eMedicine Specialties > Oncology > Carcinomas of the Genitourinary Tract
Testicular Cancer
Updated: Jul 29, 2009
Introduction
Background
Primary testicular tumors are the most common solid malignant tumor in men between the ages of 20 and 35 years in United States. For unknown reasons, the incidence of this cancer increased during the last century. Over the past decade, the incidence of testicular cancer has risen approximately 1.2% per year but the absolute mortality rate has been stable or decreasing; approximately 9,000 new cases have been diagnosed in United States every year, and only about 350 to 400 deaths have occurred annually. The American Cancer Society estimates that about 8,400 new cases of testicular cancer will be diagnosed during 2009 in the United States.1 It is estimated that 380 men will die of testicular cancer in 2009. The lifetime chance of developing testicular cancer is about 1 in 300 and the risk of dying is very low—about 1 in 5,000.
In the past, metastatic testicular cancer was usually fatal, but recent advances in treatment, including high-dose chemotherapy and stem cell rescue, have considerably improved the prognosis. Indeed, testicular cancer is a bright spot in the oncological landscape and are now considered the model for the treatment of solid tumors.
Testicular cancers are very sensitive to chemotherapy and are curable even when metastatic. Cure rates for good-risk disease cure rates are 90-95%. On , there were approximately 190,265 men alive in the United States who had a history of cancer of the testis.
Pathophysiology
The cause of testicular cancer is not known. The characteristic genetic change found is an isochromosome of the short arm of chromosome 12 [i(12p)], which is often seen in sporadic cancers. This suggests that genes in this region are important in the development of germ cell tumors. A number of other genes that have a relatively weak effect are also involved in the development of testicular cancer.
That genetic factors have a role in the development of testicular cancer is shown by the fact that the risk for the disease is higher in first-degree relatives of cancer patients than in the general population. About 2% of testicular cancer patients report having an affected relative. Siblings are at particularly increased risk, with a relative risk of 8–10. For sons of affected men, the relative risk is 4–6.
Two models of testicular carcinoma in situ have been proposed. The first posits that fetal gonocytes whose development into spermatogonia is blocked may undergo abnormal cell division and then invasive growth mediated by postnatal and pubertal gonadotropin stimulation.
The second model postulates that the most likely target cell for transformation is the zygotene-pachytene spermatocyte. During this stage of germ cell development, aberrant chromatid exchange events associated with crossing over can occur. Normally, these cells are eliminated by apoptosis. On occasion, this crossing over may lead to increased 12p copy number and overexpression of the cyclin D2 gene (CCND2). The cell carrying this abnormality is relatively protected against apoptotic death because of the oncogenic effect of CCND2, leading to re-initiation of the cell cycle and genomic instability.
Malignant transformation of germ cells is the result of a multistep process of genetic changes. One of the earliest events is the increased copy number of 12p, either as 1 or more copies of i(12p) or as tandem duplications of chromosome arm 12p. This abnormality is found in occult carcinoma in situ lesions as well as more advanced disease. Further studies indicate that CCND2 is present at chromosome band 12p13 and that CCND2 is overexpressed in most germ cell tumors, including carcinoma in situ. Amplification of CCND2 activates cdk4/6, allowing the cell to progress through the G1-S checkpoint.
Frequency
United States
Testicular cancers are not a common malignancy. Approximately 9,000 new cases are diagnosed in the United States each year. From 2002–2006, the median age at diagnosis was 34 years of age.
In the United States, the incidence increased by 100% from 1988 to 2001. Diagnoses of seminomas increased 124% during that period and diagnoses of nonseminomas increased by 64%. No significant increase occurred in the incidence of early-stage disease in proportion to all diagnoses in this population, indicating that the increase was not due to more widespread screening or earlier detection.2
According to Surveillance, Epidemiology, and End Results (SEER) data from 17 geographic areas, the age-adjusted annual incidence of testicular cancer from 2002–2006 was 5.4 per 100,000 men. However, the incidence varies widely by race/ethnicity (see below).
International
Studies published between 1980 and 2002 showed a clear trend towards an increased testicular cancer incidence in the last 30 years in the majority of industrialized countries in North America, Europe, and Oceania. Differences in incidence were seen between neighboring countries (2.5/100,000 cases in Finland versus 9.2/100,000 cases in Denmark) as well as among regions of the same country (2.8 to 7.9/100,000 within France). The increase in incidence was significantly associated with a birth cohort effect in the United States and in European countries. Substantial differences in the incidence and trends were observed among ethnic groups. Incidence by race are described above.
Mortality/Morbidity
Testicular cancers are highly curable, even in patients with metastatic disease at diagnosis. The prognosis depends upon the histologic type of cancer (seminoma versus nonseminoma), stage, and other features such as tumor marker and type of metastatic disease.
Patients with seminomas that confer a good prognosis, which constiute about 90% of seminomas, have a 5-year survival of 86%; patients with good-prognosis nonseminomas (56% of nonseminomas) have a 5-year survival of 92%. With intermediate-prognosis cancers (28% of nonseminomas), 5-year survival is 72% with seminomas and 80% with nonseminomas. With poor-prognosis nonseminomas (about 16% of nonseminomas) 5-year survival is 48%.
Those survival data are based on patients treated between 1975 and 1990; more recent studies has shown much better survival with nonseminomatous germ cell tumors (NSGCT). Pooled 5-year survival estimates for NSGCT were 94% for good-prognosis, 83% for intermediate-prognosis, and 71% for poor-prognosis tumors.
Race
The incidence of testicular cancer is fivefold higher in whites than in African Americans; however, African Americans tend to present with higher-grade disease and have much worse prognosis than whites.3
Open table in new window
Table
| Incidence of Testicular Cancer by Race | |
| Race/Ethnicity | Annual rate per 100,000 men |
| All Races | 5.4 |
| White | 6.3 |
| Black | 1.3 |
| Asian/Pacific Islander | 1.7 |
| American Indian/Alaska Native | 4.6 |
| Hispanic | 4.0 |
| Incidence of Testicular Cancer by Race | |
| Race/Ethnicity | Annual rate per 100,000 men |
| All Races | 5.4 |
| White | 6.3 |
| Black | 1.3 |
| Asian/Pacific Islander | 1.7 |
| American Indian/Alaska Native | 4.6 |
| Hispanic | 4.0 |
Age
Testicular cancer can occur at any age but is most common between the ages of 15 and 35 years. There is also secondary peak in incidence after age 60. Seminoma is rare in boys younger than 10 years of age but is the most common histologic type in men older than 60.
Clinical
History
Localized disease:
Painless swelling or nodule of one testicle is the most common presenting symptom. On the physical exam this mass/nodule can not be separated from the testis. Patients with atrophic testes will feel enlargement. Dull ache or heavy sensation in the lowed abdomen could be presenting symptom. Patients who experience a hematoma with trauma should undergo evaluation to rule out testicular cancer.
Metastatic disease:
Disseminated disease have symptom of lymphatic or hematogenous spread. Presenting symptom could be neck mass in supraclavicular lymph node metastatic disease, anorexia, nausea and other gastrointestinal symptom. Bulky retroperitoneal disease could present as back pain. Cough, chest pain, hemoptysis and shortness of breath could be presenting symptom of mediastinal adenopathy or lung metastatic disease. Central nervous system disease could rarely present as neurological symptoms. Bone pain is rare.
Gynecomastia may occur in about 5% of patients with testicular germ cell tumor that produce human chorionic gonadotropin (HCG), such as choriocarcinoma and is a systemic manifestation. Marked overproduction of hCG can develop hyperthyroidism since hCG and thyroid stimulating hormone have a common alpha-subunit and a beta-subunit with considerable homology.
Physical
Any solid, firm mass within the testis should be considered testicular cancer until proven otherwise. Prompt diagnosis and early treatment are required for cure.
Testicular cancer may be painless, in which case they are sometimes ignored by the patient. In patients with scrotal pain, testicular cancer must be differentiated form epididymitis. The clinician should consider the full differential diagnosis of a testicular mass, which includes not only epididymitis but epididymo-orchitis, testicular torsion, hydrocele, hernia, hematoma, spermatocele, varicocele, and syphilitic gumma.
Unilateral or bilateral lower extremity swelling may be present in iliac or caval venous obstruction or thrombosis.
Physical examination of the testicles is performed by fully palpating all areas of the testicle between thumb and fingers. Examination should begin with bimanual examination of the scrotal contents, starting with the normal testis. This permits the examiner to evaluate the relative size, contour, and consistency of the normal testis. Other areas of emphasis include examination of the abdomen for lymphadenopathy and hepatomegaly. The examination should also include evaluation for supraclavicular nodes, bone tenderness, and gynecomastia.
Causes
Various risk factors have been associated with testicular tumors, but the specific etiology is not known.
Cryptorchidism
In patients with cryptorchidism, the riskof developing germ cell tumor is increased fourfold to eightfold. The risk of developing germ cell tumor when a cryptorchid testis is intra-abdominal is about 5%. The risk is 1% if the testis is retained in the inguinal canal. Surgical placement of the undescended testis in the scrotum—orchiopexy—when the patient is younger than 6 years lowers the risk further. About 5-20% of patients with a history of cryptorchid testis develop tumors in the normally descended testis.
In Sweden from 1965 to 2000, a total of 16,983 men underwent orchiopexy and 56 cases of testicular cancer were reported. The relative risk of testicular cancer among those who underwent orchiopexy before reaching 13 years of age was 2.23, compared with that of the Swedish general population. For those treated at 13 years of age or older, the relative risk was 5.4.4
Prior Testicular CancerA previous history of testicular cancer is the strongest risk factor for germ cell tumor. Approximately 1-2% of testicular cancer patients will develop a second primary testicular cancer contralaterally—a 500-fold higher rate than in the general population.
Genetics
Patients with Klinefelter syndrome (47XXY) have higher incidence of germ cell tumor, particularly primary mediastinal germ cell tumor. Family members of Klinefelter syndrome patients has a sixfold to 10-fold increased risk of germ cell tumor. Patients with Down’s syndrome also are at increased risk for germ cell tumors. Increased risk has also been reported in patients with cutaneous ichthyosis, mullerian syndrome, androgen insensitivity syndrome (testicular feminization), and mixed gonadal dysgenesis.
Family history
First-degree relatives have a higher risk of developing testicular cancer than the general population, although the inscidence is low. About 2% of testicular cancer patients report having an affected relative. Brothers are at particularly high risk, with a relative risk of 8–10. Among sons of affected men, twofold to sixfold increases in testicular cancer have been reported.
Infertility
Walsh et al have reported that men with male factor infertility are nearly 3 times more likely to develop subsequent testicular cancer.5 Intratubular germ cell neoplasia (testicular carcinoma in situ) has been found in 0.4–1.1% of men undergoing testicular biopsy because of infertility.
Environmental exposure
Exposure to diethylstilbestrol (DES) in utero is associated with cryptorchidism. Increased risk has been suggested with Agent Orange exposure and numerous industrial occupations. Recurrent activity such as horseback or motorcycle riding, local trauma, and increased scrotal temperature have not been associated with increased risk.
More on Testicular Cancer |
 Overview: Testicular Cancer |
| Differential Diagnoses & Workup: Testicular Cancer |
| Treatment & Medication: Testicular Cancer |
| Follow-up: Testicular Cancer |
| References |
| Next Page » |
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Further Reading
Keywords
testicular cancer symptoms, testicular cancer diagnosis, testicular cancer treatment, germ cell tumors, GCT, seminoma, embryonal carcinoma, teratoma, choriocarcinoma, yolk sac tumor
