AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Testicular tumors in children are rare, accounting for only 1-2% of all solid tumors in this age group. In both children and adults, the vast majority of testis tumors arise from germ cells. Seminoma is one type of testicular germ cell tumor that is believed to originate from the germinal epithelium of the seminiferous tubules. In recent years, these tumors have been shown to have dramatic sensitivity to both radiotherapy and cytotoxic chemotherapy. In most patients with testis tumors (including seminoma), the disease is cured readily with minimal long-term morbidity. The management of childhood seminoma is similar to that of adult seminoma.

Pathophysiology

Germ cell tumors account for 95% of testicular tumors and include seminomas, teratomas, choriocarcinomas, and mixed tumors. Seminomas comprise approximately 50% of all germ cell tumors. Seminomas are generally believed to arise from the germinal epithelium of the seminiferous tubules because "seminoma cells" are morphologically similar to spermatogonia and also because seminomas are frequently found within the seminiferous tubules in early stages.

Most researchers believe that seminomas can arise from any or all of the spermatocytic elements because undifferentiated seminomas can resemble primordial germ cells, spermatogonia, or spermatocytes. Unlike the nonseminomatous germ cell tumors, pure seminoma tends to remain localized or to involve only lymph nodes. Seminoma is confined to the testis in 85% of patients at presentation. It spreads in an orderly fashion, initially to draining lymph nodes in the retroperitoneum; from there it spreads proximally to involve the next echelon of draining lymphatics in the mediastinum and supraclavicular fossa. Only rarely does pure seminoma spread hematogenously to involve lung parenchyma, bone, liver, or brain (ie, stage IV). Fewer than 5% of patients present with stage III or IV disease.

Frequency

United States

Germ cell tumors are the most common solid tumor in men aged 15-35 years. The worldwide incidence has more than doubled over the past 40 years, and approximately 7500 cases are diagnosed annually in the United States. Seminomas account for nearly 50% of these cases.

Mortality/Morbidity

With recent advances in radiologic staging, serum tumor marker surveillance, and platinum-based chemotherapy for advanced disease, overall survival (ie, cure) rates for patients with seminoma have increased to greater than 90%. Nearly 100% of patients with stage I testicular seminoma are cured. Potential adverse effects/morbidity related to therapy for this malignancy are discussed below; in general, morbidity includes infertility, second cancers, chemotherapy-related nausea and vomiting, nephrotoxicity, and cardiovascular toxicity or peptic ulcer disease from mediastinal or retroperitoneal irradiation, respectively.

Race

Geographic distribution of testicular cancer varies considerably, with the highest rates in North American whites, Scandinavians, and Western Europeans. The lowest rates occur in Asians, Africans, Puerto Ricans, and North American blacks. Recent data show a white-to-black incidence ratio of approximately 5:1, and a report from the US military showed a relative white-to-black incidence ratio of 40:1.

Sex

Seminomas arise from the male testicle.

Age

• As noted above, germ cell tumors are the most common solid tumors in men aged 15-35 years. Seminoma (the most common germ cell tumor) occurs most commonly in the fourth decade of life.
• Children represent only 2-5% of all patients with testicular cancer. Seminoma is considered a postpubertal tumor, although it has been reported in a patient as young as 8 years.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• The most common presenting symptom is a painless testicular mass. Other symptoms can include testicular pain (45%) or heaviness.
• A history of previous testicular trauma is common, although usually coincidental. The trauma typically draws the patient's attention to the mass.
• Seminoma that has spread to retroperitoneal lymph nodes can cause back pain or abdominal discomfort.
• Widely disseminated metastatic disease to lungs, liver, bone, or brain is rare but may produce systemic symptoms.
• A history of cryptorchidism or other genitourinary anomalies can be elicited in some patients (see Causes).

Physical

• When a testicular mass is suspected, physical examination should include transillumination of the scrotum, which can differentiate a solid mass from a fluid-filled hydrocele or varicocele.
• The contralateral testis should be examined carefully because patients with seminoma have a higher risk of contralateral testis cancer than the general population of healthy males.
• Pay careful attention to possible sites of lymph node metastases. Specifically, the abdomen should be examined to rule out the presence of large abdominal masses (suggesting bulky paraaortic/retroperitoneal lymphadenopathy), and both supraclavicular fossae should be palpated to rule out metastatic lymphadenopathy in those locations.
• A general physical examination that includes lungs, liver, nervous system, and musculoskeletal structures can aid in ruling out widespread metastatic disease.

Causes

• The cause of germ cell tumors is unknown. Familial clustering has been observed, particularly among siblings.
• Prior testicular cancer is a major risk factor for a contralateral malignancy. The cumulative risk 25 years after original diagnosis is 3.6% for patients with seminoma.
• Cryptorchidism is a predisposing factor in the development of germ cell tumors arising from the testis. In fact, 7-10% of testis tumors occur in association with cryptorchidism. Orchiopexy performed before puberty reduces the risk of germ cell tumors and improves the ability to observe the testis. Interestingly, however, 25% of the cancers found in association with cryptorchidism occur in the contralateral normally descended testis, which suggests that a developmental defect is responsible for both the maldescent and the tumor. The risk of a cryptorchid patient developing testicular cancer is related directly to the degree of maldescent: 1 in 20 if the testis is intra-abdominal and 1 in 80 if it is within the inguinal canal. Hypospadias and hydrocele are other genitourinary anomalies that have been associated with testicular cancers.
• Klinefelter syndrome is associated with the development of mediastinal germ cell tumors.
• HIV infection may be associated with an increased risk of germ cell tumors. Other possible associations include mumps, orchitis, history of testicular trauma, immunosuppression after organ transplant, and prior vasectomy.
• No clear association between seminoma or other testicular germ cell tumors and previous exposure to diethylstilbestrol has been identified.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Testicular torsion
Spermatocele
Epididymitis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Measurements of alpha-fetoprotein (AFP), human chorionic gonadotropin (beta-hCG), and lactate dehydrogenase (LDH) are important in the management of patients with testis tumors. In fact, these tests are incorporated in the current staging system for testis tumors (see Staging).
• Beta-human chorionic gonadotropin
• • Beta-hCG is a glycoprotein typically produced by the placenta.
  • Elevations in this protein are found in the serum of approximately 15% of patients with seminoma.
  • The half-life of beta-hCG is approximately 22 hours.
• Alpha-fetoprotein
• • AFP is a glycoprotein typically associated with the human fetus and is the fetal equivalent of albumin.
  • It occurs in nonseminomatous germ cell tumors, as well as in hepatocellular carcinomas, cirrhosis, hepatitis, and pregnancy.
  • The half-life of AFP is approximately 5 days.
  • AFP elevation is rare in pure seminomas and indicates that nonseminomatous elements are also present (ie, mixed tumor).
• Both AFP and beta-hCG are suggestive of malignancy when elevated before orchiectomy. The rate of decline after orchiectomy indicates the likelihood of residual tumor. Tumor marker levels are used to assess response to treatment and to predict the likelihood of complete remission, and, in regular follow-up, tumor marker levels indicate recurrence, often in the absence of symptoms, physical findings, or abnormal findings on imaging studies.
• Lactate dehydrogenase: LDH level is an independent prognostic factor in patients with germ cell tumors (including seminoma). It is thought to reflect tumor burden.

Imaging Studies

• Plain chest radiography, computed tomography (CT) imaging of the abdomen and pelvis, and bipedal lymphangiography (LAG) are the most important radiologic investigations in determining the extent of disease in patients with seminoma.
• • Chest radiography is adequate screening to rule out pulmonary parenchymal metastases.
  • CT imaging of the abdomen is the best technique for identifying the presence and extent of retroperitoneal lymphadenopathy and is necessary in all patients; it has largely replaced bipedal LAG in the radiographic staging of patients with seminoma. Retroperitoneal lymph nodes measuring 1-2 cm are confirmed to be involved pathologically with metastatic tumor in approximately 70% of cases.
  • Although radiologists skilled in the technique are increasingly difficult to find, bipedal LAG is uniquely able to define abnormal lymph nodes by both size and internal architecture, unlike CT imaging. In addition, LAG is useful to the radiation oncologist, who is able to minimize irradiation of normal tissues when such a study is available to facilitate portal design.
  • Further radiologic investigation is obtained only if the patient has symptoms suggesting further metastatic disease, eg, bone imaging in the setting of skeletal pain or brain CT imaging when neurologic signs are elicited.
• Scrotal ultrasonography
• • The typical testicular tumor is intratesticular and may produce one or more discrete hypoechoic masses or diffuse abnormalities with microcalcifications.
  • Calcifications are more frequent in seminoma than in nonseminomatous tumors.

Histologic Findings

Grossly, seminomas are pale gray to yellow nodules that are uniform or slightly lobulated. Pure seminomas are subdivided into 3 subtypes based upon histopathologic characteristics.

• Classic seminomas (85%) demonstrate a monotonous sheet of large cells with abundant cytoplasm and round hyperchromatic nuclei with prominent nucleoli. A lymphocytic infiltrate or granulomatous reaction with giant cells or both is frequently present. Trophoblastic giant cells capable of producing hCG are present in 15-20% of tumors. Mitoses are infrequent.
• Anaplastic seminoma (10%) is an older term used to describe seminomas with 3 or more mitotic figures per high-power field. This finding has no clinical or prognostic significance because the response of anaplastic seminomas to standard therapy is equivalent to that of classic seminomas.
• Spermatocytic seminoma (5%) is a rare histologic variant that is not associated with carcinoma in situ. These well-differentiated tumors usually contain cells resembling secondary spermatids or spermatocytes. Spermatocytic seminomas rarely metastasize, and they occur almost exclusively in elderly men. The only recommended treatment is orchiectomy.

Staging

Testicular seminoma is staged according to the American Joint Committee on Cancer (AJCC) 2002 staging guidelines. This is a TNM staging system comprising separate categorizations for the primary tumor, regional lymph nodes, distant metastases, and serum tumor markers; these 4 categories are used to determine the stage of the patient's disease. Modern treatment decisions are based, in part, on the subdivisions of this staging system. Formal staging is a complex process involving particular required and allowable tests and procedures; the following is a quick overview. (For full staging information, see the AJCC Staging Manual.)

• Primary tumor staging
  • Tis - Intratubular germ cell neoplasia (carcinoma in situ)
  • T1 - Tumor limited to testis/epididymis without vascular or lymphatic invasion; tumor may invade into the tunica albuginea but not the tunica vaginalis
  • T2 - Tumor limited to testis/epididymis with vascular or lymphatic invasion or tumor extending through tunica albuginea with involvement of the tunica vaginalis
  • T3 - Tumor invading spermatic cord with or without vascular/lymphatic invasion
  • T4 - Tumor invading scrotum with or without vascular/lymphatic invasion
• Regional lymph node staging
  • N0 - No regional lymph node metastases
  • N1 - Metastasis with lymph node(s) 2 cm or less in greatest dimension or multiple lymph nodes, none more than 2 cm in greatest dimension
  • N2 - Metastasis with lymph node(s) greater than 2 cm but not greater than 5 cm in greatest dimension, or multiple lymph nodes, any 1 mass greater than 2 cm, but not more than 5 cm, in greatest dimension
  • N3 - Metastasis with lymph node(s) greater than 5 cm in greatest dimension
• Distant metastatic staging
  • M0 - No distant metastases
  • M1a - Nonregional nodal or pulmonary metastasis
  • M1b - Distant metastases other than M1a
• Serum tumor marker staging
  • S0 - Marker studies within normal limits
  • S1 - LDH less than 1.5 times the reference range, beta-hCG less than 5000 mIU/mL, and AFP less than 1000 ng/mL
  • S2 - LDH 1.5-10 times the reference range , beta-hCG 5,000-50,000 mIU/mL, or AFP 1,000-10,000 ng/mL
  • S3 - LDH greater than 10 times the reference range, beta-hCG greater than 50,000 mIU/mL, or AFP greater than 10,000 ng/mL
• Stage grouping
  • Stage IA - T1 N0 M0 S0
  • Stage IB - T2,3,4 N0 M0 S0
  • Stage IS - Any T N0 M0 S1,2,3
  • Stage IIA - Any T N1 M0 S0,1
  • Stage IIB - Any T N2 M0 S0,1
  • Stage IIC - Any T N3 M0 S0,1
  • Stage IIIA - Any T Any N M1a S0,1
  • Stage IIIB - Any T Any N M0,1a S2
  • Stage IIIC - Any T Any N M1a,1b S3

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

See Further Outpatient Care for more information about postsurgical adjuvant radiation therapy and chemotherapy.

Surgical Care

The appropriate surgical treatment for any patient with suspected testicular tumor is radical inguinal orchiectomy with high ligation of the spermatic cord. Transscrotal biopsy or transscrotal orchiectomy is inappropriate because the testis and scrotum have different lymphatic drainage patterns and these procedures can result in tumor recurrence in the scrotal skin or inguinal/pelvic lymph nodes. In addition, an inguinal approach allows for more generous resection of the spermatic cord, improving surgical margins. Orchiectomy provides pathologic material for histologic diagnosis and primary pathologic staging information as well.

Consultations

Pediatric urologist, radiation oncologist, pediatric hematologist/oncologist, reproductive endocrinologist/sperm banking specialist

Diet

No specific dietary concerns are associated with the care of these patients.

Activity

Any activity limitations are related to surgery (orchiectomy); for example, the patient's surgeon may recommend avoidance of heavy lifting or contact sports for a short time.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

As discussed in Follow-up below, adjuvant moderate-dose pelvic and/or paraaortic radiotherapy remains the standard treatment for patients with early-stage seminoma (stage I, IIA, or IIB) after orchiectomy. However, patients who are found to have more advanced disease (stage IIC, III, IV) have a high risk of systemic relapse if treated with surgery and radiation alone, and the standard treatment for these patients is combination chemotherapy. These patients can be generally divided into good risk and poor risk categories. For good risk patients, several combination chemotherapy regimens are available; one common schedule for adults includes 3 cycles of cisplatin/etoposide/bleomycin (detailed below). Poor risk patients should be enrolled in clinical trials because the ideal chemotherapeutic strategy has not been determined.

Drug Category: Antineoplastics agents

Adjuvant chemotherapy regimens are for stages IIC and III disease.

Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs affect this growth. After cells divide, they enter a period of growth (phase G1), followed by DNA synthesis (phase S). The next phase is a premitotic phase (G2), then finally a mitotic cell division (phase M).

The rate of cell division varies for different tumors. Most common cancers increase very slowly in size compared with normal tissues, and the rate may decrease further in large tumors. This difference allows normal cells to recover more quickly than malignant ones from chemotherapy; it is the rationale behind current cyclic dosage schedules.

Antineoplastic agents interfere with cell reproduction. Some agents are cell cycle specific, while others (eg, alkylating agents, anthracyclines, cisplatin) are not phase specific. Cellular apoptosis (ie, programmed cell death) is also a potential mechanism of many antineoplastic agents.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• Fertility evaluation/sperm banking
• • As a group, patients with testicular cancer are more likely to have subfertility characteristics (eg, lower motile sperm count, decreased sperm mobility, suboptimal motility characteristics) than a healthy, age-matched cohort.
  • Modern adjuvant therapies for seminoma have a limited propensity to further negatively affect semen quality.
  • All male cancer patients of reproductive age who have treatment that may affect testicular function and who may desire children in the future should cryopreserve sperm before initiation of therapy.
• Adjuvant radiation therapy: Most men with seminoma present with clinical stage I disease (confined to the testis); only 15-20% of patients are found to have pelvic or paraaortic lymphadenopathy during postoperative radiographic staging. However, in another 15-20% of patients, disease that is apparently confined locally ultimately relapses in subdiaphragmatic lymph nodes if treated with orchiectomy alone. Adjuvant postoperative radiotherapy remains the current standard method to significantly reduce the incidence of regional nodal failure, and its use is determined by disease stage.
• • Stage I
    • After radical orchiectomy, patients with stage I seminoma are treated with moderate-dose external beam radiotherapy to retroperitoneal and ipsilateral pelvic lymph nodes, typically 2500 cGy in 20 fractions (125 cGy per fraction). Using this approach, the in-field disease control rate approaches 100%. Contraindications to the use of adjuvant radiotherapy for these patients include the presence of a horseshoe kidney (more common among these patients than among the general population), previous abdominopelvic radiotherapy, and severe inflammatory bowel disease. Recently, reports have indicated that paraaortic lymph node irradiation may suffice without adverse impact on overall survival.
    • Some patients with stage I disease prefer to avoid adjuvant radiation because their risk of relapse after orchiectomy is relatively low (15-20%) and because disease recurrences are usually treated with subsequent salvage radiation or chemotherapy. However, patients who choose this approach must understand that they will require frequent (and therefore expensive) follow-up evaluations with serum tumor markers and CT imaging of the abdomen and pelvis so that nodal recurrences may be identified early.
    • An accumulating amount of literature states that 1 or 2 courses of carboplatin may give results similar to adjuvant radiotherapy without the carcinogenic risks of irradiation.
  • Stage IIA-B
    • Patients with stage IIA or IIB seminoma are those who have been found to have regional nodal metastases no larger than 5 cm on postoperative imaging studies. Historically, these patients have been treated with external beam radiotherapy to the pelvic and paraaortic lymph nodes to a dose of 2500 cGy in 20 fractions (125 cGy per fraction) followed by a boost of 1000 cGy in 5-8 fractions (125-200 cGy per fraction); this has provided freedom from any relapse in approximately 90% of patients. As in patients with stage I disease, in-field control remains nearly universal.
    • Contraindications to the use of adjuvant radiotherapy for these patients include the presence of a horseshoe kidney (more common among these patients than among the general population), previous abdominopelvic radiotherapy, and severe inflammatory bowel disease. Adjuvant combination chemotherapy in lieu of radiotherapy has been used with increasing frequency over the past 2 decades, according to patterns of care studies; current randomized protocols are attempting to define which approach (adjuvant radiation versus adjuvant chemotherapy) carries the lowest morbidity while maximizing the cure rate.
• Adjuvant combination chemotherapy
• • In advanced seminoma (stage II-C or III), although local control with radiotherapy remains excellent, the risk of distant relapse is high. This risk mandates the use of systemic chemotherapy to achieve cure. Approximately 70-80% of these patients are curable with platinum-based chemotherapeutic regimens.
  • Patients with bulky nodal disease or systemic metastases are best treated with combination chemotherapy using cisplatin-containing regimens; a representative regimen is 4 cycles of cisplatin/etoposide administered intravenously in an outpatient setting.

Complications

• Patients treated with orchiectomy and adjuvant radiotherapy are at increased risk for subfertility, even though the contralateral testis is not located directly within the radiotherapy field. Scrotal shielding during radiation treatments reduces the dose of scattered radiation and should be employed routinely (see Further Outpatient Care).
• Second malignancies have been reported following orchiectomy and postoperative adjuvant radiotherapy for seminoma. Although such malignancies are uncommon, the actuarial risk increases with time from diagnosis; second cancer sites have included the rectum, small intestine, stomach, and bladder.
• Potential long-term complications of cisplatin/etoposide chemotherapy include loss of high-frequency hearing, nephrotoxicity, hypomagnesemia/Raynaud phenomenon, subfertility, and acute nonlymphocytic leukemia.
• Although cardiovascular toxicity has been reported following treatment of seminoma with orchiectomy and adjuvant radiotherapy, it was associated with the use of radiotherapy fields that treated the mediastinum and supraclavicular fossae. These fields no longer are treated routinely because the incidence of recurrence in these areas is low for patients with stage I, IIA, or IIB disease.

Prognosis

• Early-stage seminoma: Relapse occurs in approximately 4% of patients with stage I and 10% of patients with stage IIA or IIB seminoma. Subsequent treatment with chemotherapy cures more than 90% of patients whose disease relapses after radiotherapy. Ultimately, therefore, approximately 99% of patients with early-stage seminoma are cured.
• Advanced seminoma: With the development of effective cytotoxic chemotherapy, many patients with advanced (70-80%), recurrent (50-60%), or even metastatic (20-30%) seminomas are cured of their disease. Further studies of alternative chemotherapy regimens and high-dose regimens with stem cell support are ongoing.

Patient Education

• Patients diagnosed with testicular seminoma have an increased risk of developing a contralateral testis tumor and should be taught methods of testicular self-examination. This form of screening should be performed monthly so that a second primary tumor can be identified at the earliest possible stage.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• A painless testicular mass is pathognomonic of a primary testicular tumor, but this telltale sign is observed only in a minority of patients. More commonly, patients present with some combination of testicular pain, swelling, or hardness. Because infectious orchitis or epididymitis are much more common than testicular tumors, an antibiotic trial is often undertaken. If testicular pain does not resolve or physical findings do not revert to normal within 2-4 weeks, a testicular ultrasound examination is indicated.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• American Joint Committee on Cancer. AJCC Cancer Staging Manual. 6th ed. Philadelphia, Pa:. Lippincott-Raven Publishers;2002:347-360.
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• Schmidberger H, Bamberg M, Meisner C, et al. Radiotherapy in stage IIA and IIB testicular seminoma with reduced portals: a prospective multicenter study. Int J Radiat Oncol Biol Phys. Sep 1 1997;39(2):321-6. [Medline].
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• Thomas GM, Williams SD. Testis. In: Perez CA, ed. Principles and Practice of Radiation Oncology, 3rd ed. Philadelphia, Pa:. Lippincott Williams & Wilkins;1997:1695-1715.
• Warde P, Gospodarowicz MK, Panzarella T, et al. Stage I testicular seminoma: results of adjuvant irradiation and surveillance. J Clin Oncol. Sep 1995;13(9):2255-62. [Medline].
• Warde P, Gospodarowicz M, Panzarella T. Management of stage II seminoma. J Clin Oncol. Jan 1998;16(1):290-4. [Medline].
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• Weissbach L, Bussar-Maatz R, Mann K. The value of tumor markers in testicular seminomas. Results of a prospective multicenter study. Eur Urol. 1997;32(1):16-22. [Medline].
• Zagars GK, Babaian RJ. Stage I testicular seminoma: rationale for postorchiectomy radiation therapy. Int J Radiat Oncol Biol Phys. Feb 1987;13(2):155-62. [Medline].
• Zagars GK, Babaian RJ. The role of radiation in stage II testicular seminoma. Int J Radiat Oncol Biol Phys. Feb 1987;13(2):163-70. [Medline].
• Zapzalka DM, Redmon JB, Pryor JL. A survey of oncologists regarding sperm cryopreservation and assisted reproductive techniques for male cancer patients. Cancer. Nov 1 1999;86(9):1812-7. [Medline].

Article Last Updated: Jun 21, 2006