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Testicular tumors
- 1. Testicular tumors Dr HarshitaMehrotra Resident, General Surgery
- 2. Importance • Testicular tumorsare rare. • 1 – 2 % of all malignant tumors. • Most common malignancy in men in the 15 to 35 year age group. • Most curable solid neoplasms and serves as a paradigm for the multimodal treatment of malignancies. • Seminoma - most common bilateral primary testicular tumour; Lymphoma - most common bilateral testicular tumour
- 3. • Dramatic Improvementin Survival: • Effective diagnostic techniques • Improved tumor markers • Multi-modal treatment - Surgical + Radiotherapy/Chemotherapy • Mortality markedly decreased.
- 4. Etiology • Cryptorchidism • Intersexdisorder • Testicular atrophy • Chromosomal abnormalities - loss of chromosome 11, 13, 18, abnormal chromosome 12p. • Exogenous estrogen administration to mother during pregnancy • Carcinoma-in-situ • Previous testicular malignancy
- 5. Cryptorchidism • 7 -10% patients - history of cryptorchidism • Most common - seminoma • 5 - 10% tumors - contralateral testis • Relative risk - Intraabdominal testis (1 in 20) > Intrainguinal testis (1 in 80) • Orchidopexy - does not alter malignant potential - facilitates examination & detection
- 6. • Malignancy dueto • Abnormal germ cell morphology. • Elevated temperature - abnormal spermatocyte maturation. • Endocrinal disturbances. • Gonadal dysgenesis.
- 7. Carcinoma in-situ • Premalignant precusor of all GCT, except spermatocytic seminoma. • Incidence - 0.8%. • Testicular CIS develops from fetal gonocytes. • Characterized histologically by seminiferous tubules containing only Sertoli cells and malignant germ cells.
- 8. • Risk Factorsfor CIS: • History of testicular carcinoma (5% to 6%), • Extra gonadalGCT (40%), • Cryptorchidism (3%), • Contralateral testis with unilateral testis cancer (5% to 6%), • Somatosexual ambiguity (25% to 100%) • Atrophic testis 30 % • Infertility (0.4% to 1.1%) • TESTICULAR BIOPSY gold standard for diagnoses of CIS
- 9. Classification Germ Cell Tumors>90% Non-Seminomatous TumorsSeminomas Classical 85% Spermatocytic 5% Anaplastic 10% Embryonal Carcinoma Yolk Sac Tumor Choriocarcinoma Teratoma Mixed Tumors Interstitial Cell Tumors Leydig Cell Tumors Sertoli Cell Tumors Other Tumors Lymphoma Metastases Malignant Testicular Tumors Non-Germ Cell Tumors
- 11. Seminoma • Classical: 80- 85% • middle age • PLAP & B-hCG - raised • slow growing • good prognosis • Spermatocytic: 5 - 10% • age > 50 years • low metastatic potential • good prognosis • Anaplastic: 5 - 10% • middle age • aggressive • higher local & metastatic potential • high B-hCG production • Inguinal Orchiectomy + Radiation
- 12. Non-Seminomatous Germ Cell Tumors •Embryonal Carcinoma • 25 - 35 years • 3 - 6% testicular tumors • small, rounded, irregular mass • invades tunica albuginea • Yolk Sac Tumor/ Endodermal Sinus Tumor • most common testicular tumor in infants & children • raised AFP • histologically - cells demonstrate vacuolated cytoplasm secondary to fat and glycogen deposition, resemble 1 - 2 week old embryos
- 13. • Teratoma • raisedAFP • resistant to both chemotherapy & radiotherapy • mature teratoma - differentiated elements from 2-3 embryonic germ cell layers • immature teratoma - undifferentiated primitive tissue • malignant teratoma - malignant changes • Chorionic Carcinoma • pure choriocarcinoma - rare • second - third decades • raised PLAP, B-hCG • high incidence of distant metastases
- 14. • Leydig CellTumors • most common non-germ cell cell timor of testis - 1 - 3% testicular tumours • bimodal age distribution - 5 - 9 years; 25 - 35 years age • 25% cases - childhood; bilaterally - 5 - 10% cases • presentation - prepubertal children - virilization; adults - gynecomastia • elevated serum & urinary 17- ketosteroids & estrogens • Sertoli Cell Tumors • rare; < 1% testicular tumors • bimodal age distribution - < 1 year; 20 - 45 years age • presentation - testicular mass; virilization in children; gynecomastia in adults • Gonadoblastomas • rare • seen in patients with gonadal dysgenesis • age group - 30 years of age • clinical presentation - gonadal dysgenesis
- 15. Secondary Tumors ofTestis • Lymphoma • most common testicular tumour over age of 50 years • most common secondary neoplasm of testis • presentation - painless enlargement of testis, constitutional symptoms in 25% patients; bilateral - 50% patients • Leukemic Infiltration of Testis • relapse of children with acute lymphocytic leukaemia • bilateral - 50% cases • treatment - bilateral testicular irradiation with 20Gy & reinstitution od adj chemotherapy • Metastatic Tumor • rare • most common primary - prostate > lung > gastrointestinal tract > melanoma > kidney
- 16. Extragonadal Germ CellTumor • Rare - 3% all germ cell tumors • Sites - mediastinum > Retroperitoneum > Sacrocoocygeal > Pineal gland • Presentation - site & volume of disease • Mediastinal lesions - pulmonary symptoms • Sacrococcygeal - neonates - palpable mass, bowel/ urinary obstruction • Pineal - headache, visual/ auditory complaints, hypopituitarism • Treatment - same as testicular tumors.
- 17. Lymphatic drainage • RightTestis - Inter-aortocaval nodes > Precaval > Preaortic > Right common iliac > Right external iliac • Left Testis - Left Para-aortic > Preaortic > Left common iliac > Left external iliac • Cross over from right to left possible. • Epididymis - external iliac chain. • Inguinal node metastasis - scrotal involvement by the primary tumor, prior inguinal or scrotal surgery, or retrograde lymphatic spread secondary to massive retroperitoneal lymph node deposits. • Testicular cancer spreads in a predictable and stepwise fashion, except choriocarcinoma.
- 18. Metastatic Spread • Distantmetastases - Lung > Liver > Brain > Bone > Kidney > Adrenal Glands > Gastrointestinal Tract > Spleen • Germ cell tumors - Lymphatic spread • Choriocarcinomas - Hematogenous spread - lungs
- 19. Clinical Presentation • Painlesstesticular swelling • Dull ache/heaviness in Lower Abdomen • 10% - Acute Scrotal Pain • 10% - Metatstasis • Neck Mass /Cough /Anorexia /Vomiting /Back ache/Lower limb swelling • 5% - Gynecomastia - Estrogen producing tumors • Rarely - Infertility
- 20. Physical Examination • Firmto hard fixed area within tunica albugenia - suspicious • Seminoma expand within the testis as a painless, rubbery enlargement. • Embryonal carcinoma or teratocarcinoma may produce an irregular, rather than discrete mass. • Choriocarcinoma - no testicular enlargement
- 21. Differential Diagnosis • Testiculartorsion • Epididymitis, or epididymo-orchitis • Hydrocele • Hernia • Hematoma • Spermatocele • Syphilitic gumma
- 22. Investigations • All patientswith a solid, firm intra-testicular mass that cannot be transilluminated should be regarded as malignant unless otherwise proved. • Scrotal Ultrasound - • rapid, reliable technique • hypoechoic area within the tunica albuginea - markedly suspicious for testicular cancer.
- 23. Tumor markers • Onco-fetalSubstances: AFP & HCG • Cellular Enzymes: LDH & PLAP
- 24. Alfa-fetoprotein • NORMAL VALUE< 16 ngm/ml • Raised AFP : • Pure embryonal carcinoma • Teratocarcinoma • Yolk sac Tumor • Combined tumors • AFP not raised in pure choriocarcinoma & pure seminoma
- 25. Human Chorionic Gonadotropin •NORMAL VALUE < 1 ng/ml • Raised β hCG - • 100 % - Choriocarcinoma • 60% - Embryonal carcinoma • 55% - Teratocarcinoma • 25% - Yolk Cell Tumour • 7% - Seminomas
- 26. Role of TumorMarkers • Diagnosis • 80 - 85% testicular tumors - positive markers • post orchiectomy elevated markers - stage II/III disease • post lymphadenectomy residual disease - stage III disease • histology of timor • Burden of disease - degree of marker elevation • Follow-up • markers becoming positive on follow-up - recurrence • markers become positive earlier than x-rays
- 27. Imaging studies • USGScrotum • Chest X ray - Pulmonary Metastasis - 85 - 90% metastases • CECT abdomen & pelvis – Retroperitoneal nodes
- 28. Staging of Disease •Pre-requisites • history + clinical examination • tumor markers - hCG, AFP • Radiology - USG Scrotum, CECT Abd, X-Ray Chest • Pathology of tumor specimen
- 30. Prognostic Grouping Stage TN M S Stage 0 Tis N0 M0 S0 Stage 1a T1 N0 M0 S0 Stage 1b T2 - T4 N0 M0 S0 Stage 1c any T N0 M0 S1 - S3 Stage IIa any T N1 M0 S0 - S1 Stage IIb any T N2 M0 S0 - S1 Stage IIc any T N3 M0 S0 - S1 Stage IIIa any T any N M1 S0 - S1 Stage IIIb any T any N M0 - M1 S2 Stage IIIc any T any N M0 - M1a S3 any T any N M1b any S
- 31. Treatment • Treatment shouldbe aimed at one stage above clinical stage. • Seminomas - radio-sensitive - treat with radiotherapy. • Non-seminomatous - radio-resistant - surgery. • Advanced diseases/ metastases - chemotherapy.
- 32. Treatment (Cont.) • RADICALINGUINAL ORCHIDECTOMY - first line of therapy • Bulky Retroperitoneal Tumours/ Metastatic Tumors - Initially “DOWN-STAGED” with CHEMOTHERAPY • Transscrotal biopsy - CONDEMNED. • The inguinal approach permits early control of the vascular and lymphatic supply as well as en-bloc removal of the testis with all its tunicae.
- 35. Chemotherapy Chemotherapy Toxicity BEP - •Bleomycin Pulmonary fibrosis • Etoposide Myelosuppression Alopecia Renal insufficiency (mild) Secondary leukemia • Cisplatin Renal insufficiency Nausea, vomiting Neuropathy
- 36. Lymph Nodes DissectionFor Right & Left Sided Testicular Tumours
- 37. Prognosis Seminoma Non-Seminoma Stage I99% 95 - 99% Stage II 70 - 92% 90% Stage III 80 - 85% 70 - 80%
- 38. Conclusion • Improved OverallSurvival of Testicular Tumour due to Better Understanding of the Disease, Tumour Markers and Cis-platinum based Chemotherapy. • Current emphasis - diminishing overall morbidity of various treatment modalities.
- 39.