Seminoma
Other names	Pure seminoma, classical seminoma
Histopathology of classical seminoma, with typical features.[1]
Specialty	Urology,oncology

Aseminoma is agerm cell tumor of thetesticle or, more rarely, themediastinum or other extra-gonadal locations. It is amalignantneoplasm and is one of the most treatable and curable cancers, with a survival rate above 95% if discovered in early stages.^[3]

Testicular seminoma originates in thegerminal epithelium of theseminiferous tubules.^[4] About half of germ cell tumors of the testicles are seminomas.^[5] Treatment usually requires removal of one testicle. However, fertility is not usually affected. All other sexual functions will remain intact.

The average age of diagnosis is between 35 and 50 years. This is about 5 to 10 years older than men with other germ cell tumors of the testes. In most cases, they produce masses that are readily felt ontesticular self-examination; however, in up to 11 percent of cases, there may be no mass able to be felt, or there may betesticular atrophy. Testicular pain is reported in up to one fifth of cases. Low back pain may occur aftermetastasis to theretroperitoneum.^[6]

Some cases of seminoma can present as a primary tumour outside the testis, most commonly in themediastinum.^[6] In theovary, the tumor is called adysgerminoma, and in non-gonadal sites, particularly thecentral nervous system, it is called agerminoma.^[5]

Blood tests may detect the presence of placentalalkaline phosphatase (ALP, ALKP, ALPase, Alk Phos) in fifty percent of cases. However, Alk Phos cannot usefully stand alone as a marker for seminoma and contributes little to follow-up, due to its rise with smoking.^[7]Human chorionic gonadotropin (hCG) may be elevated in some cases, but this correlates more to the presence oftrophoblast cells within the tumour than to the stage of the tumour. A classical or pure seminoma by definition does not cause an elevated serumalpha fetoprotein.^[8]Lactate dehydrogenase (LDH) may be the only marker that is elevated in some seminomas. The degree of elevation in the serum LDH has prognostic value in advanced seminoma.^[9]

The cut surface of the tumour is fleshy and lobulated, and varies in colour from cream to tan to pink. The tumour tends to bulge from the cut surface, and small areas ofhemorrhage may be seen. These areas of hemorrhage usually correspond to trophoblastic cell clusters within the tumour.^[5]

Microscopic examination shows that seminomas are usually composed of either a sheet-like or lobular pattern of cells with a fibrousstromal network. The fibrous septa almost always contain focallymphocyte inclusions, andgranulomas are sometimes seen. The tumour cells themselves typically have abundant clear to pale pinkcytoplasm containing abundantglycogen, which is demonstrable with aperiodic acid-Schiff (PAS) stain. The nuclei are prominent and usually contain one or two large nucleoli, and have prominent nuclear membranes. Foci ofsyncytiotrophoblastic cells may be present in varied amounts. The adjacent testicular tissue commonly showsintratubular germ cell neoplasia, and may also show variable spermatocytic maturation arrest.^[5]

• 
  Gross pathology of seminoma
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  Histopathological image of metastatic seminoma in the inguinal lymph node. Hematoxylin & eosin stain.
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  Histopathological image of metastatic seminoma in the inguinal lymph node. At higher magnification. Hematoxylin & eosin stain.
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  Micrograph (high magnification) of a seminoma. H&E stain.
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  Testicular seminoma, showing a typically prominentlymphocytic infiltrate in the fibrousstroma separating the clusters of tumor cells.
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  Orchidectomy specimen showing seminoma
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  The germ cell markersOCT 3/4 andCD117 (positiveimmunohistochemistry pictured) are useful for diagnosis.^[10]

Spermatocytic tumors are not considered a subtype of seminoma and unlike other germ cell tumours do not arise fromintratubular germ cell neoplasia.^[11]

Intratesticular masses that appear suspicious on anultrasound should be treated with aninguinal orchiectomy. The pathology of the removed testicle andspermatic cord indicate the presence of the seminoma and assist in the staging. Tumors with both seminoma andnonseminoma elements or that occur with the presence of AFP should be treated as nonseminomas. Abdominal CT or MRI scans as well as chest imaging are done to detect for metastasis. The analysis of tumor markers also helps in staging.^[12]

The preferred treatment for most forms of stage 1 seminoma is active surveillance. Stage 1 seminoma is characterized by the absence of clinical evidence of metastasis. Active surveillance consists of periodic history and physical examinations, tumor marker analysis, and radiographic imaging. Around 85-95% of these cases will require no further treatment. Modern radiotherapy techniques as well as one or two cycles of single-agentcarboplatin have been shown to reduce the risk of relapse, but carry the potential of causing delayed side effects. Regardless of treatment strategy, stage 1 seminoma has nearly a 100% cure rate.^[13]

Stage 2 seminoma is indicated by the presence ofretroperitoneal metastasis. Cases require radiotherapy or, in advanced cases, combination chemotherapy. Large residual masses found after chemotherapy may require surgical resection. Second-line treatment is the same as for nonseminomas.^[12]

Stage 3 seminoma is characterized by the presence of metastasis outside the retroperitoneum—the lungs in "good risk" cases or elsewhere in "intermediate risk" cases. This is treated with combination chemotherapy. Second-line treatment follows nonseminoma protocols.^[12]

• Male genital neoplasia
• Germ cell neoplasia

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