CHAPTER X CHAPTER 4 - Cancer et environnement

A
B
C
Fig. 4.22 Seminoma. A Pseudoglandular variant of seminoma. B Cords of tumour cells in seminoma. C Cribriform variant of seminoma. D Alveolar variant of seminoma.
D
tion between seminoma and embryonal
carcinoma is difficult with respect to an
area within a tumour or the entire neoplasm.
Morphological discrimination features
include: the discrete uniform cells
of seminoma which contrast with the
pleomorphic overlapping cells of embryonal
carcinoma; the lymphocytic and
granulomatous response typical of seminoma
but rare in embryonal carcinoma.
PLAP and CD117 are distributed more
diffusely in seminoma than embryonal
Fig. 4.23 Positive staining for PLAP in typical seminoma.
carcinoma, whereas CD30 and pancytokeratin
are more pronounced in embryonal
carcinoma. The florid lymphocytic or
granulomatous response within seminoma
occasionally prompts the misdiagnosis
of an inflammatory lesion, especially
on frozen section. Extensive sampling
and a high power search for seminoma
cells (supported by PLAP and CD117
content) help reduce such errors.
Conversely, other tumours are occasionally
misinterpreted as classical seminoma,
possibly as a consequence of their
rarity, these include: spermatocytic seminoma,
Leydig cell tumours, (especially
those with clear/vacuolated cytoplasm);
Sertoli cell tumours, in which tubule formation
may resemble the tubular variant
of seminoma: metastases (e.g.
melanoma). In all these neoplasms, the
absence of IGCNU and the demonstration
of either the typical seminoma
immunophenotype or the immunocytochemical
features of Leydig, Sertoli or
the specific metastatic tumour should
limit error.
Prognosis and predictive factors
The size of the primary seminoma, necrosis,
vascular space, and tunical invasion
have all been related to clinical stage at
presentation {1626,2616}. With respect
to patients with stage I disease managed
on high surveillance protocols, retrospective
studies have emphasized the
size of the primary and invasion of the
rete testis as independent predictors of
relapse {1202,2781}. The 4 year relapse
free survivals were 94, 82 and 64% for
tumours