while an inguinal canal testis carries a 1.3% risk. A significant number of tumors also occur in the contralateral, normally descended testicle in patients with unilateral cryptorchidism. Surgical placement of the cryptorchid testis into the scrotum (i.e., orchiopexy ) does not alter the cancerous potential of the undescended testicle. However, the procedure does facilitate testicular examination and tumor detection. Whereas family clustering of testicular cancer has been described and the frequency is significantly higher among brothers and other close male relatives of those with testicular cancer, a well-defined pattern of inheritance has not been established. Cancer appears to be a multifactorial disorder in which both environmental and genetic factors play important roles. Men with disorders of testicular development, including those born with the chromosomal abnormality known as Klinefelter syndrome , have an increased risk for cancer of the testis. Testicular cancer is unique in that, unlike many other cancers, its frequency decreases with age. The highest risk appears in men ages 15–35 years and, although still possible, can- cer of the testis is extremely rare after age 40 years. Testicular cancer increases the risk 25-fold for development of cancer in the initially uninvolved testicle. There is some evidence that human immunodeficiency virus (HIV) infec- tion is also a risk factor. Pathophysiology The pathogenesis of the majority of cancers is not completely known. However, it has been established that specific mutations in the deoxyribonucleic acid (DNA) of normal cells cause them to become cancerous. Oncogenes are genes that promote cell division. Tumor suppressor genes are genes that slow down cell division, cause abnormal cells to die, or help repair DNA damage; in other words, tumor suppressor genes “hold cancer in check.” Mutations that activate oncogenes or deactivate tumor suppressor genes play a major role in the transformation of a normal cell to a cancerous one. Every human cancer that has been studied is associated with multiple genetic alterations involving activation of several oncogenes and the deactivation of two or more tumor suppressor genes. Cancer-causing chemicals, viruses, and radiation (both ultra- violet and ionizing) are responsible for causing many mutations during a person’s lifetime. Disease Summary Table 74.1 Approximate Frequencies of the Most Common Types of Testicular Cancer Type of Testicular Cancer Approximate Frequency (%) GERM CELL CANCERS 95 Seminoma 30 Non-seminoma 65 • Mixed cell tumor 40 • Embryonal carcinoma 20 • Teratoma 5 • Choriocarcinoma 1 NON-GERM CELL CANCERS 5 Adapted with permission from Morgan K, McCance KL. Cancer of the testis. In: McCance KL, Huether SE, eds. Pathophysiology—The Biologic Basis for Disease in Adults and Children. 5 th Ed. St. Louis: Elsevier Mosby, 2006;Table 23-9:812.
DS74-3 Case Study 74 ■ Testicular Cancer As cancer advances and abnormal cells continue to divide, more and more mutations occur and the cell becomes more distantly removed from its original genotype. As genes are altered,
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