Testicular Cancer
Malignant testicular tumors are the most prevalent solid tumors in men ages 20 to 40. Rare in nonwhite males, testicular cancer accounts for less than 1% of all male cancer deaths.
With few exceptions, testicular tumors originate from germ cells. About 40% become seminomas. These tumors, which are characterized by uniform, undifferentiated cells, resemble primitive gonadal cells. Other tumors—nonseminomas—show various degrees of differentiation.
Prognosis in testicular cancer depends on the cell type and stage. When treated with surgery, chemotherapy, and radiation therapy, all patients with stage I or stage II seminomas and 90% of those with stage I nonseminomas survive beyond 5 years. The prognosis is poor, however, if the disease advances beyond stage II. Typically, when the cancer extends beyond the testes, it spreads through the lymphatic system to the iliac, para-aortic, and mediastinal nodes. Metastases affect the lungs, liver, viscera, and bone.
Causes
Although researchers don’t know the immediate cause of testicular cancer, they suspect that cryptorchidism (even when surgically corrected) plays a role in the developing disease. A history of mumps orchitis, inguinal hernia in childhood, or maternal use of diethylstilbestrol (DES) or other estrogen-progestin combinations during pregnancy also increases the risk for this disease.
Complications
Disease progression may induce back or abdominal pain (from retroperitoneal adenopathy), dyspnea, cough, hemoptysis from lung metastases, and ureteral obstruction.
Assessment
The patient’s history may disclose previous injuries to the scrotum, viral infections (such as mumps), or the use of DES or other estrogen-progestin drugs by the patient’s mother during pregnancy. The patient may describe a feeling of heaviness or a dragging sensation in the scrotum. He may also report swollen testes or a painless lump found while performing testicular self-examination. In late disease stages, the patient may complain of weight loss, a cough, hemoptysis, shortness of breath, lethargy, and fatigue.
On inspection, you may notice that the patient has enlarged testes. Gynecomastia, a sign that the tumor produces chorionic gonadotropins or estrogen, may also be obvious. In later stages of testicular cancer, the patient may appear lethargic, thin, and pallid.
Palpation findings include a firm, smooth testicular mass and enlarged lymph nodes in surrounding areas. In later disease stages, palpation may disclose an abdominal mass as well.
On auscultation, you may hear decreased breath sounds.
Diagnostic tests
Serum analyses may be done to evaluate beta-subunit human chorionic gonadotropin (HCG), alpha fetoprotein (AFP), and lactate dehydrogenase levels.
Elevated levels of these proteins (tumor markers) suggest testicular cancer and can differentiate a seminoma from a nonseminoma: elevated HCG and AFP levels point to a nonseminoma; elevated HCG and normal AFP levels indicate a seminoma. In the future, genetic testing may be used to reveal testicular cancer gene. (See Detecting testicular cancer.)
Computed tomography (CT) scan can detect metastases.
Chest X-rays may show pulmonary metastases.
Lymph angiography, ultrasonography, and magnetic resonance imaging may reveal additional metastases.
Excretory urography may detect ureteral displacement, which is caused by metastases to a para-aortic lymph node.
Biopsy can confirm the diagnosis, help stage the disease, and plan treatment.
Treatment
Treatment includes surgery, radiation therapy, and chemotherapy. Treatment intensity varies with the tumor cell type and stage.
Surgical options include orchiectomy and retroperitoneal node dissection to prevent disease extension and assess its stage. Most surgeons remove just the testes and not the scrotum. The patient may need hormonal replacement therapy after bilateral orchiectomy.