1.By : Dr. Sumit S.HadgaonkarModerator : Prof. S. Rajendra Singh

2. Introduction Testicular tumors are rare. 1 2 % of all malignant tumors. Most common malignancy in men in the 15 to 35year age group. Benign lesions represent a greater percentage ofcases in children than in adults. Most curable solid neoplasm 3. Age - 3 peaks2 4 yrs20 40 yrsabove 60 yrs Testicular cancer is one of the few neoplasmsassociated with accurate serum markers. Most curable solid neoplasms and serves as aparadigm for the multimodal treatment ofmalignancies. 4. Dramatic Improvement in Survival Effective diagnostic techniques Improved tumor markers Multi-model treatment Surgical Radiotherapy Multi-drug chemotherapy regimens Mortality before 1970 50 % 1997 5 % 5. AETIOLOGY OF TESTICULAR TUMOUR Cryptorchidism Intersex disorder Klinefelters syndrome Testicular atrophy Trauma- prompts medical evaluation Chromosomal abnormalities - loss of chromosome 11, 13,18, abnormal chromosome 12p. Sex hormone fluctuations, estrogenadministration during pregnancy Race Carcinoma in situ Previous testicular cancer 6. CRYPTORCHIDISM & TESTICULAR TUMOURRisk of Carcinoma developingin undescended testis is14 to 48 times the normalexpected incidence 7. CRYPTORCHIDISM & TESTICULAR TUMOURThe cause for malignancy are as follows: Abnormal Germ Cell Morphology Elevated temperature in abdomen & Inguinal regionas opposed to scrotum Endocrinal disturbances Gonadal dysgenesis 8. Testicular Tumour & Molecular Biology Molecular & Genetic Research may help Futurepatient with Testicular Tumours:Earlier diagnosisIdentify Susceptible Individuals 9. PROTO-ONCOGENES in Germ Cell Tumours (Shuin et al)Seminoma &Embryonal - N-myc expressionCarcinomaSeminoma - c-Ki-ras expressionImmatureTeratomas - c-erb B-1 expression 10. Testicular germ cell tumour show consistentexpression of both: Parental alleles of H19 IGF-2 genes. 11. CROSS SECTION OF TESTIS TestisStroma Seminiferous Tubules(200 to 350 tubules) Interstitial Cells SupportingSpermatogoniaLeydig or(Androgen) Sertoli Cell 12. CLASSIFICATION I.Primary Neoplasms of Testis.A. Germ Cell Tumor.B. Non-Germ Cell Tumor . II. Secondary Neoplasms. III .Paratesticular Tumors. 13. Germ cell tumors 1. Seminomas - 40%(a) Classic Typical Seminoma(b) Anaplastic Seminoma(c) Spermatocytic Seminoma 2. Embryonal Carcinoma - 20 - 25% 3. Teratoma - 25 - 35%(a) Mature(b) Immature 4. Choriocarcinoma - 1% 5. Yolk Sac Tumour 14. Non Germ Cell Tumors1. Specialized gonadal stromal tumor(a) Leydig cell tumor(b) sertoli cell tumor2. Gonadoblastoma3. Miscellaneous Neoplasms(a) Carcinoid tumor(b) Tumors of ovarian epithelial subtypes 15. Favourable outcome - GCT Sensitive to both Radiotherapy Chemotherapy Differentiation Rapid rate of growth Young no co-morbidExtra Gonadal Germ Cell Tumors (EGCT) Prognosis is GCT 16. Germ cell tumor testis3 types based on Natural history Response to therapy Histological & biochemical properties Typical/ Classical Spermatocytic Anaplastic 17. Spermatocytic 2% - 12% of seminomas Old age > 50 yr Extremely low metastatic potential Good prognosis Anaplastic 5% - 10 Middle age Aggressive - lethal Greater mitotic activity Higher local invasion Higher metastatic potential Higher rate of -HCG production Inguinal orchidectomy + Radiation Typical/ Classical 82% - 85% Middle age PLAP 90% Syncytiottrophoblsts Beta HCG (10%) Very slow growth Inguinal orchidectomy + Radiation 18. Painless testicular swellingHard, loss of testicular sensation/ infertility Seminoma rubbery Teratoma, EC irregularHydroceleRarely pain Hemorrhage Infection 19. Metastasis manifestations (10%) Neck mass Cough/ dyspnoea Back pain Psoas muscle/ nerve roots Bone pain Lower limb swelling Iliac/ caval obstruction/ thrombosis Gynaecomastia 5% Systemic endocrine manifestation incompletely defined P/A LN VIscera 20. Painless enlargemt of testis (>10 times)Extragonadal seminoma Mediastinum Pituitary gland Pineal gland 21. Cut potato appearance 22. Embryonal carcinoma 25yr 35yr 3 6 % of TT Small, rounded irregulr mass Invading tunica vaginalis Cut surface Greyish white, fleshy Areas of necrosis, hemorrhage Poorly defined capsule 23. Chorionic carcinoma (1 2%) 2ND, 3RD decades Palpable nodule -HCG - >99%, PLAP Size extent of hemorrhage Advanced distant metastasis (lung, brain) paradoxically small primary Histology Syncytiotrophoblasts Cytotrophoblasts 24. Teratoma Children 38% - benign Adults 3% - metastatic potential AFP - 20% 25% Metastasis Resistent both Chemo, Radiation Mature Teratoma Differentiated elements form 2 or more embryonic germ cell layers ectoderm, endoderm & mesoderm Immature Teratoma Undifferentiated primitive tissues Malignant Teratoma Malignant changes 25. Teratoma More than one germ cell layer in various stages of maturation &differentiation Large, lobulated, non-homogenous Cut surface Variably sized cysts Gelatinous, mucinous, hyalinized material Intersposed solid islands cartilage/ bone/pancreatic/ liver/intesttinal/ muscle/ neural/ connective tissue 26. Immature Teratoma Areas of fibrosis & hemorrhage Mature Teratoma 27. Yolk sac tumor Most common Infants & children Adults in combination AFP Pure form Homogenous yellowish, mucinous Histology Embryoid bodies Resemble 1 to 2 week old embryos ( 50000 >10000 48. PRINCIPLES OF TREATMENT Treatment should be aimed at one stage above theclinical stage Seminomas - Radio-Sensitive. Treat withRadiotherapy. Non-Seminomas are Radio-Resistant and besttreated by Surgery Advanced Disease or Metastasis - Responds well toChemotherapy 49. PRINCIPLES OF TREATMENT Radical INGUINAL ORCHIDECTOMY is Standardfirst line of therapy Lymphatic spread initially goes toRETRO-PERITONEAL NODES Early hematogenous spread RARE Bulky Retroperitoneal Tumours or MetastaticTumors Initially DOWN-STAGED withCHEMOTHERAPY 50. PRINCIPLES OF TREATMENT Transscrotal biopsy is to be condemned. The inguinal approach permits early control of thevascular and lymphatic supply as well as en-blocremoval of the testis with all its tunicae. Frozen section in case of dilemma. 51. Treatment of SeminomasStage I, IIA, ?IIB Radical Inguinal Orchidectomy followed byradiotherapy to Ipsilateral Retroperitonium &Ipsilateral Iliac group Lymph nodes (2500-3500 rads)Bulky stage II and III Seminomas -Radical Inguinal Orchidectomy is followed byChemotherapy 52. Treatment of Non-SeminomaStage I and IIA:RADICAL ORCHIDECTOMYfollowed by RETROPERITONEAL LYMPH NODESDISSECTIONStage IIB:RPLND with possible ADJUVANT CHEMOTHERAPYStage IIC and Stage III Disease:Initial CHEMOTHERAPY followed by SURGERY for Residual Disease 53. Lymph Nodes Dissection For Right &Left Sided Testicular Tumours 54. Lymphatic drainage The primary drainage of the right testis is within theinteraortocaval region. Left testis drainage , the para-aortic region in thecompartment bounded by the left ureter, the left renalvein, the aorta, and the origin of the inferiormesenteric artery. Cross over from right to left is possible. 55. STANDARD CHEMOTHERAPY FORNON-SEMINOMATOUS GERM CELL TUMOURSChemotherapy ToxicityBEP -Bleomycin Pulmonary fibrosisEtoposide (VP-16) MyelosuppressionAlopeciaRenal insufficiency (mild)Secondary leukemiaCis-platin Renal insufficiencyNausea, vomitingNeuropathy 56. PROGNOSISSeminoma NonseminomaStage I 99% 95% to 99%Stage II 70% to 92% 90%Stage III 80% to 85% 70% to 80% 57. CONCLUSION Improved Overall Survival of Testicular Tumour due toBetter Understanding of the Disease, Tumour Markersand Cis-platinum based Chemotherapy Current Emphasis is on Diminishing overall Morbidityof Various Treatment Modalities 58. I always had the size differencethere, but I didnt knowI wouldvestill been waiting if it hadnt startedhurting, it just got so painful I couldntsit on my bike anymore.-Lance ArmstrongI always had the size differencethere, but I didnt knowI wouldvestill been waiting if it hadnt startedhurting, it just got so painful I couldntsit on my bike anymore.-Lance ArmstrongI always had the size differencethere, but I didnt knowI wouldvestill been waiting if it hadnt startedhurting, it just got so painful I couldntsit on my bike anymore.-Lance Armstrong 59. Yuvraj Singh extragonadal seminoma 60. Thank you