Bleeding & fat embolism.

Mastectomy
❖ Indications: Cases contraindicated for BCT.
❖ Techniques:
1. Extended radical:
➢ Urban = Radical + removal of supraclavicular LNs only.
➢ Iverson: Radical + removal of supraclavicular LNs + internal mammary LNs.
2. Super radical:
➢ As Iverson + removal of mediastinal LNs via thoracotomy.
3. Radical:
➢ Now only indicated if pectoralis muscles are directly infiltrated.
➢ Enbloc resection of whole breast tissue + overlying skin + pectoralis major & minor + axillary dissection (level
I, II, III).

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➢ Either:
• Halsted Op: breast removed including NAC ,then axilla or
• Meyer Op: axilla removed ,then breast removed including NAC.
4. MRM:
➢ lower morbidity with same survival rate as Halsted Op.
➢ Traditional incision: Steward or D incision.
➢ Patey operation: as radical + preservation of pectoralis major.
➢ Auchincloss operation:
• as radical mastectomy + preservation of pectoralis major & minor.
• Level III LNs not dissected.
• Dissection of Level III LNs not necessary for staging.
• If grossly involved LNs are identified intraoperatively → Do level III dissection to maximize local
control.
5. Simple = Total = Palliative:
➢ Breast removed including NAC + pectoral fascia + without axillary surgery.
6. SSM = Skin Sparing Mastectomy:
➢ Complete removal of breast including NAC + pectoral fascia + axillary clearance. Skin envelope preserved
for immediate reconstruction with improved cosmetic results.
➢ Type I SSM:
• used in prophylactic cases & for nonpalpable cancers diagnosed by CNB.
• If small diameter areola → lateral extension or tennis racquet incision for exposure of axillary tail &
facilitate access for breast reconstruction.
➢ Type II SSM: used if superficial tumor or previous biopsy is in proximity to areola.
➢ Type III SSM: used if superficial tumor or previous incision is remote from areola & usually in upper
quadrants.
➢ Type IV SSM = Skin reducing mastectomy: used if large ptotic breasts & reduction is planned on opposite
side.

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 7. Nipple & Areola Sparing Mastectomy (NSM):
➢ As SSM + preservation of NAC in selected cases with low recurrence rates (NCCN guidelines) if no direct
areola infiltration & subareolar frozen reveals no Mg.
8. Tumescent mastectomy:
➢ - local anaesthetics & epinephrine mixture +/- systemic analgesics.
➢ In elderly & cardiac patients.
9. Aesthetic mastectomy:
➢ = SSM type IV.
10. Goldilocks mastectomy:
➢ Aesthetic mastectomy in obese patients with large breasts by preserving lower flap bulk & de-epithelialization.
11. Prophylactic mastectomy:
➢ contralateral to unilateral breast cancer is discouraged.

❖ Important notes about mastectomy:

➢ Skin flap thickness is about 5mm.
➢ Removal of pectoral fascia:
▪ The standard of care.
▪ but debatable.
▪ RCT found that preservation of fascia → high incidence of chest wall recurrence.
➢ PO Drain:
▪ removed when output <30ml/24 h in 2 consecutive days or after 3 W whatever the amount.
▪ Drain should be inserted no > 5 cm from scar to be within field of RT if indicated.
LNs:
1. Clinically suspicious or Radiologically > 3 suspicious → US guided biopsy → If:
➢ -ve → SLNB.
➢ +ve →

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 • If No NAC → ALND level I & II.
• If NAC →
▪ ALND for residual disease or
▪ SLNB in selected cases when LNs become -ve.
2. Clinically -ve or Radiologically < 2 suspicious or Pathologically confirmed -ve → SLNB → if:
➢ –ve SLNB → No further surgery,
➢ SLN can’t be identified → ALND level I& II. C. If +ve SLNB:
• Micromets only: no further surgery.
• Omit further surgery if the following criteria met (ACOSOG Z0011 trial):
o T1-2 & clinical N0. o No NAC.
o 1-2 +ve SLNB. o WBRT is planned.
o BCS is planned.
o can be considered in mastectomy patients according to EORTC AMAROS trial ,but limited data exist.
➢ Classically ALND was recommended in all SLN +ve cases ,but recent studies suggest low yield of non-SLN
dissection omitting its value.

B. Surgery after NACT:

➢ For breast:
• Choice of surgical approach: Mastectomy & BCS & OPS → depends on response to NACT & patient
choice.
• Routine assessment after 3rd cycle by patient photograph & tattoo & clips.

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 • M.D. Anderson Prognostic Index:
o pT >2 cm.
o LVI.
o Multifocal tumor pattern.
o Clinically N2,3.
• Risk of recurrence:
o 0-1: low risk.
o 2: intermediate risk.
o 3-4: high risk.
• Some authors prefer mastectomy for high risk gp (consensus doesn’t exist).
• Issues to consider in margins after NACT if BCS will be used:
o Use cavity rather than lumpectomy margin.
o Orientation of specimen (easy mnemonic for thread orientation → SS short superior & LL long lateral
& DD double depth.
o IO clips (better 5).
o Routine adoption of frozen section or tissue imprint → may help adequate resection.
o New vs Old margin resection is still debatable.
o 1mm free SM + complete cavity excision.
o Inking of margins.
o Consider intraoperative US to help complete resection.
o Consider reduction mammoplasty to facilitate RT should be considered.
o When to do re-resection is debatable.
• Adoption of OPS techniques is specially recommended.
• The main factors considered in choosing adequate OPS techniques:
o Breast size.
o Breast/tumor size.
o Degree of ptosis.
• if EBRT is planned:
o CIS after NACT is considered by some authors as accepted -ve margin.
o Delayed immediate reconstruction is considered.

➢ For axilla:
• Before NACT:
o If +ve: FNAC + Clip marking.
o If -ve: may consider SLNB.
• After NACT:

88
 o If still +ve: ALND.
o If still -ve: SLNB if not done before.
o If converted from +ve to -ve: SLNB + excision of marked clip → then ALND if +ve SLNB other than
micrometastasis.
• Axillary management in the neoadjuvant setting:

❖ PORT
➢ Indications:
• After mastectomy if:
o 1ry tumor > 5 cm.
o -ve margin < 1mm.
o > 4 +ve AX LNs (strongly consider in 1-3 +ve AX LNs).

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 • After BCS:
o All cases except > 70 y old + T1N0 + ER +ve.
➢ Types:
A. Conventional EBRT:
• Dose: 5000 cGy (rad) divided on 5 days/W over 5 W (25 fractions).
• Timing: Must be taken within 6 M.
• Given after chemo.
• Field:
o Skin flaps.
o LNs: Internal mammary & infra/supraclavicular LNs especially if tumor in UIQ.
o Axilla if extranodal disease or ALND not done.
• Additional boost radiation:
o 10 cGy in 5 fractions - 16 cGy in 8 fractions →
o to tumor bed after BCS → reduces risk of local recurrence.
o The greatest absolute benefit in cases < 50 y.
B. PBI = Partial breast irradiation:
• Focusing ttt on index breast quadrant alone after BCS in axilla -ve patients.
• Techniques:
o Local conformal EBRT.
o Brachytherapy via bead & seed implants or multiple catheters & balloon catheter inserted into
cavity.
o IORT = Intraoperative single-fraction.
o Systemic ttt = hormonal & Chemo & target therapy.
o Bernard Fissure’s theory: BC is systemic disease from the start & it spreads so early by blood
micromets.

❖ Systemic ttt = (Hormonal + Chemo + Target + Bisphosphonates)

1. Hormonal ttt:
➢ Advantages:
• decreases risk of local & regional & distant recurrence.

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 • decreases risk of developing contralateral BC.
➢ Indications: Luminal A & B types.
➢ Duration: continued for at least 6 M if given as NAT if tumor is responding.
➢ Precautions:
• Young women should be counselled about fertility effect of endocrinal/chemo ttt.
• If fertility desired → gynaecologist should be consulted for possibility of oocyte/embryo cryopreservation.
• Birth control is required during hormonal ttt ,but non-hormonal ttt is encouraged.
➢ Regimen:
2. Medical:
1. SERM = Selective Estrogen Receptor Modulator:
A. Tamoxifen (Nolvadex & Tamofen):
• 1st generation.
• MOA: competes with estrogen for cytoplasmic receptors that control DNA transcription.
• Dose: 10 mg twice daily for 5 y.
• S/E:
o Most common: hot flashes & vaginal discharge.
o Most serious: DVT & endometrial cancer & cataract.
B. Raloxifene:
• 2nd generation.
• less effective: 70% of Tamoxifen strength.
• fewer S/E.
• used for osteoporosis management.
2. SERD = Selective Estrogen Receptor Degrader = Fulvestrant:
• MOA: Complete antiestrogen → binds to & blocks & degrades ER.
• Efficacy: as effective as anastrazole in postmenopausal women.
• Administration method: IM injection monthly.
3. AIs = Aromatase Inhibitors:
• 2 types:
o Nonsteroidal: Anastrazole & Letrozole (Femara).
o Steroidal: Exemestane.
• MOA:
o inhibition of aromatase enzyme → inhibition of peripheral conversion of adrenal androgen into
estrogen in peripheral fat & liver & normal breast.
o inhibition of intratumoral synthesis of estrogen → decrease extraovarian estrogen in postmenopausal
women.

91
 • Should be combined with cortisone = medical adrenalectomy.
• Dose: 1 mg / day for 5 y.
4. Ovarian ablation = medical oophrectomy = LHRH agonist as Goserelin (Zoladex):
• MOA: decreases level of circulating estrogen → induction of reversible chemical menopause.
• For premenopausal women.
• Administration method: SC injection into AAW monthly.
3. Surgical:
➢ Ovarian ablation.
➢ Either open or laparoscopic.
➢ For premenopausal women.
➢ Only indicated if:
• failed medical ablation (persistent elevated FSH with progressing or mets after adequate LHRH ttt).
• complications from drugs.
➢ RT induced ovarian ablation:
4. Chemo:
❖ Indications:
A. Adjuvant for:
➢ Mg LNs.
➢ Invasive tumor > 0.5cm:
➢ Luminal A > 0.5cm if oncotype DX score > 31.
➢ Considered if score 18-30 or test not available.
➢ Luminal A > 0.5cm + LN -ve + favourable histology = No Chemo.
➢ Considered in HER2 enriched < 0.5cm.
B. NACT:
➢ Indications: ‫وتذكر‬
➢ Timing:
• Surgery is followed after NACT within 6 W.
• Chemo should be given within 6 W PO & after 12 W it may be ineffective.
➢ Cycles: 6-8.
➢ Regimen: combination chemo either →
A. Anthracycline based:
➢ AC: Adriamycin & Cyclophosphamide (dd or normal regimen).
➢ CMF: Cyclophosphamide & Methotrexate & 5-FU.
➢ FEC: 5-FU & Epirubicin & Cyclophosphamide

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 B. Taxane based.
5. Target therapy = Trastuzumab (Herceptin) & Pertuzumab (Perjeta):
• MOA: humanized monoclonal antibody targeting human epidermal growth factor HER2 (Anti-
HER2/neu).
• Indications: Cases with overexpression of HER2/neu (25% of BC) detected by IHC or FISH.
• Single or combination:
o has some activity as single agent → response rates 20-50%.
o high survival when added to taxane.
• Duration: / 3 W for 9 W.
• S/E:
o The only significant toxicity is cardiotoxicity.
o not pass BBB → brain mets can occur.
6. Immunotherapy = Pembrolizumab: as neoadjuvant & adjuvant in high risk TNBC cases.
7. Adjuvant bisphosphonates: considered for risk reduction of distant mets for 3-5 y in
postmenopausal high-risk N-ve or N+ve tumors.
8. Adjuvant systemic ttt after preoperative systemic therapy:
➢ Early stage BC completed NACT 6-8 cycles → PO surveillance.
➢ If pCR not achieved after NACT → evidence of benefit for more adjuvant therapy.
➢ TNBC:
• If pCR → adjuvant Pembrolizumab if given preoperatively.
• If non-pCR → adjuvant Pembrolizumab if given preoperatively or 6-8 cycles Capecitabine or Olaparib if
BRCA mutated.
➢ HER2-enriched: 1y Trastuzumab +/- Pertuzumab.
➢ Luminal: Adjuvant endocrine therapy + Olaparib if BRCA mutated.
➢ Residual DCIS is not considered as non-pCR in above regimens.

93
94
 Breast reconstruction
❖ Timing:

Immediate Delayed

- Single operation.
- Lower cost.
- Enough time for patient decision.
- Preservation of maximum breast skin.
- Less operative time.
- Preservation of intramammary fold.
Advantages - Avoid delay of adjuvant treatment.
- Good quality skin flap.
- Avoid adverse effects of radiotherapy on
- Better cosmetic results with SSM. the flap.
- Reduced need for balancing surgery
for the contralateral breast.
- Double operation
- High cost.
- Limited time for patient decision. -Requires replacement of a large amount
- Increased operating time. of breast skin.
Disadvantages - May delay adjuvant treatment. - Mastectomy flaps may be thin, scarred,
contracted, or irradiated.
- Difficulties in coordinating 2 surgical
teams when required. - Mastectomy scar may be poorly
positioned.
- Less aesthetically pleasing outcome
❖ Delayed immediate:
• SSM + tissue expander insertion to maintain skin envelope expand immediately after surgery & deflate during
RT & re-inflate 2 W after completion of RT.

95
 • Myocutaneous flap with or without implant performed 6-12 M later using skin envelop to minimize size of
skin paddle needed from abdomen or back.

❖ Contraindications:
➢ Non resectable chest wall disease.
➢ Serious comorbidity.
➢ Rapidly progressive systemic disease.
➢ Psychological instability.
➢ IBC is contraindication for immediate reconstruction & delayed reconstruction can be done in selected cases.
❖ Techniques:
1. Implant-based technique:
➢ Types of implants:
• According to their content:
o Saline based.
o Silicone based.
o Double lumen (chamber for saline & chamber for silicon).
• According to surface: Smooth & Textured.
• According to shape: Round & Teardrop.
• According to profile: low & medium & high & maximum.
➢ Types of pockets:
• Total Muscular Pocket (Pectoralis M & Serratus).
• Partial Muscular Pocket (Pectoralis M).
• Pectoralis M Muscle & mesh (Synthetic or Biological).
• Biological only mesh = Acellular dermal matrix = ADM:
o the 1st biological mesh available.

96
 o collagen tissue matrix + cellular debris.
o devoid of DNA & RNA.
o acts as interposition graft between muscle & skin.
o acts as control of pocket.
o acts as scaffold for neovascularization.
❖ Complications of implants:
• Infection (staph aureus & epidermidis).
o Hematoma
o Seroma.
o Flap necrosis.
o NAC necrosis.
• Implant rotation.
• Implant rupture: acute or silent leakage.
• Capsular contracture.
• Anaplastic large cell lymphoma (retracted from market in many countries). ‫اكتب السؤال‬
2. Autogenous tissue reconstruction:
➢ TRAM = Transverse Rectus Abdominis Myocutanous flap:
• based on superior epigastric artery.
• may be bipedicled & unipedicled & supercharged & Turbo.
• The arc of rotation should not exceed 180©️.
• Vascular delay can be done by ligation of inferior epigastric artery 3 days before index surgery.
➢ LDF = Latissmus Dorsi flap:
• based on thoracodorsal artery.
• may be conventional LDF or mini LDF.
➢ TDAP perforator flap:
• based on 3 perforators of descending branch of thoracodorsal artery.
➢ LICAP perforator flap:
• based on lateral branch of posterior intercostal artery.
➢ TUG (Transverse Upper Gracilis) & PAP (Profunda Artery perforator flap):
• based on profunda femoris artery.
➢ Free flap: anastomosed to thoracodorsal & subscapular & internal mammary vessels.
• DIEP: the commonest.
• SIEP.
• Free TRAM based on inferior epigastric vessels.
• Free Gluteus maximus.

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 3. Hybrid breast reconstruction = Flap used with implants.

4. NAC reconstruction (immediate or delayed):

➢ Nipple reconstruction: relies on local skin flaps (skate & star flaps) or segment of redundant contralateral
nipple.
➢ Areola reconstruction relies on full thickness skin graft or tattooing of skin.
5. Contralateral Breast Management (CBM):
• Mastopexy.
• Reduction mammoplasty.
• Augmentation mammoplasty.
• Prophylactic mastectomy in genetic BC only.

ICAP = Intercostal Artery perforators Flaps:

➢ Definition: cutaneous perforator branches of posterior & anterior intercostal arteries.
➢ The vessels form arcade between aorta posteriorly & internal mammary vessels anteriorly.

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 ➢ There are 4 segments of intercostal vessels:
- Vertebral.
- Intercostal.
- Intermuscular.
- Rectus segments.
➢ Classification of ICAP flaps:
1. DICAP = Dorsal intercostal artery perforator flap: based on perforators originating from the
vertebral segment of the intercostal vessels.
2. LICAP = lateral intercostal artery perforator flap: based on perforators arising from intercostal
segment of intercostal vessels which is the longest (12 cm). It gives off 5 to 6 musculo-cutaneous
perforators on which flap can be designed and raised.
3. AICAP = anterior intercostal artery perforator flap: based on muscular or rectus segment of
intercostal vessels

TDAP = Thoracodorsal Artery Perforator Flap:

➢ The major vascular axis supplying the TDAP flap = The same that supplies LD muscle = Thoracodorsal (TD)
vessels.
➢ After originating from subscapular vessels, TD vessels course toward LD muscle → after giving SA branch,
they reach deep surface of muscle where they most commonly divide into 2 1ry muscular branches:
transverse branch & lateral or descending or vertical branch.
➢ These branches usually diverge at near 45-degree angles to one another. Both travel from deep surface of
muscle to become intramuscular.
➢ Lateral branch courses vertically & at 2-3 cm inside lateral border of muscle.
➢ The TD vessel supplies muscle by its course in muscle parallel to its fibers and supplies overlying skin by
perforators coursing perpendicularly to skin surface.

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➢ The 1st perforator is located 6-8 cm below posterior axillary fold and may either be branch of distal main
TD or arise from its lateral branch.
➢ Subsequent perforators up to total of 3 arise at 1.5-4 cm intervals inferiorly off lateral branch. The 1st & 2nd
perforators are found in most people.
➢ Each perforator displays 3-5 cm oblique course through substance of muscle, giving off numerous muscular
branches before penetrating through dorsal thoracic fascia to supply overlying skin and SC fat layers.
➢ Each perforator is 0.3-0.6 mm in diameter & accompanied by 2 venae comitantes.
➢ 2 rows of perforators arising from main pedicle at lateral border of LD muscle. The lateral row does not
pierce the muscle and provides for the direct TDAP perforators. The medial row courses through the muscle
(perforating it) before reaching the skin and SC tissues.

Metastatic breast cancer (Stage IV)

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 A. Palliative systemic ttt:
1. Hormonal ttt:
❖ Indications:
➢ ER +ve BC.
➢ Slowly growing disease.
➢ Bone Mets.
➢ Elderly or unfit.
❖ Regimen: as before

Premenopausal Postmenopausal

1st line hormonal therapy Tamoxifen AI

2nd line hormonal therapy LHRH agonist Tamoxifen
3rd line hormonal therapy Oophrectomy Fulvestrant & Progestagens

2. Chemo:
❖ Indications:
➢ ER -ve BC.
➢ Rapidly growing disease.
➢ Visceral Mets.
➢ Failure of response to hormonal ttt.
➢ IBC.
❖ Regimen:
➢ Drug combinations Vs single agents:
• more effective → high efficacy & low risk of drug resistance.
• more toxicity.
➢ The choice affected by:
• prior ttt. • general health.
• most useful palliation with minimal S/E.
➢ Main drugs are:
• Anthracyclines (epirubicin).
• Alkylating agents (cyclophosphamide).
• Antimetabolites (5FU). • Taxanes (paclitaxel).
• Vinca alkaloids (vinorelbine).
• Platinum (cisplatinum).
➢ S/E:

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 • Fatigue.
• N & V.
• BM suppression.
• Amenorrhea in premenopausal women.
• Alopecia.
• Anthracycline limited in cardiomyopathy.
3. Anti-HER2/neu therapy: If HER2 overexpression.
4. Bisphosphonates:
• Indications: bone Mets.
• MOA: inhibit osteoclast activity → decreased bone absorption → decrease pain.
• Duration: Regular ttt with bisphosphonates for 6 M or longer → reduces skeletal morbidity → reduction
in pathological fractures → low need for palliative RT & hypercalcaemia.
• Example: Zoledronate (Zometa®️).
5. CDK4/6 inhibitors:
• Indications: Recent ttt for postmenopausal with luminal metastatic BC in combination with Letrozole
or Fulvestrant.
• Examples: Abemacicilib & Palbociclib & Ribociclib.
6. mTOR inhibitors: Everolimus.
7. PARP inhibitors: Olaparib & Talazoparib for BRCA mutant BC.
8. Monoclonal antibodies (Immunotherapy):
• Indication: MSI-H/dMMR mutant solid BC.
• MOA: targeting PD-L1 expression (in TNBC).
• Example: Pembrolizumab.
9. Other targeted therapies:
• Alpelisib: for PIK3CA mutation in HR+ve HER2- ve.
• Larotrectinib: kinase receptor inhibitor for NTRK fusion mutation.
B. Locoregional ttt:
Surgical ttt:
A. For 1ry tumor:
❖ Simple = toilet = Palliative mastectomy for:
• Fungating BC.
• Infected BC.
• Bleeding BC.
• Infected BC.

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 ❖ Simple mastectomy or lumpectomy in known mets disease → may improve survival depending on many
biologic theories:
• Surgery prevents continued dissemination of disease from 1ry.
• Increase immune recognition.
• Remove GFs produced by 1ry tumors.
• Stage IV disease may be incorrectly staged as CT may show what Bg lung lesions as pulmonary mets.
B. For Mets:
❖ Laminectomy for SC compression.
❖ Internal fixation of pathological long bone fractures.
❖ Pleurodesis = chest tube + intra-pleural Bleomycin for mg pleural effusion.
❖ Metastasectomy considered in:
➢ Long DFS.
➢ Young age.
➢ Oligomets.
➢ However, The role for localized visceral mets is still not well defined.
RT:
❖ Indications:
➢ Breast if tumor not removed.
➢ LNs:
• Axillary LNs.
• Supraclavicular LNs.
• Mediastinal LNs to avoid SVC syndrome.
➢ Painful bone Mets.
➢ Whole Brain irradiation in symptomatic widespread brain Mets or stereotactic radiosurgery if localized
resectable disease in fit patient & favourable DFS & biology.
❖ BC in lymphoma survivors:
➢ Tends to be:
• high grade.
• high Ki67.
• aggressive behaviour.
➢ TTT: BCS + tolerable doses of RT/IMRT/ IORT/ PBI or total mastectomy based on: Patient desire & Age
(younger better) & long time of remission from lymphoma.

Algorithm for metastatic disease management:

103
Staging ---------- Bone metastases ------ Bisphosphonates

ER +ve -----------------------------------------------------------------------ER -ve

Hormonal therapy + CDK4/6 inhibitors

Failure of response to hormonal therapy --------------------------- Chemo

HER-2 +ve HER-2 -ve

Chemo + Trastuzumab chemo only

104
 SLNB = Sentinel Lymph node biopsy:
❖ Definition: 1st LN to receive drainage from cancer containing area of breast.
❖ Site:
➢ Typically Axilla.
➢ Also Internal mammary or Clavicular.
❖ Rational for SLNB: Because ALND →
➢ Lymphedema.
➢ Shoulder stiffness.
➢ Arm numbness.
➢ Fluid collection under arm.
➢ Long incision (10-15 cm).
➢ Long recovery period.
➢ 70% preoperative diagnosis of DCIS → No Mg LNs.
❖ SLN mapping & biopsy:
➢ Diagnostic procedure to determine whether BC has metastasized to LN without having to do
traditional ALND.
❖ Aim of technique:
➢ to identify & remove just SLNB and no others.
➢ The normal variant of SLNB seen is between 1-3 on average.
➢ If BC cells were to escape into lymphatics, → 1st LN detected will most likely be the 1st affected
by mets.
➢ Indications:
• Invasive BC with clinically & radiologically LN -ve at time of diagnosis.
• Invasive BC with clinically LN-ve at time of diagnosis with radiologically 1-2 suspicious
LNs & but -ve FNAC.
• DCIS ,especially those undergoing mastectomy.
❖ Contraindications:
➢ Previous RT or surgery to breast/axilla area.
➢ Mg Ax LNs.
➢ Occult BC.

105
 ➢ IBC.
❖ S/E:
➢ Blue urine.
➢ Blue staining of skin over breast.
➢ 1-2% mild allergy to blue dye & rare severe anaphylaxis.
➢ Wound in breast & armpit & maybe sternum.
➢ Lymphedema: 1-2% risk with SLNB & 7% risk with ALND.
➢ Possible nerve damage → numbness.
➢ False -ve result.
❖ Advantages of SLNB over ALND:
➢ Shorter hospital stay.
➢ Smaller scar.
➢ Rapid recovery time.
➢ Fewer LNs removed → lower risk of lymphedema & pain & numbness.
❖ Detection methods:
➢ Blue dye: patent blue or methylene blue.
➢ Radioisometric 99mTc labelled colloid: measured by handheld radiation detection probe in
theatre.
➢ Combination of both: sensitivity 97%.
❖ Sites of injection:
➢ Subareolar.
➢ Subdermal.
➢ Peritumoral.
❖ Radiocolloid SLNB technique:
➢ 4 small intradermal radioactive injections of Tc labelled Senti-scint: 1st & easiest approach.
➢ 2 peri-tumoral injections can be positioned on either side of BC under US guidance.
• Done in medial BC.
• Imperative to establish if tumor drainage into intra-mammary LNs as opposed to axillary
LNs.
➢ Periareolar.
➢ Subareolar.

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❖ Senti-scint Localization in LN:
➢ The tracer pathway from tumor to SLN:
• Radiocolloid particles are filtered into lymphatic capillaries → move freely along lymphatics
→ trapped into reticular cells of functional LNs.
• Breast massage just after injections helps process.
➢ Scanning:
• Protocols differ from one department to another.
• Can commence immediately. • Must be done within 6 h window.
➢ Marking:
• At completion of imaging in both planes → mark skin with permanent pen over SLN in both
projections.
• Guide or Map to SLNB at surgery.
➢ Lymphatic mapping: can be performed either on day preceding or few hours prior to surgery.
➢ Dosage of tracer must be calculated according to surgery time.
➢ Technique:
• Small amount of blue dye injected around breast nipple at beginning of surgery.
• Moves into lymphatic channels → turns SLN blue.
• Hand-held gamma probe used by surgeon to pinpoint radioactivity in SLN by emitting
audible tone.
• Small incision made & when blue LN is found → removed & examined under microscopy.
❖ Results:
➢ About 8% False-ve finding: when LNs removed as SLN not containing cancer cells & another
LNs containing cancer cells left in armpit → undertreatment & not receiving chemo.
➢ Long term consequences of leaving cancer cells behind in axilla are not known yet due to short
clinical trials.
➢ These cells could eventually form lumps of cancer felt in axilla → can be removed by full
ALND.
❖ Novel tracers:
➢ ICG = Indocyanine Green: SLN localization by fluorescent imaging system.
➢ SPIO = Superparamagnetic Iron Oxide: SLN localization by handheld magnetometer.
➢ Microbubble contrast agent.

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❖ SLNB after NACT in patients with known axillary LN involvement before NAC:
➢ It is feasible.
➢ To optimize its performance → several steps are needed:
• Appropriate patient selection: T1-3 & N1.
• Dual-agent lymphatic mapping (isotope + blue dye).
• Identification & Removal of > 2 SLNs.
• Clip placement in +ve LN + Clip localization + Retrieval at SLNB.
• Consideration of performing IHC staining in SLN + Completion ALND even if N0.
❖ SLNB before NACT in patients with clinically -ve axilla:
➢ Timing of SLNB before or after NACT is controversial.
➢ It is standard for operable BC.
➢ Depends on downstaging effect of NACT on subclinical involved axillary LNs.
➢ Main advantage of SLNB before NACT: provides information on Ax LN status without
confounding effects of NACT which can be helpful if -ve SLN.
➢ Main limitation of SLNB before NACT:
• If SLN proves to be +ve → lost potential for axillary LN downstaging with NACT → need
ALND either before or after NAC.
• SLNB before NACT needs 2nd surgical procedure for definitive management whether SLN
is -ve or +ve.
• Prognostic significance of -ve Ax LNs after NACT & prior +ve SLNB is questionable
because pathologically -ve Ax LNs may reflect axillary LN downstaging from NACT or just
prior removal of +ve LNs by SLNB.
❖ Emerging trials for management of axilla:
➢ Axillary RT versus observation in cases with -ve SLNB after NAT.
➢ Omission of ALND with +ve SLNB in patients undergoing mastectomy or large BC.
➢ Omission of SLNB in cases with early breast cancer cT1N0.
➢ TAD in cases with LN+ve BC: removing +ve LNs with limiting number of -ve LNs removed.
➢ The use of one step nucleic acid amplification (OSNA) assay in detecting SLN.
❖ TAD = Targeted Axillary Dissection = Technique where +ve LNs marked pre-NAC followed by
excision of marked LN along with SLNB for accurate staging.
❖ Carbon tattooing of Ax LNs: safe & cheap & reliable & durable tissue staining + alternative to
marker clips without need for image guidance to locate marked LN.

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109
 Management of axilla among cases undergoing NACT for BC
Locally recurrent BC
A. Non-invasive BC:
❖ Incidence of local recurrence:
➢ After BCS: 20% at 15 y FU.
➢ 50% non-invasive &r 50% invasive.
➢ Chest wall recurrence after MRM: 1%.
❖ Factors predicting recurrence:
➢ Inadequate margin after BCS (<5 mm): the most important.
➢ Pathologic features:
o Grade: High > low.
o Pathological type: Solid & Comedo & Cribriform DCIS > Papillary/Micropapillary.
o Molecular type: Hormonal -ve > hormonal +ve.
➢ Age at diagnosis: more in < 40y.
❖ Management of recurrence:
➢ If 1ry treated with BCS alone: Re-WLE ensuring clear SM → followed by PORT.
➢ If 1ry treated with BCS + RT: Mastectomy + reconstruction.
➢ If invasive recurrence: axillary staging if not done before.
➢ Adjuvant ttt as usual protocol.
B. IBTR = invasive breast tumor recurrence:
A. Recurrent 1ry tumor:
❖ Incidence:
• After BCS: 10-15% at 10 y FU.
• Most recurrences after 10 y are new tumors.
• Chest wall recurrence after MRM: 5-10% at 10 y FU.
❖ Factors predicting recurrence:
• Patient factors:
o young age < 40 y.
o BRCA1/BRCA2 carriers.
• Tumor factors:

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 o EIC: Extensive Intraduct Component.
o LVI.
o Grade & Multifocality.
o Tumor size + tumor histology + LN positivity: the most important predicative factors for
OS + No impact on local failure.
• TTT factors:
o Incomplete excision: tumor at margin → unacceptable LRR rate.
❖ Management:
1. Mastectomy:
➢ After BCS + RT: MRM if No distant mets.
• About 85% operability rate in most series.
• MRM at time of recurrence → not prevent further recurrence involving chest wall.
• The likelihood of 2nd recurrence depends on histology of 1st recurrence.
➢ Causes for non-operability:
• Locally extensive recurrence.
• Inoperable regional LN disease.
• Simultaneous distant mets.
➢ For non-operable recurrence → palliative mastectomy can be done.
➢ Causes of recurrence with poor prognosis: (needs systemic ttt prior to locoregional ttt) as:
• Skin involvement.
• IBC.
• Locally fixed tumors.
• Large tumors.
➢ Other causes associated with poor prognosis following mastectomy for isolated IBTR:
• Age: < 35 y at initial diagnosis.
• LN-+ve status at initial diagnosis.
• ER -ve BC.
• Adjuvant Chemo administration.
• DF interval from mastectomy: Distant relapse within 2 y after mastectomy has 35% 5 y
survival compared with 50% in those who remained DF for at least 2 y.

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➢ Locoregional control rate:
• Def: absence of further recurrence of breast or chest wall cancer following mastectomy.
• Range: from 48-95%.
➢ RT after mastectomy:
• No data address benefit of chest wall or regional LNs RT after postrecurrence mastectomy.
• regional LNs RT: if not initially given at time of BCT + > 4 +ve LNs or ≥5 cm tumor size
or perinodal fat extension at time of postrecurrence mastectomy.
• Re-irradiation of chest wall after WBRT in very high risk recurrences + long time interval
from prior RT.
2. BCS:
➢ Repeat BCS with or without RT:
• Alternative to mastectomy in local recurrence.
• Not standard ttt.
➢ Indications:
• 1ry BC treated with BCS alone without RT → repeat BCS followed by RT.
• 1ry BC treated with BCS + RT.
• Local recurrence confined to biopsy site with concordance between MM & physical exam.
• Tumor size ≤2 cm & >2 y time to relapse.
• If refusing mastectomy.
• Small size recurrence.
• Significant comorbidity.
➢ Contraindications for repeat BCS:
• BRCA1 or BRCA2 mutation.
• High risk of multicentric disease: ER -ve 1ry BC & >3 cm tumor size & IBTR detected by
physical exam.
➢ Catheter-based interstitial brachytherapy + standard EBRT to previously radiated breast:
• without significant S/E in most patients +
• with acceptable cosmesis in some patients.

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 ➢ Re-irradiation of whole breast after Repeat BCS is not recommended because of high risk of
normal tissue morbidity as:
• Tissue necrosis.
• Left sided lesions.
• Cardiac damage.
• Lung damage.
• Rib damage.
➢ Efficacy: Pilot studies → acceptable local control rates that range from 57-93% + acceptable
acute toxicity in case of repeat BCS with interstitial brachytherapy or PBIR in highly selected
cases:
• Small size recurrence.
• Relapse >4 y.
B. Management of axilla
❖ MDT decision.
❖ Factors taken into account:
➢ Previous axillary surgery +/- RT.
➢ Initial disease stage + likelihood of distant mets.
➢ Recurrence pathology: in situ Vs invasive.
➢ Impact of regional disease on adjuvant ttt decisions.
❖ Axillary evaluation of patient with IBTR = thorough physical examination + Axillary US + FNAC
of any clinically suspicious LNs.
❖ IBTR + not undergo initial ALND → repeat axillary staging with lymphatic mapping.
❖ Most surgeons explore axilla at time of mastectomy resecting any obvious LNs.
❖ SLNB:
➢ If No Clinical or Rad susp AX LNs.
➢ Feasible even if undergone prior SLNB.
➢ Not done if previous ALND was done as it is frequently not identified + often maps to
contralateral axilla.
➢ Interest in reoperative SLNB after previous ALND is increasing ,especially when
lymphoscintigraphy is added to identify sites of non-axillary drainage.

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❖ Systemic therapy:
➢ It is the mainstay for systemic ttt of mets disease.
➢ It is controversial for cases with successful control of limited disease + No distant mets.
➢ Chemo therapy is 1ry ttt for cases with ER -ve disease.
➢ HER2-directed agent therapy is 1ry ttt for cases with HER2+ve disease.
➢ Endocrine therapy is 1ry ttt for cases with ER +ve disease
➢ CALOR = (Chemo As Adjuvant For Locally Recurrent BC trial) → Adjuvant chemo reduces
distant + 2nd local failures & prolong OS in cases with isolated ipsilateral local or regional breast
recurrences.
• ER -ve disease: the most benefit from chemo.

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 Chest wall recurrence:
A. Isolated ulcerated recurrence:
❖ Local excision:
➢ +/- flap to cover defect.
➢ The commonly used flap: medially or laterally based Thoroacoepigastric flap.
❖ R.th to chest wall & supraclavicular region.
❖ Appropriate chemo & hormonal therapy.
B. Widespread recurrence:
❖ R.th: in tolerance dose.
❖ S/E if exceeds tolerance dose:
➢ CNS & PNS damage. ➢ lung & bone & skin damage.
➢ Worse than disease.
❖ Appropriate chemo & hormonal ttt.

Regional nodal recurrences:

❖ Incidence:
➢ 1-6% after BCT.
➢ Higher with widespread use of SLNB.
➢ Lower with -ve SLNB without completion ALND.
❖ C/P: palpable mass on routine FU.
❖ Site:
➢ Axilla: the commonest.
➢ Higher rate of failure in the supraclavicular nodes.
❖ Approach:
➢ Rule out distant mets.
➢ Whenever possible → resection of recurrent disease.
❖ Prognosis:
➢ Non axillary nodal recurrence → more to develop distant mets → poor outcome.
➢ 5 y distant disease free survival rate in isolated axillary recurrence Vs supraclavicular
recurrence: 32 Vs 12%.

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❖ TTT:
1. Isolated axillary recurrence:
➢ Multimodality ttt → prolonged DFS.
➢ Cases with initial -ve SLNB: complete ALND (levels I & II).
➢ Cases with prior ALND: resection.
➢ Cases not previously received regional nodal RT: RT.
➢ Cases previously received regional nodal RT: systemic therapy alone.
➢ Cases with non-resectable recurrence: systemic therapy to decrease extent of disease prior
to RT.
➢ RT pitfalls:
• ALND followed by RT → higher lymphedema rates.
• ALND followed by RT +/- systemic therapy → favourable outcome.
• No RT if recurrence is completely resected.
• Regional RT is not repeated for fear of brachial plexopathy.
• No data proving benefit for RT after ALND.
2. Isolated supraclavicular nodal recurrence:
➢ TNM staging:
• Ipsilat supraclavicular LNs: N3c.
• Contralat supraclavicular LNs: M.
➢ Debate: whether isolated supraclavicular recurrence is considered as disseminated or
locoregional disease.
➢ Study: No RCTs ,but only retrospective analysis.
➢ Multimodality ttt → prolonged DFS in small number of cases.
➢ For cases candidates for systemic therapy: initial systemic therapy.
➢ For cases not previously received RT: RT alone.
➢ For cases previously received RT: Surgery alone.
➢ For cases with incomplete response to chemo: Combined surgery + RT.
➢ For cases without distant mets: Surgery +/- RT.

❖ Prognosis: (6)
1) Axillary LN status: The most important & accurate single prognostic factor.

116
2) Patient related factors: (Age & Sex & Pregnancy)
➢ Age: worse in young due to stimulatory effect of sex hormones on tumor.
➢ Sex: worse in males as > 1/3 of cases inoperable at time of diagnosis despite early
presentation due to:
o Early fixed as no bulk of breast tissue.
o Early mets to axillary LNs.
o Difficult operation due to insufficient skin.
➢ Pregnancy: worse as Usual diagnosis at advanced stage due to:
o High density & nodular breast making clinical exam & imaging less accurate.
o Commonly mistaken for lactational mastitis & abscess.
o Common TNBC & Bad histology.
o Suboptimal ttt.
3) Tumor related factors:
➢ Site: Worse in LIQ due to early spread to abdomen.
➢ Size:
o Worse in larger tumor due to early spread to regional LNs.
o Tumor < 1 cm & without LNs → good prognosis.
➢ Histologic type:
• Bad:
o IDC NOS.
o IDC with extensive intraductal component.
o Inflammatory BC. o Signet ring carcinoma.
o Paget with mass
• Good:
o Lobular. o Tubular.
o Mucinous. o Papillary
o Medullary. o Paget without mass.

➢ Grade: 10 y survival →
• Grade I: 90%.
• Grade II: 60%.
• Grade III: 40%.

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 ➢ Stage: 5 y survival is →
• Stage I: 94%.
• Stage IIa: 85%.
• Stage IIb: 70%.
• Stage IIIa: 52%.
• Stage IIIb: 48%.
• Stage IV: 18%.
➢ HR status: ER & PR +ve tumor → Good.
4) Mets related factors → Worse if:
➢ Distant mets.
➢ Loss of mets suppressor gene nm23.
➢ Angiogenesis measured by intratumor microvessel density.
5) Genetic factors → Worse if
➢ Inactivation of tumor suppressor gene:
o Loss of p53 gene: worse.
➢ Over expression of:
o VEGF.
o EGFR.
o HER2/neu.
o C-erb-B2/neu.
o PCNA.
o Ki-67.
6) Others:
➢ Peritumoral lymphatic angioinvasion → Worse esp in LN -ve patients.
➢ Nottingham prognostic index (NPI) = 0.2 x tumor size in cm + Grade + LN status.
➢ Flow cytometry → Worse if:
o S-phase fraction >12%.
o DNA Aneuploidy.
➢ Invasion associated enzymes → Worse if:
o Proteolytic enzymes (cathepsin D).
o Metalloproteinases (type IVcollagenases).

118
❖ FU of BC patients:
➢ Clinical Examination / 6 M.
➢ Lab: CA15-3.
➢ Rad:
o BBMM after BCS / y.
o MRI after BCS to differentiate between recurrence & fibrosis.

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 Miscellanous topics in breast
Gynaecomastia
❖ Def: Hypertrophy of male breast stroma & ducts resembling that of female → later on more
fibrous tissue & less ducts.
❖ Pathognomonic: Excess estrogen in relation to testosterone
❖ Types:
➢ 1ry (idiopathic):
▪ Neonatal:
- Since birth & Self limited.
- Due to maternal sex hormones.
▪ Pubertal:
- At puberty & Self limited.
- Due to imbalance of Estrogen/Androgen.
▪ Senile:
- Between 50-70 years, like pubertal,
- Due to imbalance of LH/FSH.
➢ 2ry: (CTIN MD)
▪ Congenital: Klinefelter syndrome 47XXY: tall & hypogonadism.
▪ Traumatic atrophy of testis or castration.
▪ Infection:
- Leprosy: bilateral testicular atrophy.
- HIV.
- Mumps orchitis.
▪ Neoplastic:
a) Testicular tumors:
- Atrophy of testis or
- Hormonal secretion: Estrogen or HCG.
b) Adrenal tumors: Steroid secretion.
c) Lung cancer: Ectopic ACTH secretion.
▪ Metabolic: Liver cirrhosis due to failure to metabolize Estrogen.

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 ▪ Drugs: (ABCDE)
- Aldactone.
- Bacteria: INH.
- Cimetidine.
- Digitalis.
- Estrogen for prostate cancer.
❖ C/P: Bilateral & RA & Discoid & Mobile & Tender mass.
❖ Investigations:
➢ Function tests: LFTs & KFTs & TFTs.
➢ Hormonal assay: HCG & LH & Testosterone & Estradiol.
❖ D.D:

Gynaecomastia Male breast cancer

Site RA Eccentric

Laterality Bilateral Unilateral

Shape Discoid Ulcerating

Consistency Not-hard Hard

Mobility Mobile Very early loss of motility

Nipple retraction -ve +ve

❖ TTT:
1. General:
➢ Observation only: in early proliferative phase < 1 y & in most adolescents.
➢ TTT of cause: hypogonadism or hyperthyroidism.
➢ Drugs stoppage: regression of glandular tissue within 1 M during early proliferative painful
phase.

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 2. Medical:
➢ Androgens:
▪ For patients with hypogonadism.
▪ Not for patients with Eugonadism as it may actually worsen gynecomastia due to aromatization
of testosterone to E2.
▪ Danazol: less successful & androgenic S/E.
➢ Antiestrogens:
▪ Tamoxifen: 20mg/d for 3-6 M for relief of symptoms.
▪ SERMs: if No identifiable cause & tender gynecomastia > 3 M.
▪ AIs: block estrogen biosynthesis → decreasing estrogen to androgen ratio ,but clinical trials not
demonstrated important benefit of AIs for gynecomastia in either adolescents or men with
prostate cancer with unknown etiology.
3. Surgical:
➢ Indication:
▪ Progressive non responsive cases to other therapies.
▪ NO spontaneous regression & Fibrotic stage.
▪ Discomfort or psychological Distress & Longstanding > 12 M.
➢ Procedures:
B. SC mastectomy:
▪ Incision: Webester lower circumareolar incision can be extended medially + laterally for
additional exposure.
▪ Combination of direct surgical excision of glandular tissue + liposuction of any coexisting
adipose tissue in the inferior hemisphere.
▪ Breast tissue disc should be left behind nipple with intact pectoral fascia and overlying fat to
prevent retraction & fixation to muscle (saucer deformity).
▪ Skin flaps should be kept thick to prevent deformity & skin necrosis.
C. More extensive cosmetic surgery:
▪ For marked gynecomastia.
▪ For those with excess sagging of breast tissue as with weight loss.
▪ Excision of transverse ellipse of excess skin & fat & glandular tissue.

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 ▪ Removal of redundant tissue → Removal of NAC as full thickness graft & replacement in
appropriate anatomic position.
▪ NAC may remain attached to surrounding dermis with its blood supply & rotated upward into
its proper position.

Galactorrhea
❖ Def: Non puerperal marked milky discharge from both nipples.
❖ Causes:
➢ Physiological:
▪ Menarche: around it.
▪ Menopause: marked hormonal variations occur.
▪ New born: maternal hormones that cross placental barrier (drop of estrogen &
progesterone with increase in prolactin) ‫تظبيط‬
➢ Pathological: Hyperprolactinemia due to:
▪ Pituitary disease: ‫تظبيط‬
- Prolactinoma & GH secreting adenoma. pituitary adenoma with its characteristic
triad (amenorrhea, galactorrhoea, and infertility),
- Hypothalamic disease: tumors & sarcoidosis & radiation.
- 1ry hypothyroidism.
▪ CKD.
▪ LCF.
▪ Drugs: oestrogen, verapamil, opiates, phenothiazines, metoclopramide.
▪ Pregnancy.
▪ Stress
❖ TTT:
➢ If caused by drugs:
• Assurance.
• Drug stoppage: tapering or changing.
➢ If hyperprolactinaemia:
• TTT of cause.

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 • If No identifiable cause: Cabergoline.
• If persistent high prolactin > 1000 mlU/L → search for pituitary adenoma.
➢ If transient idiopathic galactorrhoea + normal prolactin level:
• Assurance that it is benign & Reassessment in 2-3 M.
➢ Total duct excision may be needed.

Zuska's disease: ‫قراءة فقط‬

❖ Def: squamous metaplasia of lacteriferous sinus.
❖ C/P:
➢ Periareolar chronic abscess + sinus.
➢ Intermittent nipple discharge + infection.
❖ TTT: Total duct excision

Mastalgia
❖ Def: Brest pain +/- lump.
❖ Causes:
1. Breast mastalgia:
➢ Cyclic mastalgia:
• Pain 3-7 days preceding each menstrual cycle & disappear after cessation of menstrual flow.
• Symptoms will get better after menopause.
➢ Noncyclic mastalgia: pain not associated with menstrual cycle.
• Fibroadenosis (commonest).
• Milk engorgement.
• Acute breast abscess.
• Carcinoma: painless unless advanced & infected & inflammatory (10%).
2. Non breast mastalgia:
➢ Angina pectoris.
➢ Spondylosis.
➢ GB stones.
➢ Pneumonia.

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➢ Pleurisy.
➢ Thoracic outlet syndrome.
➢ GERD.
➢ Musculoskeletal = Tietze disease:
• The commonest.
• Idiopathic painful & non suppurative swelling of 2nd or 3rd costal cartilages.
• X-ray: -ve.
• local heat to relieve pain & hydrocortisone injection into perichondrium → encourage
resolution.
• Reassurance: self limiting disease.
• Resolution may occur alone without ttt after few months.
❖ TTT (for 3-6 M):
1. For 80% →
➢ Reassure that cause is not cancer..
➢ Supportive bra at night-time.
➢ Diet:
• Olive oil containing linolenic acid & vitamin A B E.
• Avoid consumption of caffeine & excess fat.
• Salt restriction.
➢ Drugs: Simple analgesics as NSAIDs (systemic or topical).
2. For 20% → added ttt:
➢ Gamolenic acid 240 mg/d (3g evening primrose oil).
➢ Bromocriptine = antiprolactine:
• slowly to maximum dose of 2.5 mg bid.
• S/E: nausea & dizziness so antiemetic is given.
➢ Danazole = Antigonadotropin:
• 200-300 reducing to 100mg/d when symptoms are under control.
• Patient must stop OCP.
• S/E: weight gain & acne & hirsutism.
➢ Goserelin = Zoladex® (LHRH analogue): in resistant cases.

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 ➢ Tamoxifen.
➢ Vitamin A: for duct re-epithelization.
➢ Alphintern: to reduce breast oedema.
➢ Efficacy of ttt: 80% of the residual 20% will have relief of symptoms after this regimen.
F. Surgery: not used to treat breast pain under any circumstances

Breast swellings

1. Hard swellings:
❖ Traumatic:
➢ Traumatic fat necrosis.
➢ Calcified hematoma.
❖ Inflammatory:
➢ Plasma cell mastitis.
➢ Granulomatous mastitis.
➢ Chronic non-specific breast abscess.
➢ Chronic specific breast abscess: T.B & Gumma.
❖ Neoplastic:
➢ Bg: Hard fibroadenoma.
➢ Mg: Breast cancer: scirrhous.

2. Cystic swellings:
❖ Acinar or Ductal: (PCG)
➢ Papillary cystadenoma.
➢ Papilliferous intracystic carcinoma.
➢ Papilloma of duct → retention cyst.
➢ Phyllodes tumor.
➢ Cysts of fibroadenosis (solitary or multiple).
➢ Galactocele (milk cyst):
• Retention cyst due to block of milk duct by inspissated milk or epithelial debris during
lactation → distension of duct with milk.

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 • C/P: RA cyst → may extrude milk on pressure.
• Complications: rarely infected.
• TTT: Left for spontaneous regression after weaning & Aspiration & Excision if persists.
❖ Interacinar or Stromal:
➢ Traumatic: Blood cyst.
➢ Inflammatory: Cold abscess.
➢ Neoplastic:
• Bg: Lipoma & Hamartoma.
• Mg: Degenerated carcinoma.
➢ Parasitic: Hydatid cyst.
➢ Skin cysts: Dermoid & Sebaceous & Lymphatic cysts.

Management of breast cysts:

1) Single cysts:
❖ Aspiration:
• With wide bore needle.
• If fluid is obtained → aspirate cyst to dryness.
• Send fluid for cytology.
• Examine after aspiration → if residual mass → FNAC or CNB.
• Review 4-8 W after cyst aspiration to check for refilling.
❖ Aspiration is considered unsafe = Excision biopsy must be done = suspicion of malignancy
if: (4R)
• Red: bloody or serosanguineous.
• Residual mass after complete aspiration.
• Revealed mg cells by cytology.
• Refill after aspiration.
2) Multiple cysts:
• Asymptomatic cysts: no ttt & regular BBMM / 1-2 y.
• Symptomatic cysts: aspiration

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❖ Massive breast swellings: MED2PS
➢ Medullary carcinoma & Elephantiasis.
➢ Diffuse hypertrophy: usually bilateral.
➢ Phyllodes tumor.
➢ Papillary cystadenoma.
➢ Soft fibroadenoma.

Nipple discharge
❖ 5% of referral to breast clinic.
❖ 5%: in situ or mg diseases.
❖ Etiology:
i. Physiological:
• Serous: during pregnancy.
• Milk: during lactation.
• Bloody nipple discharge in 20% during 2nd or 3rd trimester & lactation due to usually
hypervascularity of developing breast tissue which is benign & requires no ttt.
ii. Pathological:
➢ Bloody:
• Duct papilloma: the commonest.
• Duct carcinoma.
• Nipple adenoma.
➢ Necrotic: Degenerative carcinoma.
➢ Purulent: breast abscess.
➢ Milky:
• Galactorrhoea. • Galactocele.
• OCs.
➢ Green & Brown & Black & Serous: Fibroadenosis.
➢ Greenish or Creamy paste: Duct ectasia.
❖ Duct ectasia is the commonest cause of nipple discharge in females > 55y.
❖ Duct papilloma is the commonest cause of nipple discharge in females < 55y.

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 Approach:
❖ Hx:
➢ Age.
➢ OCs
➢ Drugs: phenothiazines & TCA & metoclopramide.
➢ Diseases: hypothyroidism & pituitary adenoma.
❖ Exam:
➢ Side: unilateral or bilateral.
➢ Localized to 1 or multiple ducts.
➢ Induced or spontaneous.
➢ Nature: frequency & color & consistency.
➢ + mass or pain.
❖ Nipple discharge: pathological if → ‫مهم‬
• Spontaneous.
• Bloody.
• Unilateral.
• Localized to 1 duct
• Age > 40 y.
• + mass.
❖ Investigations:
➢ Lab:
• Localization test by differential pressure to localize duct.
• Benzidine test: to detect occult blood.
• Pregnancy test.
• KFTs.
• Thyroid function tests.
• Serum prolactin level & If persistent elevated > 1000 mlU/l → search for pituitary adenoma
(amenorrhea & galactorrhoea & infertility).

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 ➢ Rad:
• BBUS or BBMM: to detect impalpable mass.
• Ductography = Galactography:
- Limited use.
- Diagnose intraductal lesions as Duct papilloma & DCIS.
- Not in mastitis or breast abscess as it could worsen inflammation.
- If too much contrast injected or too much pressure during injection → duct perforation
& contrast extravasation → mastitis.
• MRI: if pathologic nipple discharge & -ve MM and US.
• MR galactography: emerging technique.
➢ Endoscopy = Ductoscopy:
• Limited use.
• If solitary intraductal lesion identifiable → either surgically excised or biopsied through
separate skin incision.
• If multiple intraluminal lesions → higher rate of encountering clinically occult cancer →
WLE.
➢ Biopsy:
• Cytology or lavage: not recommended because result does not impact management.
• Biopsy of mass if present.
❖ TTT:
1. Galactorrhoea: ‫وتذكر‬
2. Pathologic nipple discharge:
a) With identifiable lesion:
• Bg lesions with high risk features as intraductal papilloma & ADH & ALH & radial scar →
surgical excision as Microdochectomy or MDE.
• Bg lesions without high risk features as usual ductal hyperplasia & fibroadenoma: debatable
& duct excision may be needed for symptomatic relief + pathologic confirmation (Awaiting
TBCRC 034 trial result)
• BC: treat according to guidelines.
b) NO identifiable lesion: Excision of discharging duct(s) for →
• Symptomatic relief. & Exclusion of lesion.
• Breast cancer with pregnancy.

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 Breast screening
❖ Aim:
➢ Reduce mortality from breast cancer.
➢ Early detection.
➢ ttt before spread.
❖ Program: UK guidelines →
➢ Breast Self Examination: females educated to examine herself in front of mirror after
each menses for:
• Change in breast size & level.
• Skin dimpling & Nipple retraction.
• Mass in breast & axilla.
➢ Breast Clinician Examination: periodically.
➢ Imaging:
• Average risk (Lifetime risk <15%):
o Mammogram / 3 y between 50-71 y.
• Moderate risk (Lifetime risk 15-20%):
o FH of breast cancer.
o No known genetic mutation.
o Mammogram / 1 y starting at 40 y.
• High risk (Lifetime risk >20%):
o Known genetic mutation.
o MRI / 1y stating at age of 20 y for P53 mutation & at age of 30 y for BRCA mutation.
➢ BIRADS classification of mammography abnormalities:
➢ If biopsy
• Non diagnostic: needle localization & excision.
• Bg: FU.
• Mg: therapy.
➢ Advantages:
• detects cancers which are smaller, less aggressive, and node -ve.
• It is also likely to detect insitu disease.

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➢ Disadvantages:
• Anxiety especially if the patient is recalled.
• Expense.
• Possible hazard of repeated exposure to diagnostic X-rays; the latter danger is minimized by
special low-dose equipment & the mammography done every 2 years.
• Unnecessary biopsy.
• Over ttt of some disease (especially insitu disease) which would never progress to cause
significant morbidity & mortality.

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 Breast cancer with pregnancy

PABC:
❖ Def: Breast cancer diagnosed during pregnancy or up to 1 y after labor or during lactation.
❖ Incidence
➢ BC is the 2nd most common malignancy in pregnant women after cervical cancer.
➢ 0.2-4% of breast cancer.
➢ Expected to increase with increasing delayed childbearing among women.
➢ Common in older age at 1st pregnancy.
➢ Often diagnosed at later stage than in non-pregnant women of same age.
➢ Tends to be aggressive in biology: -ve for both ER and PR & HER2neu over-expression & high
Ki67.
❖ Diagnosis
➢ Rad:
• US: preferred during pregnancy
• Mammogram: with abdominal shielding.
• MRI with gadolinium contrast is not recommended (without contrast can be considered)
➢ Biopsy: CNB can be safely done under LA.
➢ Mets work up:
• CT scan & Bone scan & PET-CT: contraindicated.
• PAUS + CXR with abdominal shielding.
❖ TTT:
A. Stage I & II:

➢ Plan of ttt:

• Not precious baby: TOP → not suggest survival advantage & give chance for BCT to
be given in time (if indicated).
• Precious baby:
➢ During 1st trimester
• NO TOP & Explain that postoperative ttt will be delayed.

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 • MRM regardless size of tumor.
• Delay chemo till 2nd trimester because of its teratogenicity & risk of spontaneous
abortion.
➢ During 2nd trimester
• Early: as 1st trimester.
• Late: as 3rd trimester.
➢ During 3rd trimester
• Before labor:
o MRM or BCS.
o Chemo: given safely.
o RT after labor & should not be delivered in pregnancy.
o Tamoxifen: contraindicated during pregnancy.
• After labor: Early induction of labor at 32 W + ttt as usual.
➢ Lines of ttt:

1. Surgery
➢ Can be safely done at any time during pregnancy.
➢ Precautions for surgical team: (BCD)
• Be aware to perform surgery in rapidly & safely.
• Conduct with Obs team.
• Document fetal viability before surgery.
• Discuss GA & surgery related risks on fetus with mother.
• Discuss if BCS → higher risk of local recurrence because of R.th delay.
• Discuss TOP if NACT is needed in locally advanced cases during 1st trimester.
➢ Surgical lines:
• MRM: preferred as mostly → No need for R.th → No delay in adjuvant ttt.
• BCS:
o 1st & 2nd trimester: not contraindicated, but R.th delayed after delivery.
o 3rd trimester: BCS + R.th given without delay after delivery.
• Reconstruction:
o Delayed reconstruction: preferred.

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 o Immediate reconstruction:
- Not recommend avoiding long exposure to GA.
- IF strongly desired → Implant based reconstruction is rapid & safe.
- Autologous reconstruction: discouraged.
o Immediate delayed reconstruction:
- With tissue expander & implant later on.
- The best due to changes in breast shape & symmetry during & after pregnancy.
o SLNB:
- Can be safely done when indicated.
- Radioisotope mapping: preferred with negligible radiation dose.
- Blue dye: discouraged due to low risk of anaphylactic reaction.
2. R.th: contraindicated during pregnancy + should be delayed after delivery.
3. Chemo:
➢ Can be safely given during 2nd & 3rd trimester.
➢ Not in 1st trimester or >34 W gestation.
➢ Anthracycline + cyclophosphamide (EC or AC): preferred.
➢ Taxanes can be given (Paclitaxel preferred).
➢ 5-FU + dose dense regimens: not recommended.
➢ NACT in locally advanced cases during 1st trimester → TOP should be discussed.
4. Target therapy (Anti-HER2 therapy): contraindicated during pregnancy
5. Hormonal therapy: contraindicated during pregnancy.
B. LABC:

➢ During 1st trimester:

- Chemo given before surgery +
- Contraindicated during 1st trimester because of its teratogenicity & risk of spontaneous
abortion +
- Counsel patient & family about potential risks to fetus.
➢ During 2nd & 3rd trimesters: Chemo → then surgery → then RT after delivery & if ER/PR
+ve → tamoxifen.

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 ➢ Immediate reconstruction with tissue flaps: contraindicated during pregnancy →
• Risk of fetus +
• Prolonged anesthesia +
• Blood loss +
• Inability to obtain symmetry with postpartum contralateral breast.
➢ Axillary staging: ALND + Not SLNB ??.
C. Mets BC: TOP + ttt as usual.

❖ Prognosis: worse as usual diagnosis at advanced stage due to:

➢ High density & nodular breast making clinical exam & imaging less accurate.
➢ Commonly mistaken for lactational mastitis & abscess.
➢ Common TNBC.
➢ Suboptimal ttt.

Pregnancy and fertility after treatment of breast cancer

(Pregnancy & Fertility-Contraception & Breast feeding in BC survivors)
1. Pregnancy in BC survivors:
➢ Reassurance that pregnancy after breast cancer ttt is safe.
➢ No high risk of recurrence or mortality from pregnancy in BC survivors.
➢ BC survivors have 70% lower chance of pregnancy compared to healthy women due to
cancer ttt.
➢ Advise to wait for 2 y before pregnancy as 80% relapses occur within this period.
➢ 5-10 y of hormonal ttt may → natural menopause before finishing adjuvant ttt
➢ If try to get pregnant → break from hormonal ttt.
➢ Patients should not become pregnant during cancer ttt (chemo & RT & Hormonal).
➢ Before trying to get pregnant → should wait at least:
- 2 M after Hormonal.
- 4-6 M after chemo.
- 7 M after anti-HER2.

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2. Fertility & Contraception in BC survivors:
➢ All young BC patients should be:
- informed about impact of adjuvant ttt (chemo & hormonal) on fertility.
- referred to fertility specialist.
➢ The most efficient method of fertility preservation is Oocyte/Embryo cryopreservation.
➢ ART after completion of cancer ttt (in limited RCTs) → Not affect OS & DFS.
➢ Some claim protective effect of pregnancy in HR -ve BC.
➢ LHRH agonist for Ovarian function suppression during chemo → protect ovary from
chemo induced amenorrhea in premenopausal ER-ve BC (conflicting data in ER+ve).
➢ Contraception required during ttt as chemo & hormonal & anti-HER2.
➢ Hormonal contraception: contraindicated & alternatives should be considered.
3. Breast feeding in BC survivors:
➢ Safe & Should be encouraged.
➢ Women treated with CBS can feed her baby without any side effect on mother or baby.
➢ Milk production is affected by Surgeries involving NAC or duct system + R.th.

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 Breast sarcoma ‫قراءة‬
❖ Incidence: Rare (0.5% of breast mg tumors).
❖ Etiology:
➢ Genetic:
• Li fraumeni syndrome,
• Gardner syndrome and
• NF type 1 syndrome.
➢ Chemical: exposure to vinyl choloride & arsenic & herbicides.
➢ Physical: ionizing radiation.
➢ Biological: HIV.
❖ Pathology:
➢ Origin: de novo or on top of soft fibroadenoma.
➢ N/E: rapid growth → may fungate through skin.
➢ M/E: The Commonest types are →
• Fibrosarcoma.
• Angiosarcoma (1ry or 2ry after R.th).
• Mg Fibrous Histiocytoma.
• Myofibrosarcoma.
• Leiomyosarcoma.
❖ C/P:
➢ Age: common in 30-40 y.
➢ Breast: Enlarged & Tender & Dilated veins on surface.
➢ Skin: Hot & Dusky & Non pitting edema.
➢ DD: breast abscess: Red skin & Pitting edema & throbbing pain.
❖ TTT:
➢ WLE or Mastectomy without axillary dissection followed by R.th & Chemo.
➢ Axillary dissection if enlarged LNs.
❖ Prognosis: Worse & Recurrence rate: 40%.

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 1ry Breast lymphoma
❖ Incidence: rare.
❖ Pathology:
➢ Origin: intramammary LNs or periductal-lobular lymphoid tissue.
➢ Side: Bilateral 25%.
➢ M/E: The commonest DLBCL.
➢ Age: common in 50-70 y.
❖ Diagnosis:
❖ C/P:
➢ Mass: Painless & Rubbery.
➢ CNB + IHC.
➢ No clinical & No mammo appearance is diagnostic.
➢ Routine investigations of lymphoma done later.
❖ TTT:
➢ Chemo followed by R.th according to stage & pathologic type.
➢ No role of surgery except for obtaining tissue for diagnosis.
❖ Prognosis: favourable.

Breast melanoma
❖ Incidence: more in male than female.
❖ Origin: Breast skin.
❖ Diagnosis: Same as melanoma in other parts of body.
❖ TTT:
➢ Same as melanoma in other parts of body.
➢ Mastectomy is not needed.

139
 Male breast cancer
❖ Epidemiology:
❖ Incidence:
➢ Age: common 60-70 y.
➢ Female : Male = 99:1.
❖ Etiology:
➢ Predisposing factors:
1) Genetic:
• Klinefelter syndrome (47XXY):
o Gynecomastia.
o Small firm testes.
• Cowden syndrome.
• Mutation of BRCA2 gene.
2) Familial: FH of breast cancer (15-20%).
3) High prolactin.
4) High estrogen (ECHO):
• Estrogen therapy for prostate cancer.
• Cirrhosis.
• High endogenous oestrogen in testicular feminization syndrome.
• Obesity.
5) Trauma.
6) Previous chest irradiation.
➢ Precancerous conditions:
o Previous Bg breast diseases.
o Gynaecomastia: no high risk.
❖ Pathology:
➢ Invasive: 90%
• IDC 80%.
• ILC 1% due to paucity of terminal lobules.
• Papillary 5%.

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 • Paget disease & IBC: similar frequency.
• Medullary & Mucinous & Tubular & Squamous: lower frequency in male.
➢ CIS: 10%
• Common DCIS: mainly papillary & cribriform.
• Rare LCIS & usually + ILC.
➢ Molecular types:
• 80%: ER +ve.
• 75%: PR + ve.
• More than female.
❖ Complications: as female.
❖ C/P: as female.
❖ Investigations: as female.
❖ TTT:
1) CIS: total mastectomy with removal of NAC.
2) Invasive carcinoma:
A. No-Mets:
➢ Surgical:
• Stage I, II: MRM.
• Local advanced: NACT followed by MRM.
➢ R.th.
➢ Cytotoxic Chemo.
➢ Endocrinal therapy:
• Based on HR status.
• Following guidelines in postmenopausal.
B. Mets:
➢ Endocrinal therapy: the mainstay of ttt.
➢ Anti androgens: prolong survival if AR +ve.
➢ Cytotoxic Chemo: the mainstay if HR -ve.

141
❖ Prognosis: worse as > 1/3 of cases inoperable at time of diagnosis despite early presentation
due to:
➢ Early fixed as no bulk of breast tissue.
➢ Early mets to axillary LNs.
➢ Difficult operation due to insufficient skin.

Metastasis to breast:
❖ Incidence:
➢ uncommon.
➢ The contralateral breast is the commonest site.
➢ Other common: lymphoma & melanoma & rhabdomyosarcoma & small cell lung cancer.
❖ CNB + IHC to differentiate 1ry from 2ry tumors.
❖ TTT: directed to 1ry.
❖ Prognosis: is poor.

142
 BIA-ALCL = Breast implant associated Anaplastic Large
Cell Lymphoma
❖ Definition: peripheral T cell lymphoma arising around textured surface breast implants placed
for either reconstructive or cosmetic purpose.
❖ Epidemiology: Uncommon → 1:2000 - 1:86000 in textured implants.
❖ Etiology:
➢ Mainly linked to textured implants.
• ALLERGAN BIOCELL implant → 6 times higher risk.
➢ May be caused by: (BCG)
• Biofilm formation around capsule.
• Chronic T cell stimulation.
• Capsular contracture.
• Genetic.
❖ Pathology (TNM staging):
T1 Confined to effusion only or layer on luminal side of capsule

T2 Early capsule infiltration

T
T3 Cell aggregates or sheets infiltrating capsule

T4 Lymphoma infiltrates beyond capsule

N0 No LNs

N N1 1 regional LNs

N2 Multiple regional LNs

M0 No distant spread
M
M1 Spread to other organs/distant sites

143
❖ C/P:
➢ Late onset seroma in implant capsule (60%):
• Average 7-10 y.
• High clinical suspicions if seroma > 1 y from implant insertion.
➢ Mass adjacent to implant (20%).
➢ Axillary lymphadenopathy (20%).
❖ Investigations:
➢ Imaging
• US: Modality of choice → aspiration of seroma + biopsy from capsule or mass
• Breast MRI.
• BBMM: not helpful.
• PET CT for lymphoma staging.
➢ Biopsy:
• Aspiration of seroma.
• Biopsy from capsule or mass.
• Cytology: Anaplastic large cells.
• Flow cytometry: T cell population.
• IHC: CD30 +ve & ALK -ve.
❖ DD:
➢ 1ry breast cancer.
➢ 1ry breast lymphoma.
➢ Non malignant implant complications: rupture.
➢ Systemic ALCL.
➢ Cutaneous ALCL. ➢ Nodal ALCL.
❖ TTT:
➢ For all cases with BIA-ALCL:
• Implant removal including contralateral normal implant.
• Total capsulectomy including contralateral capsule.
• Resection of any associated mass with -ve margins.
• Sampling of any suspicious Ax LNs.

144
 ➢ For cases with localized disease if complete surgical resection:
• Adjuvant chemo or RT not indicated.
➢ Chemo:
• Indications:
o If failed surgical ttt.
o Regional LN involvement.
o Disseminated disease.
• Drug choice:
o Anthracycline based regimen: CHOP.
❖ Prognosis
➢ Indolent & good prognosis if complete surgical resection.
➢ Worse with extracapsular infiltration & mass lesion.
❖ Medicolegal aspects:
➢ Reporting to PROFILE registry.
➢ Counseling about existence of disease + self examination + symptoms.

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 TNBC = Triple Negative Breast Cancer
❖ Def: according to ASCO/CAP guidelines →
➢ <1% expression of ER & PR by IHC +
➢ Her2neu 0 or 1 by IHC or -ve by FISH (not amplified)
❖ Incidence:
➢ 15-20% of all BC cases.
➢ Most BRCA mutated BCs are TNBC.
➢ BRCA mutated TNBCs are radiosensitive.
❖ Risk factors:
➢ BRCA gene mutation: Up to 20% of TNBC
➢ African American: Higher risk for recurrence.
➢ Premenopausal.
➢ Obesity.
➢ Higher parity young age of 1st pregnancy.
❖ Pathological characters of TNBC:
➢ High proliferative rate.
➢ High grade.
➢ Central & Geographic necrosis.
➢ Frequent apoptosis.
➢ Solid sheets.
➢ Stromal lymphocytic response.
➢ High N/C rates.
➢ Marked nuclear pleomorphism.
➢ High mitosis index.
➢ Pushing border of invasion.
➢ Brisk lymphocytic infiltrates.
➢ More likely to be diagnosed clinically rather than mammographically.
❖ Molecular class of TNBC subtypes (Heterologous):
➢ Claudin-low subtype: (Epithelial mesenchymal transition phenotype).
➢ Molecular apocrine subtype: (Activation of AR pathway).

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❖ Subtypes of TNBC:
➢ Basal like / immune suppressed.
➢ Basal like / immune activated.
• TNBC is not ideal substitute for basal type.
• BRCA 1 gene associated BC is mainly Basal like molecular subtype.

➢ Luminal AR:
• The most stable.
• Clinical similarity between luminal type and luminal AR TNBC.

➢ Mesenchymal.
❖ There are 6 subtypes of TNBC:
➢ Basal like (BL1).
➢ Basal like (BL2).
➢ Immunemodulatory.
➢ Mesenchymal.
➢ MSC = Mesenchymal Stem Cell.
➢ LAR.
❖ TIL = Tumor infiltrating lymphocytes :
➢ The 1st biological prognostic response for TNBC.
➢ higher rate of CPR after NACT (up to 30%).
➢ LPBC = Lymphocyte predominant BC: > 60% of either stromal or intratumor lymphocytes
→ > 40% CPR rate.
❖ Most TNBC are IDC of NST.
❖ High grade TNBC of special type:
➢ Carcinoma with apocrine differentiation.
➢ Carcinoma with medullary features.
➢ Metaplastic BC.
❖ NCCN guidelines for TTT of TNBC:
➢ TTT of TNBC depends on:
• Prior ttt.
• PD-L 1 expression.

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 • BRCA Germline mutation.

➢ BCT or MRM +/- reconstruction.

➢ NACT:
• If:
- locally advanced BC or
- No good cosmetic outcomes after BCS.
• If CPR after NACT → higher DFS + lower LR rate.
• After NACT →
- If tumor size decreases → BCS or OPS according to tumor to breast ratio.
- If tumor disappears → remove tumor bed after guide wire localization at clip site.
- If No change in size → MRM +/- reconstruction + consider SLNB or TAD.

➢ Tumor marking:
• Radio-opaque clip.
• Us visible clip.
• Tatoo ink.

➢ No role for hormonal therapy.

➢ No role for target therapy.
➢ Systemic chemo:
• If:
- Tumor > ,5 cm or
- +ve LNs.
• Types:
A. Anthracyclines:
- Alkylators.
- Taxanes.
B. Non-Anthracyclines based regimen: for low risk TNBC (<1cm) or cardiac patients.
• Benefit:
- Adjuvant chemo increase DFs > 20% & OS > 15%.
- Large benefit from adjuvant chemo as compared to luminal types.
- Additional chemo for residual disease after complete NACT course is beneficial.

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 - Addition of antimetabolites as for cases who complete course of adjuvant chemo not
improve outcome in early cases.
- Add platinum to NACT → increase rate of PCR.
- <,5 cm tumor → favourable prognosis + small benefit from adjuvant chemo > 95% 5y
relapse free survival.

➢ Target therapy for TNBC:

• Select candidates by IHC for PD-L1.
• PARP inhibitors + Immunecheek points:
- Olaparib: improve DFS in BRCA mutated TNBC.
- Veliparib + Temzolomide (alkylating agents): improve OS.
- PARP inhibitors + DNA damaging chemo → render tumors lacking BRCA sensitive.
- Immune therapy + Chemo + PD-L1 antibody (Pembrolizumab) → CPR.

➢ TTT of visceral metastatic disease:

A. Progressive visceral disease → Combination Chemo.
B. Without rapidly Progressive visceral disease →

1. No BRCA germline mutation:

• PDL1 -ve: Single agent chemo (platinum or taxanes) + better combination chemo.
• PDL1 +ve: Atezolizumab + Paclitaxel or Pembrolizumab & Avelumab.

2. BRCA germline mutation:

• PARP inhibitors: initially used for those who have had NACT.
• Chemo if not received before or if progressed on PARP inhibitors.
• PD-L1 -ve: Single agent chemo (Platinum or Taxanes).
• PD-L1 +ve: Atezolizumab + Nabpaclitaxel as initial.

❖ Future TTT options for TNBC:

➢ The most well known protein expression in TNBC is EGF/Her1.
• EGF/Her1 receptor inhibitors as Cetuximab = anti EGFR MCA.

➢ Anti Trop-2 antibody drug conjugate sacituzumab govitecan recognizes Trop-2 covalently
attached to Topoisomerase I inhibitor SN-38.

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 ➢ AR inhibitors: Bicalutamide.
➢ Angiogenesis inhibitors: Bevacizumab as adjuvant + 1st line in mets.
❖ FU: No specific post ttt surveillance guidelines for TNBC.
❖ Prognosis:
➢ Risk of distant recurrence or death peaks at 3 y & rapid decline afterthere.
➢ Higher death rate in 1st 2 y.
➢ Higher relapse rate during 3y compared with luminal that continues to recur for decades later
& TNBC tends not to do this.
➢ Late recurrence risk declines & reach 0 after 6 y.
➢ TNBC tends to recur in locoregional & visceral organs .
➢ TNBC less likely recur initially in bone as luminal types.
➢ Brain may be 1st site for mets & Median survival after brain mets < 6 M.

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 TAD = Targeted Axillary Dissection
1. ALND:
➢ The standard technique in LNs +ve BC.
➢ Benefit: ALND improves locoregional control & provides key pathologic information to guide
post-operative ttt.
➢ Risk: as compared to SLND → ALND is associated with increased morbidity:
- Higher lymphedema.
- Paresthesia.
- Sensory loss in arm.
- Impairment in shoulder function.
➢ Over past 2 decades: ALND has been largely replaced by SLND in early stage BC.
➢ In Locally dvanced BC:
- NAC followed by ALND is the standard management.
- There is high rates of PCR in axillary LNs after NAT → about 60% in TNBC & 70% in
HER2 +ve BC when trastuzumab combined with chemo & 97% when dual HER2 blockage
is used.
2. SLND:
➢ Benefit:
- Fewer infections.
- Better quality of life.
➢ In ACOSOG Z1071 trial: false -ve rate (FNR) of SLND Post-chemo was 13% in T0-4 &
N1-2 & M0.
➢ High FNRs in SENTINA study → precluding use of standard SLND in cases converted
to clinically LNs -ve status after completion of chemo.
➢ These studies demonstrated lower FNRs & higher rates of SLN identification when:
- Use of Dual-tracer technique (both blue dye + radioisotope).
- At least 2 LNs retrieved.
- Metallic marker placed to retrieve biopsy proven +ve LNs.

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➢ SLNB after NAT in initially node +ve disease:
- ALND was the standard of care regardless of response to NAT.
3. TAD:

➢ It was emerged to select patients in whom ALND may be avoided postNAC and for
further decrease in FNR of SLND.
➢ Benefit of TAD:
• Safe.
• Less invasive.
• Fewer risks than ALND.
• Higher oncologic safety than SLND.

➢ Technique:
• MDT decision to perform TAD is required.
• All TAD procedures performed together with breast surgery.
• TAD is performed together with SLND using Dual-tracer technique = preoperative
retroareolar injection of both blue dye & Tc-99. Guide wire can be inserted rather than
I-125 seed.
• All cases had CNB or FNAC of radiologically abnormal LNs: increased diameter &
cortical thickness & round shape & hilar compression & irregular margins.
• Prior to NAC in cases with axillary disease → metallic clip inserted or radioactive seed
implanted in the most suspicious LN only if proven metastatic → Then, NAC is given.
• Intraoperative frozen section of all excised Ax LNs.
• Paraffin study of all LNs by staining with H & E + IHC → increased detection of
micrometastases.
• ALND: when one or more proven Mg LNs = micrometastasis & ITCs & failed TAD.

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 Targeted lymph node by black stain & SLN by blue stain

(Done by Dr Mohamed Yousry)

➢ I-125 seed insertion:
• Dual-tracer method (Tc-99 & blue dye) is not always used.
• Targeted implantation of radioactive I-125 seed under US guidance after completion
of chemo.
• In cases where iodine seed was used → No clip is inserted.
• No difficulty with concomitant utilization of radioactive seed in both axilla & breast
during BCS.
• Radiography of axillary specimen in operating room to confirm metallic marker &
radioactive seed prior to pathologic evaluation.
• Radioactive probe was used to retrieve the seed LN & to distinguish I-125 seed from
metallic marker within LNs.

➢ Contraindications:
• Radioactive seed placed in axillary LNs for another 1ry malignancy.
• If not receive NAC.
• Underwent TAD with single-tracer method.

➢ Success rate & Procedural safety:

• TAD is successful (97%) when targeted LN removed with seed using radioactive probe.
• Radioactive seed insertion is successful when I-125 seed implanted in targeted node
and its position confirmed after procedure.

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 • Clip + Radioactive seed in targeted LN increases likelihood of successful identification
since radioactive seed malposition or displacement can occur.
• ALND can be avoided in about 50% if TAD is successfully completed.
• Cases with normal targeted LN aspect on post-NAC imaging or regression in size →
should still undergo TAD as about 57% had residual disease in axilla.

➢ S/E:
• No adverse events during implantation of radioactive seed in axilla.
• Cases with residual disease have to undergo subsequent ALND.
• Higher costs for hospital.

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 Goldilocks mastectomy
❖ Def: technique of breast reconstruction using the redundant lower pole of Skin + SC tissue →
preserved → de-epithelialized → rolled up to create breast mound around which the superior pole
skin flaps are draped.
❖ Indications:
➢ Obese with large ptotic breasts to obtain sufficient tissue volume.
➢ Contraindications for complex reconstruction procedures.
➢ Poor candidates for traditional postmastectomy reconstruction.
➢ Reconstruction of breast mounds after 1ry failure following breast reconstruction.
➢ A salvage technique in patients with implant-induced complications.
❖ Contraindications:
➢ Inflammatory BC. ➢ Previous RT may compromise flap
➢ Large inferior pole tumors. vascularity.
➢ Inferior pole skin involvement.
❖ Technique:
➢ The standard SSM: Wise pattern skin incisions (Inverted T approach).
➢ Retain SC fat thickness in area distant from tumor.
➢ Use de-epithelialized inferior pole dermal flaps as local autologous dermal–cutaneous flaps to
reconstruct breast mound.
➢ Wrapping lateral 1/3 and medial 1/3 behind central 1/3 → Creation of breast mound.
➢ Drapping of superior skin flaps around the new breast mound.
➢ May need neo-NAC creation by leaving skin disc at appropriate position on dermal flap.
➢ Closure of skin incisions with no tension at the T junction.
❖ Advantages:
➢ Suitable for poor surgical candidates.
➢ Simple & Safe.
➢ One stage autologous breast reconstruction.
➢ No donor site morbidity.
➢ No implant complications.
➢ Tolerate PORT.

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❖ Disadvantages:
➢ Limited applicability.
➢ Challenging to achieve acceptable cosmetic outcome.
➢ Not suitable for small-moderate sized breasts with limited ptosis.
➢ Risk of dermal flap fat necrosis , particularly where breast scars meet (T-junction).
➢ Difficult to get aesthetic outcome comparable to autologous or implant.

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 Pictures Done By: Dr/ Khaled Belal

Traditional Goldilocks

Insitu-Nipple Preservation

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intra-operative rt sided reduction with lt sided Nipple preserved goldilocks

The Skin Flaps After Sc Mastectomy And Skin De-Epithelization

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Intra-Operative Filed During De-Epithelization

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