Disease relevance of Seminoma

• Cells of prostate carcinomas, a seminoma, various bladder carcinomas and teratocarcinomas showed proliferation rates that were 10% of those of the controls when incubated with some ALP for longer than 24 hours [1].
• Focal expression of the Y antigen was identified in 5 of 17 seminomas and in the majority of embryonal carcinomas and yolk sac tumors [2].
• In a pilot study, we have examined Ape1/ref-1 expression by immunohistochemistry in sections of germ cell tumors (GCTs) from 10 patients with testicular cancer of various histologies including seminomas, yolk sac tumors, and malignant teratomas [3].
• Single-agent carboplatin should be considered the treatment of choice for advanced stages of malignant seminoma when limitation of toxicity is considered important; however, the rarity, especially of extranodal metastases from seminoma, leads to the need for further investigation using this approach [4].
• PURPOSE: Activation of the KIT tyrosine kinase by somatic mutation has been documented in a number of human malignancies, including gastrointestinal stromal tumor (GIST), seminoma, acute myelogenous leukemia (AML), and mastocytosis [5].

High impact information on Seminoma

• Seminoma and epididymal cysts in a young man with known diethylstilbestrol exposure in utero [6].
• One patient with a diagnosis of extragonadal seminoma failed to respond to cisplatin-based chemotherapy and had a second tumor biopsy performed that demonstrated a t(8;14) (q24;q32) [7].
• False positivity with one-step and conventional ELISA for alpha-fetoprotein in seminoma [8].
• The gr/gr deletion was more strongly associated with seminoma (aOR 3.0; 95% CI 1.6-5.4; P = .0004) than with nonseminoma TGCT (aOR 1.5; 95% CI 0.72-3.0; P = .29) [9].
• TCL1 participates in early embryonic development and is overexpressed in human seminomas [10].

Chemical compound and disease context of Seminoma

• Simple nontoxic treatment of advanced metastatic seminoma with carboplatin [4].
• CONCLUSION: Most patients with advanced seminoma are cured with standard first-line programs of cisplatin and etoposide with or without bleomycin [11].
• We therefore feel that gallium scans have minimal value in the prechemotherapy or postchemotherapy evaluation of metastatic seminoma [12].
• Two patients had concomitant malignancy (chronic monomyelogenous leukemia and retroperitoneal seminoma respectively) and 1 patient developed immunoblastic sarcoma in the opposite hemisphere after biopsy diagnosis and steroid treatment of her demyelinating lesion [13].
• The alpha 5 integrin subunit was weakly expressed in primary seminomas in all stages [14].

Biological context of Seminoma

• In contrast, seminomas lacking a restricted 12p amplification, showing significantly lower levels of DAD-R with pronounced apoptosis, manifest clinically in the fourth decade of life [15].
• This is the first description of an activating c-kit mutation in GCTs and is evidence that the KIT signal transduction pathway is important in the pathogenesis of neoplasms with seminoma differentiation [16].
• RASSF1A methylation was detected in four of 10 (40%) seminomas and 15 of 18 (83%) nonseminoma TGCT (NSTGCT) components (P=0.0346) [17].
• These results indicate to a major difference in telomeric length between seminomas and nonseminomas, which is apparently unrelated to the presence of telomerase activity, and suggest a germline-like homeostasis of telomeric length is preserved in human nonseminomas [18].
• Storage of Cx43 in the Golgi apparatus may correspond during spermatogenesis to an intermittent physiological process that becomes permanent in malignant seminoma cells as a result of the tumourigenic process [19].

Anatomical context of Seminoma

• Increases were noted in the frequencies of Aw33, B5, DR5, and DRw6 among the patients with pure seminoma, A3 and B7 among the patients with embryonal carcinoma with or without seminoma, and Aw32 among the patients with yolk sac tumor components [20].
• The number of CD3(+), CD8(+), TIA-1(+), and granzyme B(+) cells in tumour cell nests was markedly increased in testicular seminomas, compared with NSTGCTs (p<0.01) [21].
• These similarities suggest that the increased expression of PLAP-like enzymes in seminomas results from enhanced eutopic expression of enzymes found in normal testis [22].
• The ETV4 protein was localised to nuclei of spermatogonia and revealed an intense staining in seminoma cells [23].
• METHODS AND MATERIALS: The study was carried out in 25 centers in Germany. Patients with pure seminoma, negative AFP-values, and retroperitoneal lymph node metastases of less than 5 cm in diameter were entered into the study [24].

Gene context of Seminoma

• In addition, our results also imply differences in expression regulation of DAD-R between seminomas and nonseminomas [15].
• Immunohistological analysis confirmed the loss of expression of SMAD4 protein in the seminoma tissues with the insertional mutation [25].
• Sixty-four percent of the seminomas and 23% of the non-seminomas had decreased expression of CDK6 by a mean factor of 5 (P = 0.009) [26].
• The classical seminomas showed vimentin positivity, but this was usually observed in a small number of tumor cells [27].
• In the second mixed germ cell tumour, the NSTGCT component was methylated for RASSF1A and MGMT, while the seminoma component was methylated only for RASSF1A [17].

Analytical, diagnostic and therapeutic context of Seminoma

• Thirty-six of 39 previously untreated evaluable patients with advanced metastatic seminoma (stage greater than or equal to IIb) obtained a complete response (CR) and three a partial response (PR) after cisplatin-based combination chemotherapy with or without surgery/radiotherapy (group 1) [28].
• Cisplatin-based combination chemotherapy in advanced seminoma patients is highly effective, but includes a significant risk of severe complications [28].
• PATIENTS AND METHODS: Between July 1989 and May 1993, 478 men with testicular seminoma stage I (T1 to T3; no ipsilateral inguinoscrotal operation before orchiectomy) were randomized (PA, 236 patients; DL, 242 patients) [29].
• Final proof that hCG beta and hCG alpha are indeed produced by these previously termed "marker negative" seminomas has been achieved by reverse transcriptase-polymerase chain reaction with primers specific for the alpha-subunit and the four most abundantly transcribed hCG beta genes 3, 5, 7, and 8 [30].
• In seminoma, placental alkaline phosphatase (PLAP) and germ cell alkaline phosphatase (PLAP-like) could be separated by isoelectric focusing following isolation by immunoaffinity [31].

References