Testicular ca [edmond]

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Testicular Cancer

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  • 1.Testicular Ca Dr. Edmond Wong EAU 2010 EAU 2011EGCCCG 2008 (EU) 1

2. Epidemiology 1-1.5% of male neoplasm 5% of urological tumors 3-6 new case per 100,000 male/ year Increasing trend towards increase incidence 1-2% bilateral Histological variance: Germ cell tumors (90%) Non- GCT (10%) Peak incidence: 30s for seminoma 40s for pure seminoma Familial clustering among sibilings 2 3. Risk factors1. Familial hx of Ca testis in 1st degree relative (father/brother)2. History of cryptorchidism3. Infertility4. Klinefelters syndrome5. Contralateral tumor or Tin6. HIV7. Maternal oestrogen exposure8. Race: scandanavian3 4. Genetics Specific genetic marker: Isochromosome of theshort arm of chromosome 12 i(12p) in all germcell tumors Intratubular germ cell neoplasia (testicularintraepithelial neoplasia, Tin) : samechromosomal change with alterantion in p53locus (66%) Deregulation in pluripotent programme of fetalgerm cells (markers: M2A, C-KIT,OCT4/NANOG) 4 5. Germ Cell TumorsSeminoma (40% of all GCTs): Typical/ Classic (85%) Anaplastic (5-10%) Spermatocytic (2-12%) Nonseminomatoustumour embryonal cell carcinoma yolk sac tumor teratoma choriocarcinoma5 6. Pathology: WHO classification 6 7. Classic Seminoma Peak at 30s, also in > 60s Composed of islands/ sheets of relatively largecells with clear cytoplasm and densely stainingnuclei Syncystiotrophoblastic element in 10 15 % correspond to -hCG production Lymphocystic infiltrationin 20 % Slow growth rate7 8. Anaplastic seminoma Morphology similar to that of classic / typicalseminoma Characteristics being more aggressive andpotentially more lethal: Higher mitotic activity Higer local invasion Increased rate of metastatic spread Higher rate of -hCG production Inguinal orchiectomy + RT is equally effectivein controlling both anaplastic and classicseminoma8 9. Spermatocytic seminoma Composed of cells with variable size anddeeply pigmented cytoplasm, resembledifferent phase of maturing spermatogonia Metastatic potential: extremely low Prognosis is accordingly favorable9 10. Embryonal carcinoma Highly malignant Small, rounded, but irregular mass invading the tunicavaginalis testis, may involve contiguous cordstructures Cut surface: a variegated, grayish white, fleshy tumor,often with areas of necrosis or hemorrhage and apoorly defined capsule Histology: distinctly malignant epithelioid cellsarranged in glands or tubules; cytoplasm pale orvacuolated, and the nuclei rounded with coarsechromatin and one or more large nucleoli 10 11. Choriocarcinoma May occur as a palpable nodule; the sizedepends on the extent of local hemorrhage May present with advanced distant metastasisbut a paradoxically small intratesticular lesion Histology: two distinct and appropriatelyoriented cell types must be demonstrated: syncytiotrophoblasts (large, multinucleated cells) cytotrophoblasts (closely packed, intermediate-sized, uniformcells) 11 12. Teratoma More than one germ cell layer in various stages ofmaturation and differentiation Mature and immature elements Variably sized cysts containing gelatinous, mucinous,or hyalinized material interspersed with islands of solidtissue often containing cartilage or bone Histology: the cysts may be lined by squamous,cuboidal, columnar, or transitional epithelium, and thesolid component may contain any combination ofcartilage; bone; intestinal, pancreatic, or liver tissue;smooth or skeletal muscle; and neural or connectivetissue elements12 13. Yolk sac tumor The most common testis tumor of infants and children In adults, it occurs most frequently in combination withother histologic types Responsible for the production of AFP Histology: composed of epithelioid cells that formglandular and ductal structures Embryoid bodies: measuring < 1 mm in diameter,consist of a cavity surrounded by loose mesenchymacontaining syncytiotrophoblasts and cytotrophoblasts,resembling 1- to 2-week-old embryos13 14. History: History related to the mass- Duration, painful/painless, change in size, previous history of genitalia surgery, sexualhistory, trauma, associated urinary tract symptoms Previous relevant history and risk factor(s)- Cryptorchidism (Undescend 4-13x risk)- Family History (6-8x risk)- Racial Origin (Highest in Scandinavia)- Maternal exposure of estrogen (2.8-5.3x risk)- Subfertility (1.6-20x risk)- Contralateral testicular tumour (5-10% risk)- HIV14 15. Clinical examination General: SC LN Palpable abdominal mass Gynaecomastia (7%) more common in NSGTC Back and flank pain (11%) Scrotum: Painless , unilateral mass in scrotum Reduction in testis size precede testicular tumor Casual finding of intrascrotal mass Scrotal pain (20%) Local pain (27%) Mimic orchioepididymitis (10%) 15 16. Extragoadal Ca testis 1/3 ITGCN 1/3 USG testis reveal burned out tissue 1/3 Primary extragonadal germ cell tumor Supported by elevated AFP / beta-hCG Dx must be confirmed by bx ofextragonadal mass Histology of undifferentiated Ca immunohistological marker (isochrom i12p)16 17. Blood test Serum marker has prognostic value: AFP (produced by yolk sac cells) : life 5 day Increase in 50-70% of NSGCT hCG (expression of trophoblasts): life 36hr Increase in 40-60% of NSGCT Increase in 30% of Seminomas 90% NSGCT present with rise both marker LDH (marker of tissue destruction) For pt with metastatic disease Elevated in 10 - 20% of seminomas, correlating with tumor burden Useful in monitoring of Rx response in advanced seminoma Increase in 51% of ca testis Other marker : PLAP (placental like alkaline phosphatase): monitoring pt with pure seminoma -ve maker do not exclude the dx of GCT AFB, hCG & LDH in advanced cancer is mandatory , while PLAP isoptional 17 18. Imaging of testis Scrotal USG: > 7.5 MHz Confirm presence of testicular mass Diff intra or extratesticular Explore contralateral testis Sensitivity (100%) Also indicated in pt with retroperitoneal or visceral mass & elevated hCG or AFP FU of contralateral testis on FU pt at risk Seminoma : a homogeneous hypoechoic, intratesticular mass; larger lesions may be more inhomogeneous calcifications and cystic areas are less common Nonseminomatous tumour : may contain microcalcifications and areas of hemorrhage, typically heterogeneous in appearance teratoma elements: may demonstrate well-defined structures of ectodermal derivation18 19. Testicular microcalcifications Divided into classic and limited: Classic: presence of five or more microliths on one or more images of the testes Aassociated in both benign and malignant conditions: Klinefelter syndrome male pseudohermaphroditism Down syndrome subfertility infertility cryptorchism hypogonadism fragile X syndrome pseudoxanthoma elasticum pulmonary microlithiasis19 20. CT scan of the abdomen and pelvis with IVand oral contrast To identify metastatic disease to the retroperitoneallymph nodes (sensitivity 70-80%) Understages approximately 15-20% of patientsthought to be at stage I Left-sided NSGCTs LN bounded by left renal vein,left ureter, IMA and aorta Right-sided tumors interaortocaval LN at the level ofL2 ( Echelon LN ) Lymphatic drainage cross over from right to left, and20% of right-sided NSGCTs, lymph node involvementis found on the left side 20 21. Chest XR / CT to help identify any possible pulmonarymetastases the only thoracic examination in seminoma whenretroperitoneal and pelvic CT are -ve Chest CT is recommended for NSGCT Chest CT increases the sensitivity of diagnosis,but the presence of small, benign granulomas ofthe lung may be misdiagnosed as metastaticdisease in as many as 30% of patients withclinically low-stage disease21 22. MRI: Higher SV (100%) and SP (95%) than USGfor diagnosis Able to differentiate Seminomatous from non-seminomatour tumors No adv over CT PET : No adv over CT, because both are insensitivefor microscopic LN metastasis22 23. 23 24. Inguinal exploration andorchidectomy Should be performed within 1 week Immediate orchidectomy with division of spermatic cordat internal inguinal ring must be performed if tumor isfound scrotal skin lymphatics are different from testicular lymphatics and drain into the inguinal nodes perform all orchidectomies for solid masses through an inguinal route to avoid tumor spill into the inguinal drainage basin If a patient is explored scrotally, subsequent therapy may necessitate hemiscrotectomy and radiation treatment of the inguinal nodes If dx not clear: testicular bx is taken for frozen section In case of disseminated disease or life-threateningmetastasis up-front chemotherapy and thenorchidectomy later when clinically stabilized 24 25. Before orchidectomyDiscuss the issue of: Sperm banking Contralateral testicular biopsy (10%) in no risk (34%) in risk gp (refer to TIN) Testicular prothesis: Prothesis infection (2%) may delay post-op chemo Extrusion from scrotum (5%) Scrotal contraction or migration (3%) Chronic pain (3%) Hematoma (< 1%)25 26. Radical Inguinal Orchidectomy Inguinal incision Cord isolation Pedicle control with a non-crushing vascular clamp Dissection of the spermatic cord with 1 2 cm into theinternal spermatic ring Leave a long nonabsorbable tie on the patient side ofthe spermatic cord. This is to facilitate identification ifretroperitoneal lymph node dissection (RPLND)becomes necessary and the patient requiresdissection of the remaining spermatic cord structuresfrom the abdominal exposure.26 27. Organ sparing surgery Contraindication: presence of non-tumoral contralateraltestis Indications: Bilateral testicular tumors Metachronous contralateral tumors Tumor in solitary testis with normal pre-op testosterone level Tumor volume 70% embryonal carcinoma > 50% (predict vascularinvasion)63 64. 64 65. Fertility associated issue Sperm abnormality are common in Ca testis Chemotherapy and RT impair fertility Pre-treatment fertility assessment: Testosterone LH & FSH level Semen analysis & cryopreservation should be offered