Bamidele A. Adesunloye and Ravi A. Madan
Testicular carcinoma is the most common malignancy in men between the ages of 20 and 35, but represents only 1% of all malignancies in males. The disease is believed to originate from the malignant transformation of primordial germ cells that may occur early in embryonic development. As late as the 1970s, testicular carcinoma was generally fatal, but can now be cured in most cases. Effective treatment paradigms have been developed to help manage acute disease and follow-up. Given the high cure rate and the resulting improved life expectancy, special considerations must be given to the side effects of therapy, especially in early-stage disease where even conservative interventions yield a cure in over 98% of patients. Whatever the therapeutic intervention, all patients should be monitored closely in ensuing years for both recurrent disease and long-term sequelae of therapy.
CLINICAL FEATURES
Epidemiology
■It was estimated that in 2013 there would be 7920 new cases of testicular carcinoma and 370 deaths due to the disease in the United States.
■Testicular cancer accounts for 1% of all malignancies in men but the majority of cases occur between the ages of 20 to 35 years.
■There is significant variability in the incidence by ethnicity with Caucasians being five times more likely than African Americans to have testicular carcinoma.
■For unclear reasons, the incidence of testicular cancer has been increasing over the last four to five decades in most western countries. A few epidemiologic studies have attributed the increase in part to the birth cohort effect.
■Although the incidence of testicular cancer has increased over the past several decades, the peak of incidence has remained within the 25- to 29-year age group. Testicular cancer is rare after the age of 40.
Risk Factors
■Cryptorchidism: Cryptorchid testes, defined as maldescended testes located above the external inguinal ring, are associated with a two- to fourfold increase in the risk of testicular cancer with intra-abdominal testes having a higher risk than inguinal testes. There is also an increased risk in the normally descended contralateral testis.
■Second primary tumors: Synchronous or metachronous testicular carcinoma may occur in the contralateral testis in a few group of patients; 1% to 5% of patients have bilateral disease at presentation.
■Intratubular germ cell neoplasia: A premalignant condition seen in 90% of testicular carcinomas.
■Hereditary: Despite the overwhelming evidence of a strong familial component to the risk of testicular carcinoma, to date no definite oncogene has been identified. About 1.4% of patients with testicular carcinoma have a positive family history of the disease. A son of an affected father has a four- to sixfold increased risk while for a brother of an affected sibling the risk increases to 8 to 10-fold. The risk is reportedly greater than 70-fold in monozygotic twins.
■Chromosomal abnormalities: Klinefelter syndrome has been shown to be associated with increased risk of primary mediastinal germ cell tumors in a few case series and surveys. Similar studies have also suggested the possibility of an increased risk of testicular cancer with Down syndrome.
■Peutz-Jeghers syndrome: Although it is well established that females with Peutz-Jeghers syndrome have an increased risk of gonadal tumors, this association is less clear in males with the syndrome. However, functional Sertoli cell testicular tumors with feminization syndrome have been reported in some cases.
■HIV infection: The risk of seminomatous testicular tumors is considerably higher in HIV-infected men compared to age-matched HIV-negative men. There are also recent reports of non-Hodgkin lymphoma of the testicles in patients with HIV infection.
■Sarcoidosis: The likelihood of an association between sarcoidosis and testicular carcinoma has been proposed. The rationale behind this association is plausible given the chronic inflammation associated with sarcoidosis and impaired immune surveillance of tumor antigens.
■Testicular microlithiasis: Several retrospective studies have suggested a possible association between testicular microlithiasis and testicular cancer.
■Hypospadias: Analyses of data from Danish health registry have suggested a potential association between hypospadias and testicular tumor.
Presentation
■Asymptomatic testicular nodule or swelling (painful in 10% to 20% of patients)
■Feeling of testicular heaviness, dull ache, and/or hardness (up to 40% of patients)
■Disease at extragonadal site (5% to 10% of patients; symptoms vary with site):
–Dyspnea, cough, or hemoptysis (pulmonary metastases)
–Weight loss, anorexia, nausea, abdominal or back pain (retroperitoneal adenopathy)
–Mass or swelling in neck (supraclavicular lymphadenopathy)
–Superior vena cava syndrome due to mediastinal disease
■Rare presentations:
–Urinary obstruction
–Headaches, seizures, or other neurologic complaints due to brain metastases
–Bone pain due to bone metastases
–Gynecomastia due to elevated β-human chorionic gonadotropin (β-HCG).
–Anti-Ma2-associated paraneoplastic encephalitis
DIFFERENTIAL DIAGNOSIS
■Epididymitis (initial diagnosis and treatment in 18% to 33% of testicular cancer patients)
■Orchitis, hydrocele, varicocele, or spermatocele
■Lymphoma or leukemia
■Metastasis from other tumors including melanoma or lung cancer
■Infectious diseases including tuberculosis and tertiary syphilis causing gumma
FIGURE 16.1 Adjuvant treatment options for seminoma. XRT*, radiation therapy to para-aortic lymph nodes; BEP, bleomycin, etoposide, and ciplatin; EP, etoposide, and cipaltin.
DIAGNOSIS
The initial evaluation of a suspicious testicular mass should include measurement of serum tumor markers, testicular ultrasound, and a chest x-ray. Subsequently, a radical inguinal orchietomy should be performed. Post-operatively, if germ cell tumor is confirmed, abdominopelvic CT scan should be done and the tumor markers should be repeated if they were elevated prior to orchiectomy. Chest CT and brain imaging should be done if indicated.
Goals
■Every testicular mass requires a timely workup to exclude testicular carcinoma.
■Histologic determination of tumor type and stage has prognostic and therapeutic significance.
■Testicular cancer is highly curable, with 5-year survival >95%.
■Long-term sequelae of therapy should be considered and minimized when possible.
■Orchiectomy is essential for diagnosis and local tumor control. Radical inguinal orchiectomy is preferred to scrotal orchiectomy, trans-scrotal biopsy, or fine-needle aspiration due to the risk of scrotal violation that may compromise patients’ prognosis.
Laboratory
Serum α-Fetoprotein (AFP)
■A glycoprotein with a half-life of approximately 4 to 6 days
■Commonly produced by the fetal yolk sac, liver, and gastrointestinal tract
■Should not be elevated in serum of healthy men
■Not present in patients with pure seminoma. Elevated serum α-fetoprotein (AFP) levels indicate a nonseminomatous component to the patient’s testicular cancer
Serum α-Human Chorionic Gonadotropin
■Secreted by syncytiotrophoblasts; half-life of 0.5 to 1.5 days
■Most commonly elevated tumor marker in patients with testicular cancer
■Present in choriocarcinomas; may be modestly elevated in pure seminomas
■High levels may lead to gynecomastia
Serum Lactate Dehydrogenase
■Nonspecific tumor marker in testicular cancer
■Elevated in 80% of metastatic seminomas and 60% of advanced nonseminomatous tumors
■Reflects overall tumor burden, tumor growth rate, and cellular proliferation
Imaging
■Ultrasound: Ultrasound detects the presence of testicular parenchymal abnormality in both testes.
■Chest x-ray: Posterior–anterior and lateral film evaluation for pulmonary metastases.
■Computerized tomography (CT): CT scans of chest, abdomen, and pelvis determine extragonadal metastasis and are the most effective modality for staging the disease.
■Magnetic resonance imaging (MRI): MRI may provide additional information if ultrasound is indeterminate. MRI of the brain is necessary only when there are symptoms involving the central nervous system (e.g., headache, neurologic deficit, seizure).
■Positron emission tomography (PET) scan: PET scans are not indicated in primary staging, but may have limited utility for characterizing residual masses. The routine use of PET scans has not been shown to improve outcome.
Pathology
Patients with testicular masses should have surgical exploration, with complete removal of the testis and spermatic cord through the inguinal ring. Although empirical evidence supporting this is weak, trans-scrotal testicular biopsy is not recommended due to the risk of local and nodal dissemination of tumor.
■Immunohistochemical staining can be used to distinguish the different histologic subtypes of testicular carcinoma.
■Historically, CD30 and cytokeratin staining have been used to distinguish embryonal carcinoma (positive for both markers) from pure seminoma.
■Modern immunostains have made it possible to increase the accuracy of this distinction. NANOG and OCT3/4 are expressed in seminoma and embryonal carcinoma while SOX2 is only expressed in embryonal carcinoma.
■Seminoma expresses c-kit, which is expressed by neither embryonal carcinoma nor yolk sac tumor.
■SALL4, a novel stem cell marker, stains nearly all subtypes of germ cell tumors, making it a very useful marker in confirming metastatic disease. It is particularly useful for identifying yolk sac tumor, which is strongly positive for SALL4 staining but negative for OCT4.
■Germ cell tumors are frequently aneuploid and display an array of histopathology (Table 16.1).
■Several genes (either deleted or amplified) located on isochromosome 12p have been implicated in the malignant transformation of primordial germ cells. Among patients with familial testicular germ cell tumors compatible with X-linked inheritance, evidence suggests the presence of a susceptibility gene on chromosome Xq27.
STAGING
Staging is in accordance with the American Joint Committee on Cancer tumor/node/metastasis (TNM) criteria.
■T classification is based on pathologic finding after radical orchiectomy, hence the pT nomenclature. pT0 means there is no evidence of disease. pTis refers to intratubular germ cell neoplasia or carcinoma in situ. pT1 is a disease that is limited to the testis and epididymis without lymphovascular invasion, although it may invade the tunica albuginea but not the tunica vaginalis. pT2 tumor is similar to pT1 but with lymphovascular invasion or the involvement of the tunica vaginalis. In pT3 tumor, there is invasion of the spermatic cord with or without lymphovascular invasion. Involvement of the scrotum with or without lymphovascular invasion is designated as pT4. pTx is used when the primary tumor cannot be assessed.
■N classification may be pathologic (pN) or clinical. When there is no regional lymph node involvement the N0 designation is used. N1 refers to metastasis in a lymph node mass that is ≤2 cm in greatest dimension. N2 is a lymph node metastasis or multiple lymph nodes metastases with any one mass >2 cm but ≤5 cm. Lymph node metastasis >5 cm is termed N3. If lymph node metastasis is ascertained pathologically after surgery, then the pN nomenclature is used. pN0 means that there is no evidence of lymph node involvement, while pN1 is similar to N1 except that the involvement of ≤5 lymph nodes with none >2 cm in greatest dimension is also considered pN1. Likewise, pN2 is similar to N2 but also include the involvement of more than 5 lymph nodes, none more than 5 cm or evidence of extranodal extension. pN3 has similar definition as N3. When the regional lymph nodes cannot be assessed the Nx or pNx designation is used.
■M classification is based on the extent of distant metastasis. M0 means there is no distant metastasis, while M1, which is further divided to M1a and M1b, signifies distant metastasis. M1a refers to nonregional nodal or pulmonary metastasis, while M1b indicates the presence of nonregional nodal and nonpulmonary metastases.
■Very unique to testicular germ cell tumors is the use of serum tumor markers in the staging process. S0 refers to normal serum levels of tumor markers. S1 means that the lactate dehydrogenase (LDH) is <1.5 times the upper limit of normal, β-HCG is <5,000 milli-international units/mL, and AFP is <1,000 ng/mL. S2 is used when the LDH is between 1.5 and 10 times the upper limit of normal, or β-HCG is between 5,000 and 50,000 milli-international units/mL, or AFP 1000 to 10,000 ng/mL. S3 refers to LDH >10 times the upper limit of normal, or β-HCG >50,000 milli-international units/mL, or AFP >10,000 ng/mL. Sx refers to tumor markers not available or not done.
■The TNM classification is then used in the anatomic stage grouping as follows:
•Stage I: pT1-4, N0, M0, Sx/S0
•Stage IS: Any p T or Tx, N0, M0, S1-3
•Stage II: Any pT or Tx, N1-3, M0, Sx/S0-1
•Stage III: Any pT or Tx, any N, M1, Sx/S0-3
PROGNOSIS
■The prognosis is based on the International Consensus Risk Classification system that utilized postorchiectomy levels of tumor markers and the site of metastasis to predict the progression-free survival (PFS) and overall survival (OS) of patients with advanced testicular germ cell tumors (Table 16.2).
■The 5-year PFS and 5-year OS for disseminated seminomatous and nonseminomatous germ cell tumors are given in Table 16.3.
TREATMENT MODALITIES
A radical inguinal orchiectomy is the preferred surgical approach for all patients with a testicular mass. This is both diagnostic and therapeutic. Adjuvant therapy, which may include chemotherapy, radiotherapy, or further surgery, is tailored to the disease stage and histology. Due to the unique radiosensitivity of seminomas, adjuvant radiation therapy is often employed. Patients should be counseled about sperm banking before the initiation of therapy. The need for aggressive therapy with early-stage disease is currently controversial.
Seminomas
Adjuvant treatment options for seminoma are outlined in Figure 16.1.
Stage I
■Orchiectomy is curative for most patients with stage I seminoma. With a recurrence rate of up to 20%, active surveillance is an option after surgery for patients who can comply with follow-up recommendations.
■When disease does recur, usually in the retroperitoneal lymph nodes, nearly all patients can be cured with radiation or chemotherapy.
■For patients who cannot comply with active surveillance, low-dose radiation therapy to regional lymph nodes after orchiectomy results in cure over 90% of the time.
■Chemotherapy with carboplatin is an alternative adjuvant treatment option. A single cycle of carboplatin has proven to be equivalent to radiation in producing a high rate of relapse-free survival (RFS) and OS at 4 years. It is also associated with a lower risk of second germ cell tumor.
■Regardless of initial therapy, over 98% of patients will ultimately be cured. Physicians and patients must discuss the short-term and long-term advantages and disadvantages of more aggressive therapies in this stage of disease. All patients must understand the need for frequent visits and imaging during follow-up.
Stage II
■For stage IIA/B, or nonbulky disease (lymph node mass <5 cm), radical inguinal orchiectomy followed by radiation therapy (30 Gy) to ipsilateral iliac and retroperitoneal lymph nodes results in cure 90% of the time.
■In selected cases where radiation is contraindicated, cisplatin-based chemotherapy may suffice. For stage IIC or bulky disease (lymph node mass >5 cm) cisplatin-based chemotherapy is the standard after radical orchiectomy.
■Patients with good risk stage IIC may be treated with three cycles of bleomycin, etoposide, and cisplatin (BEP) or four cycles of etoposide and cisplatin (EP). Intermediate risk disease requires four cycles of BEP.
■There is no evidence that the combination of both radiation and chemotherapy increases RFS or OS.
Stage III
Stage III disease is usually still curable. Chemotherapy is required for patients following radical orchiectomy. Patients with good prognosis may be treated with three cycles of BEP; all other patients should be treated with four cycles of BEP.
Nonseminomas
Adjuvant treatment options for stage I, II, and III nonseminoma are outlined in Figures 16.2 and 16.3.
Stage I
■Stage I nonseminomatous disease (including tumors appearing to be seminomas but with elevated levels of serum AFP) is also highly curable, with several effective treatment options after radical orchiectomy.
■Retroperitoneal lymph node dissection (RPLND) has long been the mainstay of therapy in this disease and reports of cure are as high as 99%. After RPLND, 30% to 50% patients will be found to have pathologic stage II disease, although it is important to note that up to 10% of patients will have occult distant metastasis elsewhere (primarily in the lungs) that will not be detected by RPLND.
■While extremely effective, up to 70% of patients will be overtreated with RPLND and 10% may still require chemotherapy because of metastatic disease elsewhere. In patients with positive lymph nodes, two cycles of adjuvant cisplatin-based chemotherapy reduce the risk of recurrence to <2%, although this could be considered an overtreatment.
■Adjuvant chemotherapy has been suggested after orchiectomy for stage I disease if there is evidence of lymphovascular invasion or if there is predominance of embryonal carcinoma histology. Active surveillance is again an option, with 30% of all patients expected to relapse (95% within 2 years; 99% within 4 years). Regardless of the time of recurrence, more than 95% of patients are still curable with salvage chemotherapy.
■Several factors must be considered before choosing active surveillance. These include the patient’s level of anxiety, compliance, and access to a facility with experienced physicians, radiologists, and CT scanners to detect recurrence.
FIGURE 16.2 Adjuvant treatment options for stage I nonseminoma. RPLND, retroperitoneal lymph node dissection; BEP, bleomycin, etoposide, and ciplatin; EP, etoposide and ciplatin.
Stage II
■Stage IIA disease with lymph node mass ≤2 cm may be treated with RPLND after orchiectomy. If the nodal mass is completely resected and tumor markers return to normal levels, observation or two cycles of cisplatin-based chemotherapy may be considered. About 20% of patients may have disease relapse after RPLND alone, but over 95% may be still be cured with salvage chemotherapy.
■Platinum-based chemotherapy after RPLND may improve RFS in patients with lymphatic or venous invasion by tumor, although studies indicate equivalent cure rates for adjuvant chemotherapy versus chemotherapy at recurrence.
■If tumor markers do not decline after RPLND, it is indicative of residual disease and such patients should receive three to four cycles of cisplatin-based chemotherapy as systemic therapy.
■Patients with stage IIB/C tumors and nodal disease >2 cm should receive adjuvant cisplatin-based chemotherapy and residual mass after chemotherapy should be resected.
Stage III
■Just as in stages I and II, the goal of therapy in stage III testicular cancer is cure. Patients with good risk stage III should receive three cycles of BEP, while those with intermediate or poor risk stage III should receive four cycles of the same regimen.
■In patients with contraindications to bleomycin, four cycles of etoposide, ifosfamide, and cisplatin (VIP) are as effective as BEP but with more toxicity.
■Residual masses after chemotherapy should be resected. Patients with brain metastases should receive whole-brain radiation in conjunction with chemotherapy.
FIGURE 16.3 Adjuvant treatment options for stage II and III nonseminoma.
Chemotherapy Regimens
Commonly used chemotherapy regimens (Table 16.4) include BEP and EP. VIP and VeIP are used less often.
Follow-Up
Appropriate surveillance of patients with testicular cancer is essential and should be determined by the tumor’s histology, stage, and treatment (Tables 16.5 and 16.6).
Salvage Therapy
■Salvage therapy is usually reserved for disease that has not had a durable response to primary chemotherapy with platinum-based regimen. Such patients may also be considered for a clinical trial especially if they have poor prognostic features.
■Conventional dose regimens incorporate ifosfamide and cisplatin with either vinblastine (VeIP) or paclitaxel (TIP).
■High-dose chemotherapy with autologous bone marrow or peripheral stem cell support is investigational and may represent a therapeutic option for selected patients.
■Agents currently under investigation include gemcitabine, paclitaxel, epirubicin, and oxaliplatin.
High-Dose Chemotherapy with Autologous Hematopoietic Stem Cell Rescue
■The benefit of high-dose chemotherapy with hematopoietic stem cell rescue (HDT) as first-line salvage therapy has been shown in nonrandomized trials but not in randomized phase 3 studies (Table 16.7).
■In a large retrospective study, 5-year survival was 53% with HDT as the first salvage therapy.
■Cisplatin refractory germ cell tumors are less likely to have durable response to HDT as compared with tumors that are not refractory to cisplatin.
■HDT should be considered in patients with germ cell tumors that are refractory to primary chemotherapy or those that failed first-line conventional salvage chemotherapy.
Therapy-Related Toxicity
Complications of RPLND
■Surgical techniques have been refined over the years, but 1% to 2% of patients will have complications which can include bowel perforation, chylous ascites, lymphocele, vascular injuries, pancreatitis, and ejaculatory dysfunction or retrograde ejaculation.
Fertility
Although 70% to 80% of patients treated with chemotherapy may recover sperm production within 5 years, sperm banking should be discussed with all patients desiring to father children after therapy.
■At diagnosis, approximately 25% of patients have oligospermia, sperm abnormalities, or altered follicular stimulating hormone levels due in part to the association of testicular cancer with conditions such as cryptorchidism or testicular atrophy.
■Orchiectomy may further impair spermatogenesis.
■Almost all patients become azospermic or oligospermic during chemotherapy.
■Children of treated patients do not appear to have an increased risk of congenital abnormalities.
Pulmonary Toxicity
■Bleomycin may cause pneumonitis and pulmonary fibrosis, which may be fatal in up to 50% of patients.
■More frequently, asymptomatic decreases in pulmonary function resolve after completion of bleomycin therapy.
■Bleomycin should be discontinued if early signs of pulmonary toxicity develop or if there is a decline of ≥40% in diffusing capacity of lung for carbon monoxide (DLCO).
■Routine pulmonary function tests are rarely indicated and should be reserved for patients with signs and symptoms of pulmonary toxicity (e.g., dry rales on physical examination or dyspnea on exertion).
■Corticosteroids may be used to reduce lung inflammation if pulmonary toxicity occurs.
■Smokers treated with bleomycin should be particularly discouraged from tobacco use.
■Retrospective studies have suggested that low fraction of inspired oxygen and adequate intravascular volume management may reduce the incidence of postoperative bleomycin-induced pulmonary toxicity.
Nephrotoxicity
■Cisplatin-based chemotherapy may result in decreased glomerular filtration rate, which can be permanent in 20% to 30% of patients.
■Hypokalemia and hypomagnesemia are also frequent manifestations of altered kidney function in these patients.
Neurologic Toxicity
■Cisplatin-based chemotherapy may result in persistent peripheral neuropathy in 20% to 30% of patients.
■Cisplatin-induced neuropathy is sensory and distal. Peripheral digital dysesthesias and paresthesias are the most common manifestations.
■Polymorphism in the glutathione S-transferase gene may increase the susceptibility to cisplatin-induced neurotoxicity.
■Ototoxicity in the form of tinnitus or high-frequency hearing loss, usually outside the frequency of spoken language, may be seen in up to 20% of the patients treated with cisplatin-based regimen. The risk increases with increasing number of treatment cycles.
Cardiovascular Toxicity
■Bleomycin, cisplatin, and radiation alone or in combination can increase the risk of cardiovascular disease.
■Angina, myocardial infarction, and sudden cardiac death are increased by up to twofold.
■The risk of hypertension, hypercholesterolemia, and insulin resistance is increased in patients with testicular cancer treated with chemotherapy.
■Patients are also at increased risk of thromboembolism and Raynaud phenomenon.
Secondary Malignancies
■Secondary malignancies are associated with the use of cisplatin, etoposide, and radiation. Patients treated for testicular cancer with these agents reportedly have a 1.7-fold increase in their risk of developing a secondary malignancy.
■The increased risk of second malignancy may persist for up to 35 years after the completion of chemotherapy or radiotherapy for testicular carcinoma.
■Alkylating agents such as cisplatin may lead to a myelodysplastic syndrome within 5 to 7 years that can eventually progress to leukemia. Topoisomerase inhibitors such as etoposide may cause secondary leukemias within 3 years.
■There is an increased incidence of solid tumors in previous radiation fields, including the bladder, stomach, pancreas, and kidney.
REVIEW QUESTIONS
1.A 22-year-old man without significant medical history presented with right-sided chest pain. A chest radiograph showed a mass in the anterior mediastinum. Serum HCG and AFP levels were elevated but a thorough examination of the testicle was unrevealing. This patient likely has
A.Seminoma
B.Klinefelter syndrome
C.Primary mediastinal B-cell lymphoma
D.Thymoma
E.Down syndrome
2.A 29-year-old man presented with a painless right testicular mass. His serum HCG was 10,000 milli-international units/mL and the AFP was 3 ng/mL. CT scan showed a retroperitoneal lymph node mass that measured 7 cm. Immunohistochemical staining of this tumor is likely to be positive for the following markers:
A.CD30 and cytokeratin
B.SOX2 and NANOG
C.CD117
D.CD30
E.OCT4 and SOX2
3.The patient in question 2 had right inguinal orchiectomy followed by four cycles of BEP. Thereafter, his serum tumor markers were in the normal range but there was a persistent 2 cm para-aortic lymph node mass. What is the best next course of action?
A.Surgical resection
B.Radiation therapy
C.Salvage chemotherapy
D.High-dose therapy with stem cell transplant
E.Surveillance
4.A 35-year-old man with cardiac arrhythmia has been on warfarin and amiodarone for several years. Recently, he was diagnosed with nonseminomatous germ cell tumor and he had radical left inguinal orchiectomy a few weeks ago. Preoperatively his AFP was 15,000 ng/mL, left ventricular ejection fraction was 55%, estimated glomerular filtration rate was 55, and DLCO was 50% of its value 6 months ago. He has been referred to you for adjuvant chemotherapy. What is the best treatment for this patient?
A.Four cycles of BEP
B.Three cycles of etoposide and carboplatin
C.Four cycles of EP
D.Four cycles of VeIP
E.Four cycles of VIP
5.A young executive of a thriving commercial firm has just been diagnosed with a poor-risk testicular germ cell tumor with lung metastases. He wants to know his chances for survival because he has two young children. You should tell him that
A.His 5-year OS is 99%.
B.His 5-year OS is 72%.
C.His 5-year OS is 48%.
D.He is more likely to die from the treatment than from the disease.
E.His survival cannot be determined until RPLND is performed.
6.Prior to treatment for testicular germ cell tumor all patients should
A.Have a pulmonary function test with DLCO
B.Be counseled about sperm banking
C.Have an echocardiogram
D.Have genetic testing
E.Receive corticosteroid to prevent bleomycin toxicity
7.The most common genetic abnormality in testicular germ cell tumor is
A.47, XXY
B.Xq27
C.Increased copy number of 12p
D.SOX17
E.KIT
8.A 30-year-old man had a radical left inguinal orchiectomy for a nonseminomatous testicular germ cell tumor a few months ago. After four cycles of BEP there was a residual retroperitoneal lymph node mass. Excision of the mass was performed and there was evidence of yolk sac element. What will you recommend?
A.Close surveillance
B.Two cycle of EP
C.Three cycles of BEP
D.Four cycles of VIP
E.None of the above
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The opinions expressed in this chapter represent those of the authors and do not necessarily represent official positions or opinions of the US government or of the U.S. Department of Health and Human Services.