The patient is an eighteen-year-old male who visits his physician at the urging of his girlfriend. She has noted bilateral enlargement of his breasts and is concerned that he might have breast cancer. The physician confirms nontender gynecomastia (breast enlargement in a male). The patient states that he has had mild dyspnea (shortness of breath) for about a month. On questioning he notes that he has had a painless mass in the right testis in the last several months. His history is also pertinent; he had cryptorchidism that was surgically repaired at twenty-four months. He does not know which testis was cryptorchid. The physician confirms a painless hard right testicular mass by palpation with otherwise normal male genitalia showing obvious distortion visible through the scrotum. Questionable supraclavicular lymphadenopathy (enlargement of the lymph nodes above the clavicle) is also noted. The physician orders laboratory tests for hCG (chorionic gonadotrophin) and AFP (alpha fetoprotein), both of which are positive. The physician refers the patient to a urologist who performs testicular ultrasound and notes that a “fluffy” density has replaced much of the right testis. The left testis appears normal. A chest x-ray shows multiple lesions consistent with metastatic disease. The patient undergoes orchiectomy of the right testis. Histopathological examination of the testis discloses a nonseminomatous germ cell tumor (NSGCT) described as a teratocarcinoma (malignant teratoma). The patient has high stage disease with pulmonary metastases. After undergoing several cycles of chemotherapy using platinum-based agents, he has been disease free for three years.
Figure 20.12
Discussion
About 50 percent of all germ cell tumors of the testes are NSGCTs, and about two-thirds of these are teratocarcinomas. The tumors are believed to derive from embryonal carcinoma cells that have differentiated into a mixture of mature looking tissues normally found in a variety of organs (FIGURE 20-12). These tumors are often “mixed” and also contain embryonal cells that are not differentiated and maintain malignant potential. It is of interest that the mature appearing cells (as shown in Figure 20-12) may survive chemotherapy, whereas the malignant embryonal component forming metastases is eliminated. In fact, there is an excellent potential for cure even in advanced stage disease. The presence of gynecomastia can be physiological and is a common transient finding in pubertal boys. However, the occurrence of gynecomastia should prompt examination for testicular tumors. Between 5 and 10 percent of testicular germ cell tumor patients will show gynecomastia. Over 70 percent of NSGCTs secrete hCG or AFP. The hCG molecule shares components with a number of other human hormones. hCG tends to increase the level of the female hormone estrogen more than that of testosterone, and the increased ration of the former to the latter results in gynecomastia.
Etiology and Pathogenesis
Nonseminiferous germ cell tumor (NSGCT) of the subclass containing mixed differentiated tissue components (malignant teratoma) with metastatic disease to lymph nodes and lungs. Gynecomastia related to production of hCG by the tumor.
Questions
1. Considering that testicular cancer is uncommon and quite curable, propose a simple screening protocol for early detection of this disease.
2. Propose a likely mechanism for the secretion of hCG by embryonal tumors.
3. Assume you are a male of forty years of age with no prior family history of prostatic cancer. Your doctor suggests screening for this disease. (A) What tests is your doctor likely to perform? (B) Your test results are of “borderline significance” for the presence of prostatic cancer. What tests is your physician likely to suggest? (C) Would you agree to the testing procedure? Support the logic of your answer.