Sumit testicular tumors


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Sumit testicular tumors

  1. 1. By : Dr. Sumit S.HadgaonkarModerator : Prof. S. Rajendra Singh
  2. 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. 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. 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. 5. AETIOLOGY OF TESTICULAR TUMOUR Cryptorchidism Intersex disorder – Klinefelter’s 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. 6. CRYPTORCHIDISM & TESTICULAR TUMOURRisk of Carcinoma developingin undescended testis is14 to 48 times the normalexpected incidence
  7. 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. 8. Testicular Tumour & Molecular Biology Molecular & Genetic Research may help Futurepatient with Testicular Tumours:Earlier diagnosisIdentify Susceptible Individuals
  9. 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. 10. Testicular germ cell tumour show consistentexpression of both: Parental alleles of H19 IGF-2 genes.
  11. 11. CROSS SECTION OF TESTIS TestisStroma Seminiferous Tubules(200 to 350 tubules) Interstitial Cells SupportingSpermatogoniaLeydig or(Androgen) Sertoli Cell
  12. 12. CLASSIFICATION I.Primary Neoplasms of Testis.A. Germ Cell Tumor.B. Non-Germ Cell Tumor . II. Secondary Neoplasms. III .Paratesticular Tumors.
  13. 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. 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. 15. Favourable outcome - GCT Sensitive to both Radiotherapy Chemotherapy Differentiation Rapid rate of growth Young – no co-morbidExtra Gonadal Germ Cell Tumors (EGCT) Prognosis is ½ GCT
  16. 16. Germ cell tumor – testis3 types – based on Natural history Response to therapy Histological & biochemical properties Typical/ Classical Spermatocytic Anaplastic
  17. 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 β -HCG production Inguinal orchidectomy + Radiation Typical/ Classical 82% - 85% Middle age PLAP – 90% Syncytiottrophoblsts – ↑Beta HCG (10%) Very slow growth Inguinal orchidectomy + Radiation
  18. 18. Painless testicular swellingHard, loss of testicular sensation/ infertility Seminoma – rubbery Teratoma, EC – irregularHydroceleRarely pain Hemorrhage Infection
  19. 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. 20. Painless enlargemt of testis (>10 times)Extragonadal seminoma Mediastinum Pituitary gland Pineal gland
  21. 21.  Cut potato appearance
  22. 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. 23.  Chorionic carcinoma (1 – 2%) 2ND, 3RD decades Palpable nodule ↑β-HCG - >99%, ↑PLAP Size ≈ extent of hemorrhage Advanced distant metastasis (lung, brain) – paradoxically small primary Histology Syncytiotrophoblasts Cytotrophoblasts
  24. 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. 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. 26.  Immature Teratoma Areas of fibrosis & hemorrhage Mature Teratoma
  27. 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 (<1 mm) Treatment 80 % confined to testis at diagnosis Radical inguinal orchidectomy Retro peritoneal LN – RPLND Advanced disease – chemotherapy R adiotherapy Residual disease Failed to respond to chemotherapy Mean survival – 87% for all stages
  28. 28. Non Germ Cell Tumors Sex cord tumors1. Leydig cell tumors2. Sertoli cell tumors Mixed germ cell and stromal cell tumors1. Gonadoblastoma Miscellaneous primary non germ cell tumors1. Epidermoid cyst2. Adenocarcinoma of rete testis3. Adrenal rest tumors
  29. 29. Secondary Tumors of Testis Lymphoma – most common secondary tumor- most common testicular tumor in patientsabove 50 years- most common variety is histiocytic Leukamic Infilteration of testis-primary site of relapse after ALL remission-occurs mainly in the interstitial space-biopsy for diagnosis- no orchidectomy- testicular irradiation for treatment Metastases to testis- rare cases reported (200 cases till now)
  30. 30. Tumors of adnexa / Paratesticular tissue Adenomatoid tumor-most common paratesticular tumor-benign in nature Mesothelioma-metastatic in 15% cases to inguinal lymph nodes Cystadenoma- bilateral cases are associated with Von HippelLindau syndrome Rhabdomyosarcoma- most commonly seen in second decade of life
  31. 31. Carcinoma in situ {CIS} Pre invasive precusor of all GCT, exceptspermatocytic seminoma Incidence of CIS in the male population is 0.8%. Testicular CIS develops from fetal gonocytes & ischaracterized histologically by seminiferoustubules containing only Sertoli cells and malignantgerm cells.
  32. 32. Patients at risk of 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 diagnosesof CIS
  33. 33. Clinical features Painless Swelling of One testis Dull Ache or Heaviness in Lower Abdomen 10% - Acute Scrotal Pain 10% - Present with Metatstasis- Neck Mass / Cough / Anorexia / Vomiting / BackAche/ Lower limb swelling 5% - Gynecomastia Rarely - Infertility
  34. 34. Physical Examination Examine contralateral normal testis. Firm to hard fixed area within tunica albugenia issuspicious Seminoma expand within the testis as a painless,rubbery enlargement. Embryonal carcinoma or teratocarcinoma mayproduce an irregular, rather than discrete mass.
  35. 35. Differential Diagnosis Testicular torsion Epididymitis, or epididymo-orchitis Hydrocele, Hernia, Hematoma, Spermatocele, Syphilitic gumma .
  36. 36. Epididymal cyst
  37. 37. DICTUM FOR ANY SOLID SCROTAL SWELLINGSAll patients with a solid, FirmIntratesticular Mass that cannot beTransilluminated should be regardedas Malignant unless otherwise proved.
  38. 38. Scrotal ultrasound Ultrasonography of the scrotum is a rapid, reliabletechnique to exclude hydrocele or epididymitis. Ultrasonography of the scrotum is basically anextension of the physical examination. Hypoechoic area within the tunica albuginea ismarkedly suspicious for testicular cancer.
  39. 39. Tumor markersTWO MAIN CLASSESOnco-fetal Substances : AFP & HCGCellular Enzymes : LDH & PLAPAFP - Trophoblastic CellsHCG - Syncytiotrophoblastic Cells( PLAP- placental alkaline phosphatase, & LDH lactic aciddehydrogenase)
  40. 40. AFP –( Alfafetoprotein)NORMAL VALUE: Below 16 ngm / mlHALF LIFE OF AFP – 5 and 7 daysRaised AFP : Pure embryonal carcinoma Teratocarcinoma Yolk sac Tumor Combined tumors, AFP not raised in pure choriocarcinoma , & in pureseminoma
  41. 41. HCG – ( Human Chorionic Gonadotropin)Has  and  polypeptide chainNORMAL VALUE: < 1 ng / mlHALF LIFE of HCG: 24 to 36 hoursRAISED  HCG -100 % - Choriocarcinoma60% - Embryonal carcinoma55% - Teratocarcinoma25% - Yolk Cell Tumour7% - Seminomas
  42. 42. ROLE OF TUMOUR MARKERS Helps in Diagnosis - 80 to 85% of Testicular Tumours havePositive Markers Most of Non-Seminomas have raised markers Only 10 to 15% Non-Seminomas have normal marker level After Orchidectomy if Markers Elevated means ResidualDisease or Stage II or III Disease Elevation of Markers after Lymphadenectomy means a STAGEIII Disease
  43. 43. ROLE OF TUMOUR MARKERS cont... Degree of Marker Elevation Appears to be DirectlyProportional to Tumour Burden Markers indicate Histology of Tumour:If AFP elevated in Seminoma - Means Tumour has Non-Seminomatous elements Negative Tumour Markers becoming positive on follow upusually indicates -Recurrence of Tumour Markers become Positive earlier than X-Ray studies
  44. 44. Imaging studies Chest X ray CECT abdomen – retroperitoneal nodes PET- No apparent advantage over CT MRI - No apparent advantage over CT
  45. 45. Large left para aortic nodal mass due to GCTcausing hydronephrosis
  46. 46. Requirements for staging To properly Stage Testicular Tumours followingare pre-requisites:(a) Pathology of Tumour Specimen(b) History(c) Clinical Examination(d) Radiological procedure - USG / CT /MRI / Bone Scan(e) Tumour Markers -  HCG, AFP
  47. 47. Serum tumor markersLDH HCGMiu/mlAFPNg/mlS0 _< N <N <NS1 <1.5 x N < 5000 < 1000S2 1.5-10x N 5000 to500001000 to10000S3 >10x N > 50000 >10000
  48. 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. 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. 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. 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. 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. 53. Lymph Nodes Dissection For Right &Left Sided Testicular Tumours
  54. 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. 55. STANDARD CHEMOTHERAPY FORNON-SEMINOMATOUS GERM CELL TUMOURSChemotherapy ToxicityBEP -Bleomycin Pulmonary fibrosisEtoposide (VP-16) MyelosuppressionAlopeciaRenal insufficiency (mild)Secondary leukemiaCis-platin Renal insufficiencyNausea, vomitingNeuropathy
  56. 56. PROGNOSISSeminoma NonseminomaStage I 99% 95% to 99%Stage II 70% to 92% 90%Stage III 80% to 85% 70% to 80%
  57. 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. 58. “I always had the size differencethere, but I didn’t know…I would’vestill been waiting if it hadn’t startedhurting, it just got so painful I couldn’tsit on my bike anymore.”-Lance Armstrong“I always had the size differencethere, but I didn’t know…I would’vestill been waiting if it hadn’t startedhurting, it just got so painful I couldn’tsit on my bike anymore.”-Lance Armstrong“I always had the size differencethere, but I didn’t know…I would’vestill been waiting if it hadn’t startedhurting, it just got so painful I couldn’tsit on my bike anymore.”-Lance Armstrong
  59. 59. Yuvraj Singh –extragonadal seminoma
  60. 60. Thank you