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National Cancer Institute
Last Modified: January 20, 2012
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ® editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ® summary on Levels of Evidence for more information.)
Note: Estimated new cases and deaths from testicular cancer in the United States in 2012: 1
Testicular cancer is a highly treatable, usually curable, cancer that most often develops in young and middle-aged men. Most testicular cancers are germ cell tumors. For treatment planning, germ cell tumors are broadly divided into seminomas and nonseminomas because they have different prognostic and treatment algorithms. For patients with seminoma (all stages combined), the cure rate exceeds 90%. For patients with low-stage seminoma or nonseminoma, the cure rate approaches 100%. 2 3 4 5 6
Risk factors for testicular cancer include the following: 7
Surgical correction of an undescended testis (orchiopexy) before puberty appears to lower the risk of testis cancer, but this isn't certain. 8
Tumors that are 100% seminoma are considered seminomas. All other tumors, including those that have a mixture of seminoma and nonseminoma components, are considered and should be managed as nonseminomas. Most nonseminomas consist of a mixture of the different germ-cell tumor subtypes. Tumors that appear to have a seminoma histology but are accompanied by an elevated serum level of alpha-fetoprotein (AFP) should be treated as nonseminomas because seminomas do not produce AFP.
Alpha-fetoprotein (AFP), beta-human chorionic gonadotropin (beta-hCG), and lactase dehydrogenase (LDH) play an important role as serum tumor markers in the staging and monitoring of germ cell tumors and should be measured prior to removing the involved testicle. 9 For patients with nonseminomas, the degree of tumor-marker elevation after the cancerous testicular has been removed is one of the most significant predictors of prognosis. 10 Serum tumor markers are also very useful for monitoring all stages of nonseminomas and for monitoring metastatic seminomas because elevated marker levels are often the earliest sign of relapse.
AFP: Elevation of serum AFP is seen in 40% to 60% of men with nonseminomas. Seminomas do not produce AFP. Men who have an elevated serum AFP should be considered to have a mixed germ cell tumor (i.e., nonseminomatous germ cell tumors [NSGCT]) even if the pathology shows a pure seminoma, unless there is a more persuasive explanation for the elevated AFP, such as liver disease.
Beta-HCG: Elevation of the beta subunit of hCG is found in approximately 14% of the patients with stage I pure seminoma prior to orchiectomy and in about half of patients with metastatic seminoma. 11 12 13 Approximately 40% to 60% of men with nonseminomas have an elevated serum beta-hCG.
Significant and unambiguously rising levels of AFP and/or hCG are an indication of relapsed germ cell tumor in most cases and are an indication for treatment even in the absence of radiological evidence of metastatic disease. Nonetheless, tumor-marker elevations do need to be interpreted with caution. For example, false-positive hCG levels can result from cross reactivity of the assay with luteinizing hormone, in which case an intramuscular injection of testosterone should result in normalization of hCG values. There are also clinical reports of marijuana use resulting in elevations of serum hCG and some experts recommend querying patients about drug use and retesting hCG levels after a period of abstinence from marijuana use. Similarly, AFP is chronically mildly elevated in some individuals for unclear reasons and can be substantially elevated by liver disease.
LDH: Seminomas and nonseminomas alike may result in elevated lactate dehydrogenase (LDH) but such values are of less clear prognostic significance because LDH may be elevated in many different conditions unrelated to cancer. A study of the utility of LDH in 499 patients with testicular germ cell tumor undergoing surveillance after orchiectomy or after treatment of stage II or III disease reported that 7.7% of patient visits had elevations in LDH unrelated to cancer, whereas only 1.4% of visits had cancer-related increases in LDH. 14 Of 15 relapses, LDH was elevated in six and was the first sign of relapse in one. Over 9% of the men had a persistent false-positive increase in LDH. The positive predictive value for an elevated LDH was 12.8%.
A second study reported that among 494 patients with stage I germ cell tumors who subsequently relapsed, 125 had an elevated LDH at the time of relapse. Of these 125, all had other evidence of relapse: 112 had a concurrent rise in AFP and/or hCG, one had CT evidence of relapse prior to the elevation in LDH, one had palpable disease on examination and one complained of back pain that led to imaging that revealed retroperitoneal relapse. 15 Measuring LDH thus appears to have little value during surveillance of germ cell tumors for relapse. On the other hand, for patients with metastatic NSGCT, large studies of prognostic models have found the LDH level to be a significant independent predictor of survival on multivariate analysis. 10 16
There are two major prognostication models for testicular cancer: staging, 17 and for risk-stratification of men with distant and/or bulky retroperitoneal metastases, the International Germ Cell Cancer Consensus Group classification. 10 The prognosis of testicular germ cell tumors is determined by the following factors:
Thus, for men with disseminated seminomas, the main adverse prognostic variable is the presence of metastases to organs other than the lungs (e.g., bone, liver, or brain). For men with disseminated nonseminomas, the following variables are independently associated with poor prognosis:
Nonetheless, even patients with widespread metastases at presentation, including those with brain metastases, may have curable disease and should be treated with this intent. 18
Radical inguinal orchiectomy with initial high ligation of the spermatic cord is the procedure of choice in diagnosing and treating a malignant testicular mass. 19 As noted above, serum AFP, LDH, and hCG should be measured prior to orchiectomy. Transscrotal biopsy is not considered appropriate because of the risk of local dissemination of tumor into the scrotum or its spread to inguinal lymph nodes. A retrospective analysis of reported series in which transscrotal approaches had been used showed a small but statistically significant increase in local recurrence rates compared with the recurrence rates when the inguinal approach was used (2.9% vs. 0.4%). 20[Level of evidence: 3iiiDii] Distant recurrence and survival rates, however, were indistinguishable in the two approaches.
Evaluation of the retroperitoneal lymph nodes, usually by CT scanning, is an important aspect of staging and treatment planning in adults with testicular cancer. 21 22 Patients with a negative result however, have a substantial chance of having microscopic involvement of the lymph nodes. Nearly 20% of seminoma patients and 30% of nonseminoma patients with normal CT scans and serum tumor markers will subsequently relapse if not given additional treatment after orchiectomy. 23 24 25 For nonseminoma patients, retroperitoneal lymph node dissection (RPLND) increases the accuracy of staging but as many as 10% of men with normal imaging, normal tumor markers, and benign pathology at RPLND will still go on to relapse. 26 About 25% of patients with clinical stage I nonseminomatous testicular cancer will be upstaged to pathologic stage II with RPLND, and about 25% of clinical stage II patients will be downstaged to pathologic stage I with RPLND. 26 27 28 In prepubertal children, the use of serial measurements of AFP has proven sufficient for monitoring response after initial orchiectomy. Lymphangiography and para-aortic lymph node dissection do not appear to be useful or necessary in the proper staging and management of testicular cancer in prepubertal boys. 29 (Refer to the Genital/Urinary Tumors section in the PDQ® summary on Unusual Cancers of Childhood for more information.)
Patients who have been cured of testicular cancer have approximately a 2% cumulative risk of developing a cancer in the opposite testicle during the 15 years after initial diagnosis. 30 31 Within this range, men with nonseminomatous primary tumors appear to have a lower risk of subsequent contralateral testis tumors than men with seminomas.
HIV-infected men are reported to be at increased risk for developing testicular seminomas. 32 Depending on comorbid conditions such as active infection, these men are generally managed similarly to non-HIV-infected patients.
Radiation therapy, used to treat pure seminomatous testicular cancers, can cause fertility problems because of radiation scatter to the remaining testicle during radiation therapy to retroperitoneal lymph nodes (as evidenced in the SWOG-8711SWOG-8711 trial, for example). trial, for example). 37 (For more information on fertility, refer to the (For more information on fertility, refer to the Sexuality and Reproductive Issues summary.) Depending on scatter summary.) Depending on scatter dose, sperm counts fall after radiation therapy but may recover over the course of 1 dose, sperm counts fall after radiation therapy but may recover over the course of 1 to 2 years. Shielding techniques can be used to decrease the radiation scatter to 2 years. Shielding techniques can be used to decrease the radiation scatter to the remaining normal testicle. Because chemotherapy, retroperitoneal lymph node dissection, and radiation therapy can each result in infertility, men should be offered the opportunity to bank sperm before undergoing any treatment for testis cancer other than orchiectomy.to the remaining normal testicle. Because chemotherapy, retroperitoneal lymph node dissection, and radiation therapy can each result in infertility, men should be offered the opportunity to bank sperm before undergoing any treatment for testis cancer other than orchiectomy.
Although acute bleomycin pulmonary toxic effects may occur, they are rarely fatal at total cumulative doses of less than 400 units. Because life-threatening pulmonary toxic effects can occur, the drug should be discontinued if early signs of pulmonary toxic effects develop. Although decreases in pulmonary function are frequent, they are rarely symptomatic and are reversible after the completion of chemotherapy. Survivors of testis cancer who were treated with chemotherapy have been reported to be at increased risk of death from respiratory diseases, but it is unknown whether this finding is related to bleomycin exposure. 44
Radiation therapy, often used in the management of pure seminomatous germ cell cancers, has been linked to the development of secondary cancers, especially solid tumors in the radiation portal, usually after a latency period of a decade or more. 45 46 These include melanoma and cancers of the stomach, bladder, colon, rectum, pancreas, lung, pleura, prostate, kidney, connective tissue, and thyroid. Chemotherapy has also been associated with an elevated risk of secondary cancers.
More recently, men with testis cancer who have been treated with radiation therapy and/or chemotherapy have been reported to be at increased risk of cardiovascular events. 47 48 49 Other studies have reported that chemotherapy for testis cancer is associated with an increased risk of developing metabolic syndrome and hypogonadism. 50 51 Moreover, an international population-based study reported that men treated with either radiation or chemotherapy were at increased risk of death from circulatory diseases. 44
In a retrospective series of 992 patients treated for testicular cancer at the Royal Marsden Hospital between 1982 and 1992, cardiac events were increased approximately 2.5-fold in patients treated with radiation therapy and/or chemotherapy compared with those who underwent surveillance after a median of 10.2 years. The actuarial risks of cardiac events were 7.2% for patients who received radiation therapy (92% of whom did not receive mediastinal radiation therapy), 3.4% for patients who received chemotherapy (primarily platinum-based), 4.1% for patients who received combined therapy, and 1.4% for patients who underwent surveillance management after 10 years of follow-up. 48
A population-based retrospective study of 2,339 testicular cancer survivors in the Netherlands, treated between 1965 and 1995 and followed for a median of 18.4 years, found that the overall incidence of coronary heart disease (i.e., myocardial infarction and/or angina pectoris) was increased 1.17 times (95% confidence interval [CI], 1.041.31) compared with the general population. 49 Patients who received radiation therapy to the mediastinum had a 2.5-fold (95% CI, 1.83.4) increased risk of coronary heart disease, and those who also received chemotherapy had an almost 3-fold (95% CI, 1.74.8) increased risk. Patients who were treated with infradiaphragmatic radiation therapy alone had no significantly increased risk of coronary heart disease. In multivariate Cox regression analyses, the older chemotherapy regimen of cisplatin, vinblastine, and bleomycin (PVB), used until the mid-1980s, was associated with a significant 1.9-fold (95% CI, 1.22.9) increased risk of cardiovascular disease (i.e., myocardial infarction, angina pectoris, and heart failure combined). The newer regimen of bleomycin, etoposide, and cisplatin (BEP) was associated with a borderline significant 1.5-fold (95% CI, 1.02.2) increased risk of cardiovascular disease. Similarly, an international pooled analysis of population-based databases reported that the risk of death from circulatory disease was increased in men treated with chemotherapy (standardized mortality ratio 1.58) or radiation therapy (SMR = 1.70). 44[Level of evidence: 3iiiDii]
Although testicular cancer is highly curable, all newly diagnosed patients are appropriately considered candidates for clinical trials designed to decrease morbidity of treatment while further improving cure rates.
The following histologic classification of malignant testicular germ cell tumors (testicular cancer) reflects the classification used by the World Health Organization (WHO). 1 Less than 50% of malignant testicular germ cell tumors have a single cell type, of which roughly 50% are seminomas. The rest have more than one cell type, and the relative proportions of each cell type should be specified. The cell type of these tumors is important for estimating the risk of metastases and the response to chemotherapy. Polyembryoma presents an unusual growth pattern and is sometimes listed as a single histologic type, though it might better be regarded as a mixed tumor. 1 2 3
Note: This Stage Information section has been updated to include information from the 7th edition (2010) of the American Joint Committee on Cancer's AJCC Cancer Staging Manual. The PDQ® Adult Treatment Editorial Board, which is responsible for maintaining this summary, is currently reviewing the new staging categories to determine whether additional changes need to be made to other parts of the summary. Any necessary changes will be made as soon as possible.
The American Joint Committee on Cancer (AJCC) has designated staging by TNM classification to define testicular cancer. 1
|pTX||Primary tumor cannot be assessed.|
|pT0||No evidence of primary tumor (e.g., histologic scar in testis).|
|pTis||Intratubular germ cell neoplasia (carcinoma in situ).|
|pT1||Tumor limited to the testis and epididymis without vascular/lymphatic invasion; tumor may invade into the tunica albuginea but not the tunica vaginalis.|
|pT2||Tumor limited to the testis and epididymis with vascular/lymphatic invasion, or tumor extending through the tunica albuginea with involvement of the tunica vaginalis.|
|pT3||Tumor invades the spermatic cord with or without vascular/lymphatic invasion.|
|pT4||Tumor invades the scrotum with or without vascular/lymphatic invasion.|
|NX||Regional lymph nodes cannot be assessed.|
|N0||No regional lymph node metastasis.|
|N1||Metastasis with a lymph node mass 2 cm in greatest dimension; or multiple lymph nodes, none >2 cm in greatest dimension.|
|N2||Metastasis with a lymph node mass >2 cm but not >5 cm in greatest dimension; or multiple lymph nodes, any one mass >2 cm but not >5 cm in greatest dimension.|
|N3||Metastasis with a lymph node mass >5 cm in greatest dimension.|
|pNX||Regional lymph nodes cannot be assessed.|
|pN0||No regional lymph node metastasis.|
|pN1||Metastasis with a lymph node mass 2 cm in greatest dimension and 5 nodes positive, none >2 cm in greatest dimension.|
|pN2||Metastasis with a lymph node mass >2 cm but not >5 cm in greatest dimension; or >5 nodes positive, none >5 cm; or evidence of extranodal extension of tumor.|
|pN3||Metastasis with a lymph node mass >5 cm in greatest dimension.|
|M0||No distant metastasis.|
|M1a||Nonregional nodal or pulmonary metastasis.|
|M1b||Distant metastasis other than to nonregional lymph nodes and lung.|
|Group||T||N||M||S (Serum Tumor Markers)|
|III||Any pT/Tx||Any N||M1||SX|
|IIIA||Any pT/Tx||Any N||M1a||S0|
|Any pT/Tx||Any N||M1a||S1|
|Any pT/Tx||Any N||M1a||S2|
|Any pT/Tx||Any N||M1a||S3|
|Any pT/Tx||Any N||M1b||Any S|
|Serum Tumor Markers (S) Required for Staging|
|SX||Marker studies not available or not performed.|
|S0||Marker study levels within normal limits.|
|S1||LDH <1.5 í Nb and hCG (mIu/ml) <5,000 and AFP (ng/ml) <1,000.|
|S2||LDH 1.510 í N or hCG (mIu/ml) 5,00050,000 or AFP (ng/ml) 1,00010,000.|
|S3||LDH >10 í N or hCG (mIu/ml) >50,000 or AFP (ng/ml) >10,000.|
In addition to the clinical stage definitions, surgical stage may be designated based on the results of surgical removal and microscopic examination of tissue.
Stage I testicular cancer is limited to the testis. Invasion of the scrotal wall by tumor or interruption of the scrotal wall by previous surgery does not change the stage but does increase the risk of spread to the inguinal lymph nodes, and this must be considered in treatment and follow-up. Invasion of the epididymis tunica albuginea and/or the rete testis does not change the stage. Invasion of the tunica vaginalis or lymphovascular invasion signifies a T2 tumor, while invasion of the spermatic cord signifies a T3 tumor, and invasion of the scrotum signifies a T4. Increases in T stage are associated with increased risk of occult metastatic disease and recurrence. Men with stage I disease who have persistently elevated serum tumor markers after orchiectomy are staged as IS, but stage IS nonseminomas are treated as stage III. Elevated serum tumor markers in stage I or II seminoma are of unclear significance except that a persistently elevated or rising hCG usually indicates metastatic disease.
Stage II testicular cancer involves the testis and the retroperitoneal or peri-aortic lymph nodes usually in the region of the kidney. Retroperitoneal involvement should be further characterized by the number of nodes involved and the size of involved nodes. The risk of recurrence is increased if more than five nodes are involved or if the size of one or more involved nodes is more than 2 cm. Bulky stage II disease (stage IIC) describes patients with extensive retroperitoneal nodes (>5 cm), which portends a less favorable prognosis.
Stage III implies spread beyond the retroperitoneal nodes based on physical examination, imaging studies, and/or blood tests (i.e., patients with retroperitoneal adenopathy and highly elevated serum tumor markers are stage III). Stage III can be further stratified based on the location of metastasis and the degree of elevation of serum tumor markers. In the favorable group (IIIA), metastases are limited to lymph nodes and lung, and serum tumor markers are no more than mildly elevated. Stage IIIB patients have moderately elevated tumor markers, while stage IIIC patients have highly elevated markers and/or metastases to liver, bone, brain or some organ other than the lungs. These subclassifications of stage III correspond to the International Germ Cell Consensus Classification system for disseminated germ cell tumors. 2
Ms. Gambino talks about the complexity of cancer care and the need for patients and families to have help in navigating from diagnosis and treatment decisions to survivorship. Read more.
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