HoDG KIN' LYmpHOMA
m Og0ntakion *ainlea costykal LN enlagomt
Cyclicco fevet Pet-fbsteln fa)
assoucuh0nO h
f0iOnepblach Sanolap meR
O Amyloid okiy (29 AA
Aohco induted LNPeun
ods kin ydhamaHL chooacdaougéd) by
Hhe poeRente e Reecd-tean baecellg RS Cel)
Bat kgCue e Lndlammdctoiy e l
athoqenek
(EBY have Lmp-1 Lacent Mereb-paot1)
CD21
0 8-cel
Cowpowpvuh
Stecebto
sty o-2
E-K= /C-REL
protoanto gen
CREL poto ontostent
B-Cel Neoblath B-Ce1l
Pee ctS-totvbes
el
LRscell)
Ox00 yo cepheate
oFosipobhi Pormirot
Nucleg
AlOT Ool Ey abhamoante
RS-Cen CmV
(Cytomegalo vinua)
apmind OO Basopili intaahvt lean
Muclea vios rclu Sio ng.
tCyt+ Nu
cellolone iNOn-cllagnosti
HL
Ine cthio NHL
Seen
morOnUteBaIS
DLBCL
mmUno blaai)
NHL
R-S-cell Requned r PistolegteaDhqneste
Backgtoued ipflaeorocor
Cel
HL
Clace icad rmurobrenolybe Non-Clascical
NLPHL NocluloeH yphoe'
CDIS ecominau L
mokt Commevorko CD 1S CD20 4e
m CDS
Nodulps Bast ggretja
losaoti5 Paomotia
D3o eD¢SJ
ovastallNLPHL
aE edCellud aelp B Pre tase
3E bhouyle Rich mein Trdia (DeMlb ing
L D epletecC0or&e
PPgnosi
Moduba
:Sclou -Yown
M-F
medu'ca shire MOLgy
merdo
Collagu bawol
Cleo Eo Lacuhoome
Crhepop
Dnpanaffip-
Sehon LAUNAR RS-Lel)
hoblatnOmore
e
amixED CELLVLAR1T
Biasic LYgug 1blolen
mc alo BS y p
DNA, ght,
Seou
-mC al EBV
HIV
-MpNO-ANUCLePR
RSCELS
3) -RICcH
mN-RS Ce_also Dt
EO mORPHIC RS-cCL
4E LyPo e
Basobhilt
debosiH MUpmifiud
Caluom RS-TelMg
Hacdy in Cell LAtybicat hitiotybe
HL-PHL
COsyico L yAetec
DY
Axillauy
Ao A PRy ndacion
-Hisho uyhal Rich Vasuiauth RS-cell
Tob-CormR Cell
Nu
Palypoida
mulh lobaztl0d
STAGING
H L An-
Asbo Stgi
OK
SirgQe Bxchalymphat agaw@
LN inoved
Oh gam giae daphaejm
OR
x-taa lyphade Ogun )
On bDth sde el diahoagm
C0r C oct enha hyrp/oLhi 009am ovemult
Difye invo efExtaa lardohactic oeons
COr cO N-1hU0/uomeut
batik o
ll Stgu) c Awther odrded Dn-he
ou Gytyp-(B)
PoAgeMt
Abgen
ltprt Sa.aaus
Unorblained totekg
Uwiesblauned e
Baal-fay tacte"
Hb<lo 62
COLut
Ab:yCouut bro su
TLC y kBy
( L o o Albumn lenol
TLC 1bcoo/mm
NON-HODGKIN Twec MA
DISORDERS > HODGKINS LYMPHOM
HODGKIN LYMPHOMA
More often localized to dsingle More frequent involvement of
axial araun of nod (cervical, multiple peripheral nodes
mediastinal) para-aortio
Orderly spre ad by contiguity Noncontiguous spread
Mesenteric no des and Waldeyer Waldeyer ring and mesenteric
ring rarely involved nodes commonly involved
Extranodal presentation rare Extranodal presentation common
Lj Sy
Figure 13-24 Feed-Stemberg oels and variants. A, Dlagnostic Reed-Sternberg cell, with two nuclear lobes, large inclusion-like nucleol, and abundant cyto
plasm, surounded by lmphocytes, macrophages, and an eosinophil. B, Reed-Stermberg cell, mononuclear variant. C, Reed-Sternberg cell, lacunar variant
his variant has afolded or mutiobated nucleus andlieswithin aopen space, whichisanartifactcreatedbydisruption ofthe cytoplasm during tissue sec-
tioning.D,Reed-Sternberg cl,present.
mphohistiocytic variant.Severalsuch variantswith mutipyintolded nuclear membranes,smallnucleoli,fine chromatin,and
(A, Courtesy Dr. Robert W. McKerna, Department of Pathology Unversity of Texas Southwesterm Medical School,
abundant pale
Dallas, TeK)
otoplasm are
Figure 13-25 Hodgkin lymphoma, nodular sclerosis type. A low-power view
shows wel-defined bands of pink, acellular collagen that subdivide the tumor
into nodules. (Courtesy Dr. Robert W. McKenna, Department of Pathology.
University of Texas Southwestern Medical School, Dallas, Tex.)
Figure 13-26 Hodgkin lymphoma, mixed-cellularity type. A diagnostic, binu-
cleate Reed-Sternberg cellis surounded by reactive cells,including eosino-
phils (bright red cytoplasm), lymphocytes, and histiocytes. (Courtesy
Dr. Robert W. McKenna, Department of Pathology,
University of Texas
Southwestern Medical School, Dallas, Tex.)
Figure 13-27 Hodgkin lymphoma, lymphocyte predominance type. Numer
ous mature-looking ymphocytes surround scattered, large, pale-staining
lymphohistiocytic variants (popcorn" cells). (Courtesy Dr. Robert W.
McKenna, Department of Pathology, University of Texas Southwestern
Medical School, Dallas, Tex.)