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Testicular Anaplastic Seminoma

Images

Figure 1(a)

Figure 1(b)

Figure 1(c)

Figure 1(d)

Figure 1(e)

Figure 2


Clinical History:

 

44-year-old male presented with New onset right-sided testicular pain. 

Findings:

 

Figure 1 (a,b,c,d,e): Heterogenous mass is noted in right testis with mostly solid and some cystic components with increased vascular flow. Small right hydrocele is also noted. Figure 2: Small, subcentimenter aortocaval lymph node is noted. In light of history of testicular mass, possibility of metastasis cannot be ruled out.

Diagnosis:

Testicular Anaplastic Seminoma


Discussion:

 

Testicular cancer is a rare malignancy that accounts for only1% of all neoplasms in men 1. The peak prevalence is at 15–34years, but it may occur outside this age group1,2. Germcell tumors represent 95% of all testicular tumors, arise fromspermatogenic cells, and are further classified into seminomatousand nonseminomatous germ cell tumors3. Of all the testicular tumors, 61% are pure seminoma and the remainder non-seminomatous germ cell tumors (NSGCT) or mixed tumors4. Risk factors includea history of contralateral testicular cancer, cryptorchidism,exposure to carcinogens, trauma, mumps orchitis, and epididymitis2,5,6. Patients present with a painless, swollen, hardtestis, although pain may occur due to intratumoral hemorrhage. Diagnosis Testicular tumors are usually diagnosed clinically and pathologicallyat surgery. Imaging of the testis with sonography can help toconfirm the presence of an intratesticular mass or if thereis uncertainty about the clinical features. CT remains the imaging technique of choice in staging testiculartumors. Treatment Treatment options includesorchidectomy, chemotherapy and radiotherapy. Surveillance forms important part in the management of patients with testicular neoplasms. Surveillance Surveillance after treatmentas a management strategy is increasingly recognized. Surveillance protocols are designed toidentify relapse at the earliest stage, thereby enabling earliertreatment. In addition to clinical and serum marker assessments, imagingwith CT, MRI and PET forms the basis of surveillance strategies, but thefrequency of CT studies varies greatly among centers. The potentialbenefit of repeated scanning must be weighed against the financialand health costs of more frequent scanning. A thoracic CT examinationgives a radiation dose equivalent to 400 chest radiographs (8vs 0.02 mSv, respectively), whereas for CT of the chest and abdomen,the dose is increased to approximately 20 mSv, which is a dose equivalentto 1,000 chest radiographs. This radiation exposure resultsin a 1:1,000 lifetime risk of a second cancer and leukemia ina 25-year-old patient over the subsequent 40 years7. Surveillance as a management strategy in stage 1 testicular germ cell tumour (GCT) is increasing in popularity due to the recognition of the long-term side effects of treatment. There is a tendency towards less frequent use of imaging as supported by recent trials in non-seminomatous GCT but further studies are needed with respect to the assessment of seminoma and to evaluate the role of magnetic resonance imaging (MRI) instead of abdominal CT8. Given that 80–85% of patients with stage I seminoma and 70–75% with stage I NSGCT require no treatment after orchidectomy and that those with relapse are almost invariably salvaged, it follows that surveillance is a preferred approach that serves the purpose of minimizing treatment-related morbidity.   TNM classification of testicular tumor9.

 

Primary tumor (pT) Extent of primary tumor is classified after radical orchidectomy    pTX Primary tumor cannot be assessed (if radical orchidectomy has not been performed, TX is used)    pT0 No evidence of primary tumor (e.g., histologic scar in testis)    pTis Intratubular germ cell neoplasia    pT1 Tumor is limited to testis and epididymis without vascular or lymphatic invasion; tumor may invade into the tunica albuginea but not tunica vaginalis    pT2 Tumor is limited to testis and epididymis with vascular or lymphatic invasion or tumor extends through tunica albuginea with involvement of tunica vaginalis    pT3 Tumor invades spermatic cord with or without vascular or lymphatic invasion    pT4 Tumor invades scrotum with or without vascular or lymphatic invasion Regional lymph nodes (N)    Clinical involvement       NX Regional nodes cannot be assessed       N0 No regional lymph node metastasis       N1 Metastasis with a lymph node mass 2 cm in greatest dimension; or multiple lymph nodes, none > 2 cm in greatest dimension       N2 Metastasis with a lymph node mass > 2 cm but < 5 cm in greatest dimension; or metastases with multiple lymph node masses, with any one mass > 2 cm but 5 cm in greatest dimension       N3 Metastasis with a lymph node mass > 5 cm in greatest dimension    Pathologic involvement       pN0 No regional lymph node metastases       pN1 Metastasis with a lymph node mass 2 cm in greatest dimension and five or fewer positive nodes, with none > 2 cm in greatest dimension       pN2 Metastasis with a lymph node mass > 2 cm but 5 cm in greatest dimension; more than five nodes positive, with none > 5 cm; or evidence of extranodal extension of tumor       pN3 Metastasis with a lymph node mass > 5 cm in greatest dimension    Distant metastases (M)       MX Distant metastasis cannot be assessed       M0 No distant metastasis       M1 Distant metastasis       M1a Nonregional lymph node or pulmonary metastasis       M1b Distant metastasis other than to nonregional lymph nodes and lungs    Serum tumor markers (S)       SX Tumor marker studies not available or not performed       S0 Tumor marker levels within normal limits       S1 LDH < 1.5 x normal; β-HCG < 5,000 IU/L; and -fetoprotein < 1,000 ng/mL       S2 LDH 1.5–10 x normal; β-HCG 5,000–50,000 IU/L; or -fetoprotein 1,000–10,000 ng/mL       S3
LDH > 10 x normal; β-HCG > 50,000 IU/L; or -fetoprotein > 10,000 ng/mL

 

 

References / Suggested Reading:

 

1.    Greenlee RT, Hill-Harmon MB, Murray T, Thun M. Cancer statistics, 2001. CA Cancer J Clin 2001;51:15–36. 2.    Gori S, Porrozzi S, Roila F, Gatta G, De Giorgi U, Marangolo M. Germ cell tumours of the testis. Crit Rev Oncol Hematol 2005;53:141–164. 3.    Ulbright TM, Amin MB, Young RH. Tumors of the testis, adnexa, spermatic cord, and scrotum. In: Atlas of tumor pathology, fasc 25, ser 3. Washington, DC: Armed Forces Institute of Pathology, 1999; 1–290. 4.    K.A. McGlynn, S.S. Devesa, B.I. Graubard and P.E. Castle, Increasing incidence of testicular germ cell tumors among black men in the United States, J Clin Oncol 23 (24) (2005), pp. 5757–5761. 5.     Coupland CA, Chilvers CE, Davey G, Pike MC, Oliver RT, Forman D. Risk factors for testicular germ cell tumours by histological tumour type. United Kingdom Testicular Cancer Study Group. Br J Cancer 1999;80:1859–1863. 6.     Ehrengut W, Schwartau M. Mumps orchitis and testicular tumours. Br Med J 1977;2:191. 7.    Sohaib SA, Koh DM, Husband JE. The role of imaging in the diagnosis, staging, and management of testicular cancer. AJR Am J Roentgenol. 2008 Aug;191(2):387-95. 8.    Sohaib SA, Husband J. Surveillance in testicular cancer: who, when, what and how? Cancer Imaging. 2007 Oct 22;7:145-7. 9.    Sobin LH, Wittekind CH, eds. TNM: classification of malignant tumours, 6th ed. New York, NY: Wiley-Liss,2002.

Author

Ashwani Sharma Shweta Bhatt, Vikram Dogra

Instructor, Assistant professor and Professor

University of Rochester Medical Center , Rochester, NY