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EPIDEMIOLOGY

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Although testis cancer is rare when viewed across the lifespan, it is the most common malignancy in men aged 20–35 years. Thanks to the high cure rate of the disease, however, it represents fewer than 5% of cancer deaths during those ages. In 2013, there were about 7,920 new cases and 370 deaths from testicular cancer. Incidence is relatively stable while mortality has been in decline. The declining mortality rate is attributed to the development of curative chemotherapy for advanced disease, improved treatment algorithms, earlier stage at presentation, and a growing proportion of seminomas relative to nonseminomas. The U.S. male lifetime risk of being diagnosed with testis cancer is between 3 and 4 in 1000. Testis cancer is exceedingly rare in African American men, whose incidence of the disease is one-fifth that of white Americans.

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Major risk factors for testis cancer include cryptorchidism, and a family history or personal history of testicular cancer. Having a brother with testis cancer raises a man's risk about 8- to 10–fold, whereas testis cancer in the father raises the son's risk fourfold. The risk for testis cancer in men with cryptorchidism is estimated to be 10–15 times higher than in the general population, resulting in a roughly 2%–3% lifetime risk of testis cancer. Prepubertal orchiopexy is strongly recommended in men with cryptorchidism to reduce the risk of testis cancer. Men who have had testis cancer have about a 2%–3% risk of developing a second cancer in the contralateral testis.

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PATHOLOGY

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The vast majority of testicular neoplasms are germ cell tumors (GCTs), which include the following subcategories:

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  • Seminoma

  • Embryonal carcinoma

  • Teratoma

  • Yolk sac tumor (also known as endodermal sinus tumor)

  • Choriocarcinoma

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Choriocarcinomas and teratomas in men are different diseases from gestational choriocarcinomas and gestational teratomas in women. In contrast, ovarian GCTs in women and pediatric GCTs are similar but not identical to testicular GCTs in post-pubescent males. For management purposes, GCTs in men are divided into pure seminomas and nonseminomas. Pure seminomas may contain no other GCT elements. Nonseminomas, in contrast, usually consist of a mixture of two or more GCT subtypes and one of these subtypes may be seminoma.

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Serum tumor markers (STMs) are elevated in over half of all testis cancer patients. STMs are more likely to be elevated in advanced stage than localized disease. The following STMs all play a critical role in the diagnosis, staging, and management of testicular cancer:

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  • Alpha-fetoprotein (AFP) (half-life = 5–7 days)

  • Human chorionic gonadotropin (HCG) (half-life = 24–36 h)

  • Lactate dehydrogenase (LDH)

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One critical fact is that seminomas do not produce AFP. Elevated serum AFP therefore precludes a diagnosis of seminoma regardless of the histopathology unless an alternative source for the AFP is clearly identified. Likewise, a post-orchiectomy HCG greater than 1000 IU/L would be considered inconsistent with pure seminoma by many GCT ...

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