Evaluation of Five Tumor Markers (AFP, CEA, hCG, hPL and SP₁) in Monitoring Therapy and Follow-up of Patients with Testicular Germ Cell Tumors

Abstract

61 patients with seminoma and 113 with nonseminomatous germ cell tumors of the testis were treated according to the histology, stage of disease, and serum levels of tumor markers (CEA, AFP, hCG, hPL and SP₁). 33 were stage I, 63 stage II, and 78 stage III patients. Most patients with seminoma, mature teratoma, immature teratoma, and ‘pure type’ embryonal carcinoma, as well as the latter three types with seminomatous admixture, had normal serum levels of the markers. Sometimes, slightly elevated levels of hCG suggested the presence of metastases. But, serial measurements of the markers were seldom useful in monitoring therapy. The 5-year tumor-free survival rates were favorable: 100% for stage I and II disease; and 57 or 44% for, respectively, stage III seminoma or the other tumors amounting to 10% of the nonseminomatous group. The role of the five markers was significant in patients with teratoma with malignant transformation, choriocarcinoma, endodermal sinus tumor (EST), and embryonal carcinoma or teratocarcinoma with an admixture of EST or choriocarcinoma or both. Elevation of a marker was a grave prognostic sign. The 5-year survival rates were 100, 16, and 4% for stages I, II and III disease, respectively. An elevated level of one or more of the markers assayed was always useful for monitoring therapy. Decreasing level indicated regression. However, return of an elevated level to normal did not indicate eradication of all tumor and called for diagnosis by imaging modalities. Constantly elevated or increasing marker levels during treatment indicated resistance to therapy. An increasing level from any nadir during remission indicated recurrence. Elevated levels of any of the five markers tested were as important as imaging modalities, and often more sensitive.

Intracranial Malignant Germ Cell Tumor and the Klinefelter Syndrome

“…Most attractive is the theory of altered migra tion of the primitive germ cells along the urogenital ridge from the endodermal layer of the primitive yolk sac to the gonad [22,23]. GCTs in non-KS patients may occur due to failed migration secondary to inappropriate timing or other factors [24], An increased incidence of extragonadal GCTs in KS may result from abnormal hormonal in fluences misdirecting migration or an increased potential for neoplastic transformation in improperly located germ cells: multiple lines of evidence suggest that one of these influences may be the altered gonadotropin level in KS patients [25,26], The timing of malignant transformation is also unknown but may begin in utero [5], This may help to explain the earlier median age of GCT diagnosis in KS patients. Although many KS patients receive hormonal supplementation, there are currently no data to suggest that this may normalize the increased risk of GCTs in this population.…”

Clinical Usefulness of Serum Ferritin Measurements in Patients with Testicular Germ Cell Tumors

“…Of the latter group, tumors from 20 patients contained only one histological component: teratoma or embryonal carcinoma, while 14 contained two components: terato ma or embryonal carcinoma with an admixture of seminomatous elements. These nonseminomatous tumors arc known as non producing the conventional markers [1][2][3], Only 16 patients had nonseminomatous tumors producing the markers amply (table I).…”

“…Serial determinations of CEA, AFP and hCG in serum significantly contribute to the diagnosis, staging and management of patients with germ cell tumors of the testis [1][2][3]. However, serum concentrations of these markers are within normal limits in most pa tients with seminoma, pure embryonal carcinoma, pure teratoma, and the latter two types of tumors with seminomatous admixture [1][2][3].…”

“…However, serum concentrations of these markers are within normal limits in most pa tients with seminoma, pure embryonal carcinoma, pure teratoma, and the latter two types of tumors with seminomatous admixture [1][2][3].…”

Pluripotential Germinal Tumor Tissue as a Source of Transplantable Graft Tissue

“…G onadotrophic stimulation is also im portant in the genesis of GCT in cases of cryptorchidism, testicular feminization, gonadal dys genesis, certain testicular tumors which are not themselves gonado tropin secreting, and the worsened prognosis evident among GCT sec reting gonadotropins [1,9,11,18,27,29].…”