eMedicine Specialties > Radiology > Genitourinary

Testicle, Malignant Tumors

Dawn Light, MD, MPH, Clinical Assistant Professor of Radiology and Pediatrics, Department of Radiology, Consulting Staff, Dayton Children's Medical Center; Clinical Assistant Professor of Radiology, Department of Radiology, Uniformed Services University of the Health Sciences

Updated: Mar 4, 2009

Introduction

Background

Classification of malignant tumors of the testicle

Germ cell tumors (GCTs) account for nearly all (95%) of primary testicular tumors. The GCT line is fairly evenly split between seminomas (45%) and nonseminomas (50%). Of the nonseminomas, mixed GCTs are most common (40%). Teratomas and teratocarcinomas are considered malignant in adults and constitute 30% of nonseminomatous lesions. The embryonal cell tumor is the classic pure-cell, nonseminomatous tumor and is relatively uncommon (20%). Choriocarcinoma represents the most lethal but least common (1%) nonseminomatous type.

Both computed tomography (CT) scanning and ultrasonography have been used to search for metastatic retroperitoneal lymphadenopathy, but CT scanning is more commonly used.

This is a seminoma. Sometimes epididymal invasion can be noted on sonograms.

Among nongerminal testicular tumors, stromal Leydig cell tumors and Sertoli cell tumors constitute the remaining 5% of primary testicular tumors; these are rare tumors that are malignant in only about 10% of the cases.

Lymphoma, leukemia, and melanoma are the most common malignancies that metastasize to the testicle.¹

Screening for testicular cancer

Ultrasonographic screening for testicular cancer is not currently recommended, because this disease does not meet the criteria for an acceptable screening program wherein early treatment must have a success rate superior to that of the treatment initiated when the patient is clinically symptomatic.

For cancer screening to be successful, the screening tool must be highly sensitive and specific, widely available, cost-effective, and acceptable to the patients. Also, the test must allow clinicians to identify disease at a stage where they can improve the patient's clinical outcome and/or clearly identify patients at risk.

Screening for testicular cancer is not a current recommendation because patients with stage 1 or 2 (2A or 2B) testicular cancer have a long-term, disease-free survival rate greater than 95%; in patients with bulky retroperitoneal nodes and/or pulmonary or visceral metastasis, this rate is 60-80%. A birth-cohort effect is observed for testicular cancer in the United States and Europe, but the etiology of this effect is not known. The false-negative rate for ultrasonographic identification of testicular lesions is extremely low.

Pathophysiology

The specific pathophysiologic mechanisms for neoplasm induction have not been described, but testicular cancer is thought to result from the differentiation of totipotential germ cells. Studies of cancer in familial groups suggest that discordant tumor histology occurs in only 20% of identical twin pairs, whereas the discordance rate is 67% in sibling pairs. Thus, evidence supports a familial tendency toward testicular malignancy.²

A current molecular model suggests that mutations in the 12p chromosomal segment of the malignant cell sequences are associated with tumor development.³ Patients with ambiguous genitalia have the highest risk of testicular malignancy. Among patients with a known testicular cancer, the metachronous risk in the contralateral testicle is 5%. The malignancy risk in men with cryptorchidism is 2-4%, and the risk in patients with subfertility is 1% or less.⁴

The precise malignancy risk associated with testicular microlithiasis (>5 microcalcifications within a testicle) is unclear. Retrospective studies⁵ of patients with known malignancy or ultrasound for a clinical finding demonstrate high concordance between microlithiasis and malignancy, but results from a prospective analysis show only a 5-10% risk of coexisting tumors.⁶

Mature-appearing testicular teratomas are considered malignant in adults but benign in children.

Frequency

United States

Testicular cancer is the most common solid malignancy in males aged 18-35 years and currently represents 1% of all cancers in men. McKiernan et al reported that the rate of testicular cancer increased by 51% between 1973 and 1995.⁷ Strong evidence suggests a birth-cohort effect, but the etiology of this cohort has not been elucidated.

International

Carcinoma in situ (CIS) is reported to occur in less than 1% of healthy males. Incidence studies in Europe reveal a similar increase in the frequency of disease over the past 40 years.

Mortality/Morbidity

• Seminoma is highly curable when detected early. The 5-year survival is reported to be 95% for stage I disease and 85-90% for stage 2 disease.
• For nonseminomatous germ cell tumors, the results are less favorable, with a 5-year survival rate of 86% for stage I disease. The corresponding survival rate for teratocarcinomas is only 70%.
• Choriocarcinoma has a dismal prognosis; almost no patients survive 5 years after the disease presentation. Choriocarcinomas have the worst prognosis of all the testicular malignancies.

Race

Testicular cancer primarily affects white males. Blacks rarely develop this cancer: 9 cases per million population, compared with 50 cases per million population in other racial groups.

Sex

Patients with ambiguous genitalia have a 25% risk of developing testicular malignancy.

Age

Testicular cancer is the most common solid malignancy in males aged 18-35 years. Seminomas, which peak in the fourth or fifth decade of life, are most common at the extremes of age. Choriocarcinomas are most commonly reported in those aged 10-30 years. Yolk sac tumors are usually composed of pure cell lines and most often seen in patients younger than 3 years.⁸

Presentation

Staging of testicular cancer

• Stage 1: Confined to the testicle and the spermatic cord
• Stage 2: Includes metastatic lymph nodes below the diaphragm
  • Stage 2A: Involves nonpalpable nodes
  • Stage 2B: Involves bulky adenopathy
• Stage 3: Metastasis above the diaphragm
  • Stage 3A: Confined to the lymph nodes
  • Stage 3B: Extra total metastasis

Carcinoma in situ

At the time of the initial surgery, CIS is found in approximately 5% of obtained biopsy samples of the contralateral testicle. The natural history of CIS is progression to frank malignancy at 5 years in 50% of cases. However, the literature does not support routine biopsy of the opposite testis in cases of testicular cancer. The adverse effects of castration are high, and the ease with which the tumors are treated suggests thatsurveillance with treatment of early tumors is preferred.

Differential diagnosis

The differential diagnosis of intratesticular masses includes several entities. Epidermoid cysts of the testicle are seen as a round, sharply demarcated lesion in the testicle. Dilated rete testes are clusters of testicular mediastinal dilated tubules that empty into the epididymis and are often associated with epididymal cysts. Testicular abscess is commonly linked with severe epididymitis, pain, fever, and redness and induration of the scrotum. Hematoma can be associated with a history of testicular trauma, and one must be certain that these findings completely resolve, because incidental trauma is often the presentation for a subsymptomatic testicular mass.⁹

Hormonal changes

Most of the hormonal abnormalities in seminomas are elevated beta–human chorionic gonadotropin (HCG) levels; thus, the presence of elevated alpha1-fetoprotein levels decrease the likelihood that a tumor is a seminoma. Increased hormone levels occur in about 8% of patients with seminomas and 60% of those with nonseminomatous cancers.

Preferred Examination

Ultrasonography is the standard imaging technique used to identify testicular carcinoma. It has a high sensitivity, but it must be combined with physical examination to achieve the best specificity. More than 95% of testicular parenchymal abnormalities are identifiable on routine sonograms, but several other lesions commonly mimic testicular cancer. Ultrasonography is more specific in the presence of a palpable mass. Nonpalpable intratesticular lesions larger than 1 cm are unlikely to be malignant.

Differential Diagnoses

Other Problems to Be Considered

Abscess or focal orchitis
Focal atrophy
Hematoma
Infarct
Tubular ectasia of the rete testes
Sarcoid
Metastases from lymphoma or leukemia

Radiography

Findings

Plain radiographs have no role in the initial diagnosis of testicular cancer. Metastasis to the chest is fairly common and often seen on screening chest radiographs. However, computed tomography (CT) scanning is more sensitive and specific for staging the disease.

Computed Tomography

Both computed tomography (CT) scanning and ultrasonography have been used to search for metastatic retroperitoneal lymphadenopathy, but CT scanning is more commonly used.

Findings

CT scan imaging is routinely performed as part of the initial staging process, but it is not sensitive or specific enough to be useful in evaluating undiagnosed testicular masses. Chest, abdominal, and pelvic CT scan studies are indicated for the evaluation of retroperitoneal and mediastinal metastases.

CT scanning of the chest is especially useful when mediastinal or parenchymal lung disease caused by testicular cancer is suspected. This modality or magnetic resonance imaging (MRI) is also indicated in patients with neurologic signs or symptoms.

The most common site of disease recurrence is the retroperitoneum; thus, CT scanning is the best tool to detect recurrence.

False Positives/Negatives

Lymphoma can be difficult to distinguish from metastatic testicular cancer. Use tissue sampling from the abnormal testicle to make this distinction.

Magnetic Resonance Imaging

Findings

MRI is not used as the initial modality to evaluate testicular masses.

Degree of Confidence

Increased signal intensity in the testicle is seen on T2-weighted images of testicular malignancies, but it is not specific for the disease.

Ultrasonography

Testicular infarction can mimic an infiltrative tumor.

The depiction here is classic for a seminoma. Testicular malignancies appear as a hypoechoic mass in the vast majority of cases.

This is a mixed germ cell tumor. Testicular cancers can be ill-defined and subtle.

This is a seminoma. Occasionally, testicular tumors occur at a more advanced stage. If the entire testicle is involved, comparison with the normal side may show diffusely decreased echogenicity. Sometimes, epididymal invasion can be noted on sonograms.

This is a seminoma. Sometimes epididymal invasion can be noted on sonograms.

Testicular epidermoids can mimic solid malignancies.

Findings

Testicular ultrasonography is used to determine the location of a palpable mass when testicular cancer is suspected. Generally, palpable extra-testicular lesions are benign. On the other hand, intratesticular masses, especially if they are palpable, are likely to be malignant and must be surgically explored. Therefore, ultrasonography is useful for localizing palpable abnormalities and to triage them for surgical repair when indicated.¹⁰

The examination is usually performed with a high-frequency linear transducer to compare the echotexture of the 2 testicles for areas of heterogeneity. Testicular cancers are hypoechoic relative to the surrounding parenchyma in about 95% of cases. Published findings suggest that seminomas are often more homogeneously hypoechoic and that nonseminomatous lesions are often more cystic, with interspersed areas of calcification.^11,12

The tumor tissue type cannot be reliably differentiated solely by its ultrasonographic appearance. Commonly, seminomas are well defined within the tunica albuginea and homogeneously hypoechoic. Embryonal cell cancers typically are hypoechoic, with interspersed cystic components. Teratomas and choriocarcinomas are often heterogeneous with multiple internal calcifications present. Stromal cell tumors (eg, Leydig and Sertoli cell tumors) are generally well defined and hypoechoic, but calcifications are frequently found. Lymphoma and leukemia of the testicle generally present as an ill-defined, diffuse process of decreased echogenicity.

When multiple lesions are present, the differential diagnosis should be expanded to include metastatic processes, such as leukemia and lymphoma, and inflammatory processes, such as sarcoid. Testicular lymphoma can be difficult to diagnose when both testes are homogeneously hypoechoic.

Testicular microlithiasis (>5 or more microcalcifications within a testicle) results from concentric cores of calcification of intrasubstance collagen fibers.  Case studies of patients with testicular tumors suggest a high rate of microlithiasis, but prospective evaluations of patients with microlithiasis have failed to demonstrate more than a minimal increase in the frequency of such tumors. Annual ultrasound screening of patients with microlithiasis has been suggested by some authors, but prospective studies have failed to demonstrate a positive cost-benefit ratio at this time. Azzopardi tumor is the name used for a presumed "spontaneously burned out" tumor, wherein malignant cells spontaneously necrose and calcify, perhaps related to outgrowing the blood supply.

Degree of Confidence

Although the specificity and sensitivity have not been reported, general consensus exists that an ultrasonographic finding of a solid or mixed cystic and solid intratesticular mass is an indication for surgical exploration.

False Positives/Negatives

False-negative results are most common in the infiltrative malignant processes. When a condition such as leukemia or lymphoma causes bilateral diffusely decreased echogenicity, the infiltrative malignant process can be difficult to recognize.

False-positive results are seen in a variety of conditions (see Images 1-12). Dilated rete testes can be masslike, and they can simulate a predominantly cystic mass. The imaging characteristics of epidermoid tumors can be indistinguishable from those of germ cell lesions. Cho et al report that the classic appearance for an epidermoid is a heterogeneous mass, possibly with concentric hyperechoic and hypoechoic layers forming a ring.¹³ The epidermoid is often avascular. An abscess or phlegmon of the testicle is hypoechoic and often associated with increased vascularity. Testicular infarction can present as ill-defined decreased echogenicity in a testicle, suggesting a diffusely infiltrative malignant process.

A troublesome scenario can occur when a patient presents with a history of trauma and the sonogram shows a hypoechoic focus presumed to be a hematoma. Distinguishing a hematoma from a testicular tumor can be impossible on the initial images. Because such tumors can be detected after incidental trauma, ultrasonographic follow-up of suspected hematomas is recommended to ensure their complete resolution.

Intervention

The treatment of testicular cancer is orchiectomy. Ultrasonography is used only to suggest the diagnosis and exclude benign scrotal masses. When testicular malignancy is suspected, the surgeon uses an inguinal approach to avoid contaminating the scrotum. Some institutions are performing testis-sparing procedures when the ultrasonographic findings suggest a benign intratesticular mass such as an epidermoid or a teratoma.^14,15

With regard to treatment and adverse effects, radical orchiectomy with ligation of the spermatic cord at the inguinal ring is the recommended surgical procedure for suspected testicular cancer. Infertility may be related to retrograde ejaculation caused by retroperitoneal lymph node dissection or the toxic effects of chemotherapy or radiation therapy. Cisplatin is the mainstay of chemotherapy and is associated with nausea, vomiting, and nephrotoxicity. Hypomagnesemia-induced Raynaud phenomenon is also common.

In adults, even nonaggressive-appearing teratomas are known to develop metastasis. For this reason, careful excision of all teratomas is recommended in adults.

Patient Education: For excellent patient education resources, visit eMedicine's Men's Health Center and Cancer and Tumors Center. Also, see eMedicine's patient education articles Cancer of the Testicle and Testicular Self-Exam.

Medicolegal Pitfalls

• Tissue diagnosis should be strongly considered in any solid intratesticular mass, especially if a palpable abnormality is present.

Multimedia

Media file 1: Testicular infarction can mimic an infiltrative tumor.

Media file 2: The depiction here is classic for a seminoma. Testicular malignancies appear as a hypoechoic mass in the vast majority of cases.

Media file 3: Compared with other types of tumors, mixed germ-cell tumors are more likely to have cystic areas and calcifications scattered within the tumor.

Media file 4: This is another seminoma. On sonograms, a seminoma is often more homogeneous than nonseminomatous cancers.

Media file 5: This is a mixed germ cell tumor. Testicular cancers can be ill-defined and subtle.

Media file 6: Both computed tomography (CT) scanning and ultrasonography have been used to search for metastatic retroperitoneal lymphadenopathy, but CT scanning is more commonly used.

Media file 7: Dilated rete testes can mimic a cystic neoplasm, but they are usually elongated on orthogonal views and clearly located in the testicular mediastinum.

Media file 8: Testicular sarcoid can mimic seminoma when it presents as a solid-appearing testicular mass

Media file 9: This is a seminoma. Occasionally, testicular tumors occur at a more advanced stage. If the entire testicle is involved, comparison with the normal side may show diffusely decreased echogenicity. Sometimes, epididymal invasion can be noted on sonograms.

Media file 10: This is a seminoma. Sometimes epididymal invasion can be noted on sonograms.

Media file 11: Testicular cancer is not typically hypervascular.

Media file 12: Testicular epidermoids can mimic solid malignancies.

References

1. Katiyar RK, Singh A, Kumar D. Primary melanoma of testis. J Cancer Res Ther. Apr-Jun 2008;4(2):97-8. [Medline].

2. Hersmus R, de Leeuw BH, Wolffenbuttel KP, Drop SL, Oosterhuis JW, Cools M, et al. New insights into type II germ cell tumor pathogenesis based on studies of patients with various forms of disorders of sex development (DSD). Mol Cell Endocrinol. Sep 10 2008;291(1-2):1-10. [Medline].

3. Looijenga LH, de Munnik H, Oosterhuis JW. A molecular model for the development of germ cell cancer. Int J Cancer. Dec 10 1999;83 (6):809-14. [Medline].

4. Carmignani L, Bozzini G. Re: Increased incidence of testicular cancer in men presenting with infertility and abnormal semen analysis. J. D. Raman, C. F. Nobert and M. Goldstein [Letter]. J Urol. Apr 2006;175(4):1574; author reply, 1574.

5. Bach AM, Hann LE, Hadar O, et al. Testicular microlithiasis: what is its association with testicular cancer?. Radiology. Jul 2001;220(1):70-5. [Medline].

6. Peterson AC, Bauman JM, Light DE, et al. The prevalence of testicular microlithiasis in an asymptomatic population of men 18 to 35 years old. J Urol. Dec 2001;166(6):2061-4. [Medline].

7. McKiernan JM, Goluboff ET, Liberson GL, et al. Rising risk of testicular cancer by birth cohort in the United States from 1973 to 1995. J Urol. Aug 1999;162(2):361-3. [Medline].

8. Taskinen S, Fagerholm R, Aronniemi J, Rintala R, Taskinen M. Testicular tumors in children and adolescents. J Pediatr Urol. Apr 2008;4(2):134-7. [Medline].

9. Kao HW, Wu CJ, Chen CY, et al. Malignant tumor of testis imitating epididymo-orchitis. Arch Androl. Sep-Oct 2005;51(5):407-11.

10. Kravets FG, Cohen HL, Sheynkin Y, Sukkarieh T. Intraoperative sonographically guided needle localization of nonpalpable testicular tumors. AJR Am J Roentgenol. Jan 2006;186(1):141-3.

11. Carmignani L, Morabito A, Gadda F, et al. Prognostic parameters in adult impalpable ultrasonographic lesions of the testicle. J Urol. Sep 2005;174(3):1035-8.

12. Schwerk WB, Schwerk WN, Rodeck G. Testicular tumors: prospective analysis of real-time US patterns and abdominal staging. Radiology. Aug 1987;164(2):369-74. [Medline].

13. Cho JH, Chang JC, Park BH, et al. Sonographic and MR imaging findings of testicular epidermoid cysts [comment Dogra V. In. AJR Am J Roentgenol. 2002 Oct;179(4):1075; author reply 1075-6]. AJR Am J Roentgenol. Mar 2002;178(3):743-8. [Medline].

14. Labarthe P, Khedis M, Chevreau C, Mazerolles C, Thoulouzan M, Durand X, et al. [Management of pure teratoma of the testis in adult, results of a multicenter study over 15 years.]. Prog Urol. Dec 2008;18(13):1075-81. [Medline].

15. Soh E, Berman LH, Grant JW, Bullock N, Williams MV. Ultrasound-guided core-needle biopsy of the testis for focal indeterminate intratesticular lesions. Eur Radiol. Dec 2008;18(12):2990-6. [Medline].

16. Austoker J. Screening for ovarian, prostatic, and testicular cancers. Br Med J. Jul 30 1994;309(6950):315-20. [Medline].

17. Braga FJ, Arbex MA, Haddad J, Maes A. Bone scintigraphy in testicular tumors. Clin Nucl Med. Feb 2001;26(2):117-8. [Medline].

18. Derogee M, Bevers RF, Prins HJ, et al. Testicular microlithiasis, a premalignant condition: prevalence, histopathologic findings, and relation to testicular tumor. Urology. Jun 2001;57(6):1133-7. [Medline].

19. Dieckmann KP, Skakkebaek NE. Carcinoma in situ of the testis: review of biological and clinical features. Int J Cancer. Dec 10 1999;83(6):815-22. [Medline].

20. Doebler RW, Norbut AM. Localized testicular infarction masquerading as a testicular neoplasm. Urology. Aug 1999;54(2):366. [Medline].

21. Heidenreich A, Weissbach L, Holtl W, et al. Organ sparing surgery for malignant germ cell tumor of the testis. J Urol. Dec 2001;166(6):2161-5. [Medline].

22. Hurd DS, Olsen T. Cutaneous sarcoidosis presenting as a testicular mass. Cutis. Dec 2000;66(6):435-8. [Medline].

23. Middleton WD, Teefey SA, Santillan CS. Testicular microlithiasis: prospective analysis of prevalence and associated tumor. Radiology. Aug 2002;224(2):425-8. [Medline].

24. Resnick MI, Amis ES Jr, Bigongiari LR, et al. Staging of testicular malignancy. American College of Radiology. ACR appropriateness criteria. Radiology. Jun 2000;215 (suppl):741-6. [Medline].

25. Steinfeld AD. Testicular germ cell tumors: review of contemporary evaluation and management. Radiology. Jun 1990;175(3):603-6. [Medline].

26. von Eckardstein S, Tsakmakidis G, Kamischke A, et al. Sonographic testicular microlithiasis as an indicator of premalignant conditions in normal and infertile men. J Androl. Sep-Oct 2001;22(5):818-24. [Medline].

Keywords

malignant testicular tumors, testicular germ cell tumors, germ cell tumors, GCTs, seminomas, nonseminomas, teratomas, teratocarcinomas, testicular metastases, primary testicular tumors, testicular cancer, embryonal cell tumors, choriocarcinomas, yolk sac tumors, endodermal sinus tumors, nongerminal testicular tumors, stromal Leydig cell tumors, Sertoli cell tumors

Contributor Information and Disclosures

Author

Dawn Light, MD, MPH, Clinical Assistant Professor of Radiology and Pediatrics, Department of Radiology, Consulting Staff, Dayton Children's Medical Center; Clinical Assistant Professor of Radiology, Department of Radiology, Uniformed Services University of the Health Sciences
Dawn Light, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Family Physicians, American College of Radiology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Steven Perlmutter, MD, FACR, Associate Professor of Clinical Radiology, School of Medicine at Stony Brook University; Medical Director of Radiology, Peconic Bay Medical Center
Steven Perlmutter, MD, FACR is a member of the following medical societies: American College of Radiology, American Institute of Ultrasound in Medicine, American Medical Association, American Roentgen Ray Society, Association of Program Directors in Radiology, Association of University Radiologists, Medical Society of the State of New York, Radiological Society of North America, Society of Breast Imaging, Society of Nuclear Medicine, and Society of Uroradiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Joshua A Becker, MD, Professor, Department of Radiology, New York University School of Medicine
Joshua A Becker, MD is a member of the following medical societies: Society of Uroradiology
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

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