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Testicular Seminoma

  • Author: Michael B Williams, MD, MS; Chief Editor: Bradley Fields Schwartz, DO, FACS  more...
 
Updated: Mar 03, 2016
 

Practice Essentials

Testicular seminoma (see the image below) is a pathologic diagnosis in which only seminomatous elements are observed upon histopathologic review after a radical orchiectomy and in which serum alpha-fetoprotein (AFP) is within the reference range. Seminomas account for one third of testicular germ cell tumors (GCTs), which are the most common malignancy in men aged 15-35 years.[1] The risk of testis cancer is 10-40 times higher in patients with a history of cryptorchidism; 10% of patients with GCTs have a history of cryptorchidism.[2]

This is a classic testicular seminoma, high-power This is a classic testicular seminoma, high-power view, from a 37-year-old man with a painless mass in his right testis. Levels of serum beta-human chorionic gonadotropin and alpha-fetoprotein were within the reference range, and the metastatic workup findings were negative. Histopathology showed a pure seminoma. Metastatic workup showed no nodal or distant spread, T1N0M0 stage I. After orchiectomy, the patient underwent adjuvant external beam radiotherapy to the para-aortic nodes. At a 3-year follow-up study, the patient is disease free and has a greater than 95% chance of remaining disease free. See related image for a scrotal sonogram of this patient. Note here that tumor cells are uniform, have abundant clear cytoplasm, a large centrally located nucleus, and a variable mitotic pattern.

Signs and symptoms

The typical presentation in testicular seminoma is as follows:

  • A male aged 15-35 years presents with a painless testicular lump that has been noticeable for several days to months
  • Patients commonly have abnormal findings on semen analysis at presentation, and they may be subfertile[3]
  • Patients may present with a hydrocele, and scrotal ultrasonography may identify a nonpalpable testis tumor

Uncommon presentations include the following:

  • Testicular pain, possibly with an acute onset; may be associated with a hydrocele
  • A metastatic testis tumor may manifest as large retroperitoneal and/or chest lesions, while the primary tumor is nonpalpable

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies for testicular seminoma are as follows:

  • An elevated AFP level rules out pure seminoma, despite possible contrary histopathologic orchiectomy findings
  • Lactate dehydrogenase (LDH) is a less-specific marker for GCTs, but levels can correlate with overall tumor burden
  • Beta–human chorionic gonadotropin (beta-hCG) levels are elevated inn 5-10% of patients with seminomas; elevation may correlate with metastatic disease but not with overall survival
  • Placenta-like alkaline phosphatase levels can be elevated in patients with seminoma, especially as the tumor burden increases; however, it may also increase with smoking

Scrotal ultrasonography

  • Consider this study in any male with a palpable testicular mass that is suspicious or questionable
  • Other indications may include acute scrotal pain (especially when associated with a hydrocele), nonspecific scrotal pain, or swelling
  • If an asymptomatic hydrocele obscures physical examination of the testicle, this study may be appropriate prior to surgical intervention
  • This study may also be appropriate for males who are at the peak age range for testicular cancer (ie, 15-35 years)
  • Scrotal ultrasonography commonly shows a homogeneous hypoechoic intratesticular mass
  • Larger lesions may be more inhomogeneous
  • Calcifications and cystic areas are less common in seminomas than in nonseminomatous tumors

Other imaging studies

  • Abdominal and pelvic CT scanning: Can be used to identify metastatic disease to the retroperitoneal lymph nodes, but it results in understaging in approximately 15-20% of patients thought to be at stage I[4]
  • Chest CT scanning: Indicated only when abnormal findings are observed on a chest radiograph
  • Fluoro-2-deoxy-D-glucose (FDG) PET scanning: May be useful in restaging assessments of residual masses following chemotherapy

Histologic findings

Seminomas can have 3 histologic variants, as follows[5] :

  • Classic seminoma (the most common histologic type)
  • Anaplastic seminoma (5-15% of patients)
  • Spermatocytic seminoma (a rare variant that occurs in older adults)

See Workup for more detail.

Management

In testicular seminoma, orchiectomy provides both diagnosis and therapy. Orchiectomy alone cures most stage I seminomas. To prevent relapse, the following are standard options in stage I disease[6] :

  • Surveillance
  • Single-agent carboplatin
  • Radiotherapy

Preferred treatments for more advanced stages are as follows:

  • Stage IIA - Radiotherapy
  • Stage IIB - Chemotherapy with etoposide and cisplatin (EP) or bleomycin, etoposide, and cisplatin (BEP)  
  • Stage IIC, III - Chemotherapy with EP or BEP

After treatment, patients require lifelong follow-up. Surveillance includes the following, with the frequency determined by disease stage and duration of follow-up:

  • History and physical examination
  • Serum tumor markers (beta-hCG, LDH, AFP)
  • Chest radiography
  • CT scan of the abdomen, with or without CT scan of the pelvis

See Treatment and Medication for more detail.

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Background

The study of testicular germ cell tumors (GCTs) is a unique area of urologic oncology, as treatment algorithms have benefited from numerous randomized prospective clinical trials (unlike prostate cancer) and because metastatic disease is highly responsive to multimodal treatment (unlike renal cell carcinoma). Seminoma is a histologic subtype of GCTs, which are discussed separately as nonseminomas in Germ Cell Tumors.

The interest in GCTs is disproportional to its incidence because of its fascinating pathologic subtypes, success of multimodal therapy (even for metastatic disease), and almost universal incidence in otherwise healthy males aged 15-35 years. Testicular GCTs have various pathologic subtypes, including seminoma, embryonal, yolk sac, teratoma, and choriocarcinoma. The most important clinical distinction is between seminoma and nonseminoma, two broad categories with different treatment algorithms: (1) Seminoma as a classification refers to pure seminoma upon histopathologic review, and (2) the presence of any nonseminomatous elements (even if seminoma is prevalent) changes the classification to nonseminoma.

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Pathophysiology

Testicular seminoma is a pathologic diagnosis in which only seminomatous elements are observed upon histopathologic review after a radical orchiectomy and in which serum alpha-fetoprotein (AFP) is within the reference range. Any elevation of AFP levels or nonseminomatous elements in the testis specimen mandates diagnosis of nonseminomatous GCT (NSGCT) and an appropriate treatment change.

GCTs have the following subtypes and frequencies: seminoma (40%), embryonal (25%), teratocarcinoma (25%), teratoma (5%), and choriocarcinoma (pure; 1%). Seminomas can be further subdivided into one of three categories based on histology: classic, anaplastic, and spermatocytic (see Histologic Findings).[5]

Germ cell carcinoma in situ (CIS) is a premalignant condition with a natural history of progression to seminoma or embryonal cancer. Patients with infertility, intersex disorders, cryptorchidism, prior contralateral GCTs, or atrophic testes more commonly have CIS. Histologically, it demonstrates intratubular atypical germ cells within seminiferous tubules. Most patients with seminomas (except spermatocytic seminoma) and NSGCTs have CIS or severe atypia associated with the primary tumor.[7] In patients with GCTs, 5% of those with contralateral testes harbor CIS.[8]

Testicular microcalcifications observed on scrotal sonograms were long held to be implicated in the development of testicular carcinoma. However, an analysis of 83 patients with asymptomatic microcalcifications observed for 5 years demonstrated only one with testicular carcinoma development over the interim. This represented an odds ratio for the study population of 317 (95% CI, 36-2756), with over 98% of men with asymptomatic microcalcifications having a benign course. A recommendation of continued monthly self-examination without further intervention was given for management of this indolent finding.[9]

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Frequency

United States

Testicular GCTs are rare, representing only 1%-2% of all male malignancies and occurring in 1 of 250 men by age 65 years; however, GCT is the most common malignancy in men aged 15-35 years. Incidence rates are 3.7 and 0.9 cases per 100,000 persons per year for whites and blacks, respectively.[10]

International

The incidence of testis cancer has increased from the early 1960s to the mid 1980s. Nonwhite populations have a lower incidence than white populations. The highest rates of testis cancer are in Denmark (11.5 cases per 100,000 persons per year), Norway (9 cases per 100,000 persons per year), and Switzerland (11 cases per 100,000 persons per year). Rates vary across Europe.[11]

A review by Bray and colleagues (2006) of 41 cancer registries in 14 countries found the seminoma rates to be highest in Denmark and Switzerland (9 cases per 100,000 persons per year) and the lowest rates in Japan, Israel, and Finland (1-3 cases per 100,000 persons per year).[12]

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Mortality/Morbidity

In a review of testicular GCT patients diagnosed in Norway from 1953-2012, Kvammen et al found that although relative survival has improved in recent decades, it generally continues to decline with increasing follow-up time, particularly beyond 15-30 years, regardless of disease extent at diagnosis. Relative survival was lower in patients diagnosed before 1980 or after age 40. These authors proposed that the likely main cause is treatment-induced late effects, with the continued use of adjuvant radiotherapy in seminomas until the year 2000 as the suspected culprit.[13]

Race- and Age-related Demographics

Established data sets have consistently demonstrated a higher incidence of GCTs in whites than in African Americans—as high as a 5:1 ratio. McGlynn et al (2005) published an analysis of 9 registries of the Surveillance, Epidemiology, and End Results (SEER) database from 1973-2001. They found an increasing incidence among African Americans starting in the 1990s. The increased incidence was 100% for GCTs overall—124% for seminoma and 64% for nonseminoma. The reasons for this increase are unclear, and the author's review of the data suggests environmental or nonperinatal factors (occupation, physical activity, diet) rather than early screening as the predominant cause.[14]

Testicular GCTs represent the most common malignancy in men aged 15-35 years. Seminoma accounts for one third of these diagnoses.[1]

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Contributor Information and Disclosures
Author

Michael B Williams, MD, MS Assistant Professor, Department of Urology, Leroy T Canoles, Jr, Cancer Research Center, Eastern Virginia Medical School

Michael B Williams, MD, MS is a member of the following medical societies: American Association for Cancer Research, American Urological Association, Society of Urologic Oncology, Texas Medical Association, American Society of Clinical Oncology, American Association of Clinical Urologists

Disclosure: Nothing to disclose.

Coauthor(s)

Paul F Schellhammer, MD Professor of Urology, Eastern Virginia Medical School; Urologist, Urology of Virginia, PC

Paul F Schellhammer, MD is a member of the following medical societies: American Medical Association, American Urological Association, Society of Surgical Oncology, Society of Urologic Oncology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Bradley Fields Schwartz, DO, FACS Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine

Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, Society of Laparoendoscopic Surgeons, Society of University Urologists, Association of Military Osteopathic Physicians and Surgeons, American Urological Association, Endourological Society

Disclosure: Nothing to disclose.

Additional Contributors

Gamal Mostafa Ghoniem, MD, FACS Professor and Vice Chair of Urology, Chief, Division of Female Urology, Pelvic Reconstructive Surgery, and Voiding Dysfunction, Department of Urology, University of California, Irvine, School of Medicine

Gamal Mostafa Ghoniem, MD, FACS is a member of the following medical societies: American Urogynecologic Society, International Continence Society, International Urogynaecology Association, Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction, American College of Surgeons, American Urological Association

Disclosure: Received honoraria from Astellas for speaking and teaching; Received grant/research funds from Uroplasty for none; Partner received honoraria from Allergan for speaking and teaching.

Acknowledgements

John W Davis, MD Assistant Professor, Department of Urology, University of Texas MD Anderson Cancer Center

John W Davis, MD is a member of the following medical societies: American College of Surgeons and American Urological Association

Disclosure: Nothing to disclose.

Dan Theodorescu, MD, PhD Paul A Bunn Professor of Cancer Research, Professor of Surgery and Pharmacology, Director, University of Colorado Comprehensive Cancer Center

Dan Theodorescu, MD, PhD is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Urological Association, Medical Society of Virginia, Society for Basic Urologic Research, and Society of Urologic Oncology

Disclosure: Key Genomics Ownership interest Co-Founder-50% Stock Ownership; KromaTiD, Inc Stock Options Board membership

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Testicular seminoma. A 57-year-old man presents with abdominal pain of slow onset. CT scanning shows a large 25-cm retroperitoneal lesion encompassing the aorta and renal vasculature and displacing the right kidney laterally. The patient had a history of cryptorchidism repaired at age 8 years. Testes were normal and descended; however, ultrasonography showed a small 5-mm lesion on the right testis, which proved to be pure seminoma at orchiectomy. The beta-human chorionic gonadotropin level was 70 mIU/mL (reference range, < 5 mIU/mL), and the alpha-fetoprotein level was within the reference range; no metastatic lesions were observed above the diaphragm, indicating stage IIb (bulky), T1N3M0. The patient was referred for 4 cycles of cisplatin-based chemotherapy.
Testicular seminoma. This scrotal ultrasound of a 37-year-old man with a painless mass in his right testis shows a right testis with hypoechoic solid masses compared to the homogeneous, more hyperechoic, healthy left testis. Levels of serum beta-human chorionic gonadotropin and alpha-fetoprotein were within the reference range, and the metastatic workup findings were negative. Histopathology showed a pure seminoma. Metastatic workup showed no nodal or distant spread, T1N0M0 stage I. After orchiectomy, the patient underwent adjuvant external beam radiotherapy to the para-aortic nodes. At a 3-year follow-up study, the patient is disease free and has a greater than 95% chance of remaining disease free.
Testicular seminoma. This is a classic seminoma at low power. Uniform tumor cells are observed with mild inflammatory response (lymphocytes). Other seminoma findings not seen could include a fibrovascular stroma, syncytiotrophoblastic cells, and multinucleated histiocytes.
This is a classic testicular seminoma, high-power view, from a 37-year-old man with a painless mass in his right testis. Levels of serum beta-human chorionic gonadotropin and alpha-fetoprotein were within the reference range, and the metastatic workup findings were negative. Histopathology showed a pure seminoma. Metastatic workup showed no nodal or distant spread, T1N0M0 stage I. After orchiectomy, the patient underwent adjuvant external beam radiotherapy to the para-aortic nodes. At a 3-year follow-up study, the patient is disease free and has a greater than 95% chance of remaining disease free. See related image for a scrotal sonogram of this patient. Note here that tumor cells are uniform, have abundant clear cytoplasm, a large centrally located nucleus, and a variable mitotic pattern.
Table 1. Primary Tumor (T)
pTxPrimary tumor cannot be assessed
p0No evidence of primary tumor
pTisIntratubular germ cell neoplasia
pT1Tumor limited to the testis and epididymis
No vascular/lymphatic invasion
May invade the tunica albuginea
No invasion of the tunica vaginalis
pT2Tumor limited to the testis and epididymis
Vascular/lymphatic invasion or tumor extending through the tunica albuginea with involvement of the tunica vaginalis
Invades beyond the tunica albuginea or into the epididymis
pT3Tumor invades the spermatic cord with or without vascular/lymphatic invasion
pT4Tumor invades the scrotum with or without vascular/lymphatic invasion
Table 2A. Regional Lymph Nodes (N): Clinical
NxNodes not assessed
N0No regional lymph node metastasis
N1Lymph node mass or multiple lymph node masses ≤ 2 cm in greatest dimension
N2Lymph node mass or multiple lymph node masses >2 cm but ≤ 5 cm in greatest dimension
N3Lymph node mass >5 cm in greatest dimension
Table 2B. Regional Lymph Nodes (N): Pathologic
pN0No evidence of tumor in lymph nodes
pN1Lymph node mass ≤ 2 cm in greatest dimension
≤ 5 nodes positive
pN2Lymph node mass >2 cm but < 5 cm in greatest dimension
>5 nodes positive
Evidence of extranodal extension of tumor
pN3Lymph node mass >5 cm in greatest dimension
Table 3. Distant Metastases (M)
M0No evidence of distant metastases
M1aNonregional nodal or pulmonary metastases
M2bNonpulmonary visceral metastases
Table 4. Serum Tumor Markers (S)
SLDHhCG† (mIU/mL)AFP (ng/mL)
SxNot assessedNot assessedNot assessed
S0≤ NandNormalandNormal
S1< 1.5 x Nand< 5,000and< 1,000
S21.5-10 x Nor5,000-50,000or1,000-10,000
S3>10 x Nor>50,000or>10,000
Table 5. Stage Grouping
Stage groupingTNMS
Stage 0pTisN0M0S0
Stage IT1-T4N0M0Sx
Stage IAT1N0M0S0
Stage IBT2-4N0M0S0
Stage ISAny TN0M0S1-S3
Stage IIAny TAny NM0Sx
Stage IIAAny TN1M0S0-S1
Stage IIBAny TN2M0S0-S1
Stage IICAny TN3M0S0-S1
Stage IIIAny TAny NM1Sx
Stage IIIAAny TAny NM1aS0-S1
Stage IIIBAny TAny NM0-M1aS2
Stage IIICAny TAny NM0-M1aS3
Any TAny NM1bAny S
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