Ivan Gallegos
Director of Pathology Department, Universidad de Chile.
Chairman Pathology Department, Hospital Clínico, Universidad de Chile.
Medical Director, Biobank, Medicine Faculty, Universidad de Chile.
Executive Medical Director, Private Pathology Laboratory Citolab
Chairman Pathology Department, Hospital Clínico, Universidad de Chile.
Medical Director, Biobank, Medicine Faculty, Universidad de Chile.
Executive Medical Director, Private Pathology Laboratory Citolab
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of p53, Ki67, CD30, and CD117 and correlated it with
histological features and presence of clinical metastasis at
diagnosis of testicular seminomas.
Materials and Methods: A retrospective study of 62 patients was
performed in patients with pure seminoma. The retroperitoneum
was staged with computed tomography scan and the
thorax with simple x-rays and/or computed tomography scan.
Pathologists were unaware of the clinical stage of the patients.
Manual microarrays were created from a tissue representative
of tumor. The expression of p53, Ki67, CD30, and CD117 was
evaluated as negative, any degree of expression, and expression
in more than 50% of neoplastic cells. Univariate and multivariate
analysis were performed.
Results: Sixty-two cases were analyzed: 43 cases were in clinical
stage I (69.4%), 17 were in clinical stage II (27.4%), and 2 were
in clinical stage III (3.2%). Fifty-six cases expressed CD117
(90%), 42 p53 (68%), 8 CD30 (13%), and all cases Ki67. There
were no differences in p53, Ki67, CD30, and CD117 expression
between testicular seminoma with and without clinical metastasis
at diagnosis, regardless of the magnitude of expression.
Neither of them found positive association between these
marker expressions and morphologic risk factors such as tumor
size greater than 6 cm and rete testis invasion.
Conclusions: This study shows that expression of p53, Ki67, and
CD30 and loss of CD117 expression fail to predict the presence
of clinical metastasis at diagnosis of testicular seminoma and do
not correlate with other histopathological risk factors in clinical
stage I patients.
of p53, Ki67, CD30, and CD117 and correlated it with
histological features and presence of clinical metastasis at
diagnosis of testicular seminomas.
Materials and Methods: A retrospective study of 62 patients was
performed in patients with pure seminoma. The retroperitoneum
was staged with computed tomography scan and the
thorax with simple x-rays and/or computed tomography scan.
Pathologists were unaware of the clinical stage of the patients.
Manual microarrays were created from a tissue representative
of tumor. The expression of p53, Ki67, CD30, and CD117 was
evaluated as negative, any degree of expression, and expression
in more than 50% of neoplastic cells. Univariate and multivariate
analysis were performed.
Results: Sixty-two cases were analyzed: 43 cases were in clinical
stage I (69.4%), 17 were in clinical stage II (27.4%), and 2 were
in clinical stage III (3.2%). Fifty-six cases expressed CD117
(90%), 42 p53 (68%), 8 CD30 (13%), and all cases Ki67. There
were no differences in p53, Ki67, CD30, and CD117 expression
between testicular seminoma with and without clinical metastasis
at diagnosis, regardless of the magnitude of expression.
Neither of them found positive association between these
marker expressions and morphologic risk factors such as tumor
size greater than 6 cm and rete testis invasion.
Conclusions: This study shows that expression of p53, Ki67, and
CD30 and loss of CD117 expression fail to predict the presence
of clinical metastasis at diagnosis of testicular seminoma and do
not correlate with other histopathological risk factors in clinical
stage I patients.