Who gets testicular cancer and what causes it?Although relatively infrequent, testicular cancer is the most common solid tumor among men bet
Who gets testicular cancer and what causes it?
Although relatively infrequent, testicular cancer is the most common solid tumor among men between the ages of 20 to 34. It is estimated that there will be 7,200 new testicular cancers cases diagnosed in 2001 in the United States.
The most important risk factor for testes cancer is cryptorchidism. Cryptorchidism increases testicular cancer risk 3 to 14 fold, and it has been estimated that 10% of testicular cancer patients have a history of cryptorchidism. Early orchidopexy (before 1 year of age) may reduce, but does not eliminate this increased risk.What is testicular cancer?
Germ cell tumors account for more than 90% of all testes tumors, the majority of which are classified as pure seminomas or non-seminomas. Most non-seminomatous germ-cell tumors are comprised of a combination of the following histologic patterns; embryonal carcinoma, teratoma, teratocarcinoma and choriocarcinoma.
The most common non-germ cell testicular tumors are Sertoli and leydig cell tumors. The majority of these tumors are benign. Leydig cell tumors can present with sequela of increased androgen production such as precocious puberty in boys and virilization in girls.How is testicular cancer diagnosed?
All intra-testicular masses should be considered a malignancy until proven otherwise. Patients with testicular masses should have a scrotal sonogram to confirm the presence of a solid intra-testicular mass and to evaluate the contralateral testicle. For the most part, patients with intratesticular masses should undergo radical orchiectomy through an inguinal approach. There is no role for needle biopsy and testicular masses should not be removed by a trans-scrotal approach. Prior to orchiectomy patients should be evaluated with serum tumor markers; alpha-fetoprotein (AFP) and human chorionic gonadotropin (bHCG). More than 90% of patients with non-seminomatous germ cell tumors have either an elevated AFP, HCG or both. In contrast only 10% of seminomas are associated with an elevated HCG. AFP is never produced in pure seminomas so patients with elevated AFP should be treated as though they have non-seminomatous tumors.
Germs cell tumors spread sequentially to the retroperitoneal lymph nodes and then to other distant sites so patients diagnosis of germ-cell neoplasm should be staged with an abdominal CT scan and a chest x-ray. Other serum markers s uch as LDH can provide useful prognostic information as well.How is testicular cancer treated?
The development of cis-platinum based chemotherapy for testicular cancer has made cure possible in most cases. Today, treatment decisions are based on maximizing chance for cure while reducing treatmetn related morbidities. The primary treatment for all testicular tumors is radical orchiectomy. Subsequent treatment depends on histology and clinical stage.
Seminoma is very sensitive to radiation and effective doses can be delivered with minimal morbidity. Therefore even though only 15% of patients with clinical stage I seminoma have micrometastatic lymph node involvement it is recommended that most of these patients receive a low dose of adjuvant radiation to the retroperitoneum. Patients with lymph node metastasis <5 cm in diameter are also treated with radiation. Patients with bulky adenopathy > 5 cm or distant disease are treated with 3 - 4 courses of cis-platinum based chemotherapy.
Non-seminomas are less sensitive to radiation than seminomas but respond very well to cis-platinum based chemotherapy. Treatment options for stage I non-seminomas include; retroperitoneal lymph node dissection (RPLND), observation or primary chemotherapy. Treatment recommendations are based on histologic features of the primary tumor as well as patients desires to avoid treatment related side effects. Approximately 30% of patients with clinical stage I disease have micrometastic lymph node involvement, but the presence of more than 50% embryonal elements or lymphovascular invasion increases this risk to greater than 50%. Although RPLND is a major surgical procedure it can now be performed with minimal morbidity. Development of "template" dissection techniques preserves the sympathetic chain so that patients seminal emmision and antegrade ejaculation will be retained. Observation protocols can achieve cure rates similar to the RPLND but require intensive follow up for at least 5 years. Although excellent cure rates can also be achieved with primary chemotherapy long term morbidity has yet to be determined.
All patients with Stage II or h igher non-seminomas should be treated with 3 - 4 cycles of cis-platinum based chemotherapy. Patients with persistently elevated tumor markers following orchiectomy are presumed to have residual metastatic disease and should be treated with chemotherpay. Those with residual retroperitoneal masses larger than 3 cm usually undergo a "post-chemotherapy" RPLND.