Pathology of Germ Cell Tumors of Testis

Abstract

Since the last National Conference on Urological Tumors, there has been major progress in pathology of testicular tumors. An international histological classification of these tumors has been proposed, which is based on the sound principle that pathological examination must specify the exact components that are present in a tumor and give an estimate of relative proportions of each. The WHO classification, using generally accepted principles of tumor typing, has provided a standard method of pathological reporting of these tumors so that results of research from different parts of the world can be compared. The WHO system published in 1977 is readily convertible to the system in use in the American Testicular Tumor Registry. Its convertibility to the Friedman-Moore and Pugh-Cameron Testicular Tumor classifications is limited. Though it is generally believed that embryonal carcinoma can differentiate along extra-embryonic lines to form yolk sac tumor and choriocarcinoma or along embryonic lines to form teratoma, the malignant germ cell itself seems to have the potential to develop along any of these lines without first going through the embryonal carcinoma phase. Seminomas with high mitotic index and seminomas that contain syncytiotrophoblasts appear to have a less favorable prognosis than classic seminomas or spermatocytic seminomas. HCG is readily demonstrable in syncytiotrophoblasts whether alone or forming choriocarcinoma. AFP is demonstrable in yolk sac tumors and in some embryonal carcinomas. Histological demonstration of AFP and HCG can and should be correlated with clinical findings. Such correlation can readily be made with the WHO histological classification of these tumors.

Transcription factor AP‐2γ, a novel marker of gonocytes and seminomatous germ cell tumors

“…14,31 Also, compared to classical seminomas, AP-2g was downregulated in embryonal carcinomas and its expression was lost in yolk sac tumors and teratomas. This result is in agreement with the current model of progression of pluripotent embryonal carcinoma to more differentiated nonseminomatous GCTs.…”

“…There were 87 testicular, 13 metastatic and 11 primary extragonadal GCTs and 5 ovarian dysgerminomas (Table I). Tumors were diagnosed according to the WHO classification, 14 and routine immunohistochemistry was performed using antibodies to PLAP, a-fetoprotein, human chorionic gonadotropin and receptor tyrosine kinase c-KIT.…”

Germ cell tumors of the gonads: a selective review emphasizing problems in differential diagnosis, newly appreciated, and controversial issues

“…If the borderline findings are diffuse, impressive AE1/AE3 and CD30 reactivity should be required, rather than focally prominent positivity for one of these markers, before accepting the tumor as embryonal carcinoma. About 5% of germinomas have distinct admixed syncytiotrophoblast cells, 73,83 although additional cases with inconspicuous syncytiotrophoblast cells can be identified using immunohistochemical stains for human chorionic gonadotropin (hCG). 84 When these cells are widely dispersed, as is typically the case, this phenomenon does not usually create diagnostic confusion.…”

Human testicular germ cell tumours express inhibin subunits, activin receptors and follistatin mRNAs

“…One of these portions was snap frozen in liquid nitrogen, while the other portion was fixed in 4% buffered formalin and embedded in paraffin. Tumours were classified according to the recommendations of the World Health Organization (Mostofi et al, 1987), as described previously (Oosterhuis et al, 1989). In this study, nine seminomas, 11 non-seminomas and two spermatocytic seminomas were included.…”

“…Both these groups develop from intratubular germ cell neoplasia (carcinoma in-situ or CIS) (Skakkebek et al, 1987), but seminomas and non-seminomas differ in histology and clinical behaviour, with the non-seminomas being the more aggressive tumours (Oosterhuis et al, 1993). Histologically, non-seminomas are classified as embryonal carcinomas, teratomas, choriocarcinomas and yolk sac tumours (Mostofi, 1980;Ulbright, 1993). These components originate from pluripotent embryonal carcinoma cells (Andrews et al, 1987) and may occur as the only cell type or may be intermixed.…”