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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.

BACKGROUND The purpose of this study was to develop a reliable model to identify clinical Stage I nonseminomatous germ cell tumors (NSGCTs) associated with low risk or high risk for occult retroperitoneal metastasis, so that the model could be used to customize the therapeutic approach for patients with these tumors. The model was to be based on pathohistologic parameters and immunohistochemical expression of proliferation markers, proteases, and adhesion molecules in the primary tumor. METHODS One hundred forty‐nine patients with clinical Stage I NSGCTs underwent retroperitoneal lymphadenectomy and were included in the study. Three to five paraffin embedded, formalin fixed tissue blocks were available from each patient and were analyzed for the following histopathologic features associated with pathologic Stage I or II disease: the presence or absence of vascular invasion (VI), the presence or absence of tunic invasion, and the percentage of each histologic type present in the primary tumor. Immunohistochemical expression of MIB‐1, p53, bcl‐2, cathepsin D, and E‐cadherin was evaluated using a semiquantitative scoring system. Statistical analysis was performed with univariate and multivariate logistic regression models. RESULTS The percentage of embryonal carcinoma (%EC, P < 0.001) and the presence of VI (P < 0.0001) and tunic invasion (P < 0.002) were the most significant independent risk factors associated with pathologic Stage II disease. A combination of %EC and VI allowed correct prediction of final pathologic stage for 88% of clinical Stage I patients. Cutoff values including both variables identified the correct pathologic stage for 131 of 149 patients (88%). Less than 45% EC and the absence of VI correctly identified pathologic Stage I disease in 91.5% of patients; more than 80% EC and the presence of VI correctly predicted pathologic Stage II in 88%. In univariate analysis, only p53 (P < 0.03) and E‐cadherin (P < 0.001) expression were significantly different in the embryonal carcinoma component of pathologic Stage I and II NSGCT. To evaluate prospectively the clinical utility of the new derived cutoff points, the data were applied to 10 consecutive patients with clinical Stage I NSGCT who underwent retroperitoneal lymphadenectomy; pathologic Stage I and II were correctly predicted for 5 of 6 Stage I and 4 of 4 Stage II patients, respectively. CONCLUSIONS %EC and the presence or absence of VI appear to be reliable prognosticators to identify patients at high risk and low risk for occult retroperitoneal disease. In cases of clinical Stage I NSGCT, p53, bcl‐2, MIB‐1, cathepsin D, and E‐cadherin did not appear to be of prognostic significance. The authors recommend that all patients with clinical Stage I NSGCT have their primary orchiectomy specimens evaluated for %EC and the presence of VI to determine their risk for occult retroperitoneal metastasis. Cancer 1998;83:1002‐1011. © 1998 American Cancer Society.

Observations on 6,000 testicular tumors revealed the following: Testicular tumors constitute the fourth most common cause of deaths from neoplasia in the age group of 15–34 years of age. There is a definite geographic, racial, and age distribution. The cause of testicular tumors is unknown, but cryptorchidism, trauma, infections, and genetic and endocrine factors appear to play a role in their development. Germ cell tumors comprise the large majority of testicular tumors and present one or more of 4 bask histologic patterns: seminoma, embryonal carcinoma, choriocarcinoma, and teratoma. In 40% the tumors show admixtures of 2 or more of these basic cell types. Tumors of specialized gonadal stroma constitute about 6% of testicular tumors and consist of Leydig cell, Sertoli cell, and granulosa‐theca cell tumors, or admixtures of these. The most important metastatic tumor of the testes is malignant lymphoma, initially manifested as testicular tumor.

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