Oncology CE 2.0 3 PDF

Charlotte Eikaas 2023/24 PROSTATE CANCER EPIDEMIOLOGY: most common cancer in men; 95% AC DIAGNOSIS Occurs in 10-15% of men at some point, usually 50+ 1. PSA- prostate specific antigen (NOT CANCER SPECIFIC) Frequency increases...

Charlotte Eikaas 2023/24 PROSTATE CANCER EPIDEMIOLOGY: most common cancer in men; 95% AC DIAGNOSIS Occurs in 10-15% of men at some point, usually 50+ 1. PSA- prostate specific antigen (NOT CANCER SPECIFIC) Frequency increases with age: >50% of males have prostate Normal = 10 → 66% have cancer If 4-10 → 22% have cancer Age = #1 (male gender being a given…) Used in staging, prognosis and monitoring of treatment (+) family history with diagnosis 20) Bone scintigraphy: if PSA >10 + Gleason 9-10 + pain; check metastasis PRESENTATION Staging of PC (TMN)- combined with Gleason to give final verdict Peripheral location → asymptomatic Early transitional zone/ locally advanced peripheral T1 = barely visible, non-palpable disease: pain upon urination, increased urinary frequency, T2 = contained within capsule difficulty initiating urination, nycturia T3 = beyond capsule Progressive: hematospermia, impotence, impaired semen T4 = Infiltration beyond bladder/rectum production Advanced: bone pain- osteoblastic metastasis TREATMENT T1/T2 → either watchful waiting, prostatectomy or RT T3 → RT (NEVER operate- can’t be resected), watchful waiting SCREENING: not recommended, as many PCs are clinically T4/ N+/ M+ → hormonal therapy or watchful waiting insignificant; toxicity of treatment may worsen prognosis Watchful waiting: if expected lifespan F 2x 1. Urine sample- BLD+, LEU+, NIT – Older age groups affected (60+) 2. Renal USG- tumor is hyperechoic 3. CT with contrast- very important; 90% of RCCs can be RISK FACTORS & ETIOLOGY: most are uncertain diagnosed and staged by CT, eliminating need for biopsy 4. PET-CT: may be done to assess micrometastasis Smoking- MC Obesity & HTN +/- TMN- T = size, invasion, involvement of renal/ pelvic vessels Somatic/ hereditary mutations- VHL, tuberous Microscopic grading: Fuhrman score (I-IV) sclerosis SUBTYPES: may be determined by biopsy- done if tumor is TREATMENT: nephrectomy = only potentially curative treatment; unresectable, or if ablation is being considered should be aimed at preserving as many nephrons as possible. Renal tumors have their own capsules, easing surgical removal Clear cell carcinoma: 80-90% of RCC, tubular origin DD oncocytoma- may appear similar Main alternative to surgery = ablation Seen in VHL disease- most sporadic cancers RT- used in palliative treatment; chemo is ineffective also have loss of genes from VHL Targeted therapy: VEGFR TK + mTOR inhibitors- not much RCC most likely to invade renal vein used yet Papillary carcinoma Constant bleeding from unresectable tumor → renal a. Chromophobe carcinoma embolization PROGRESSION & PROGNOSIS PRESENTATION Invasion: may go through perinephric fat into renal vein, resulting in hematogenous metastasis Painless hematuria- MC symptom Metastatic sites: mainly lungs, bones, liver and adrenals; Abdominal mass + dull flank pain occurs in 30% Fever and weight loss- due to SAA amyloidosis Hypertension IVC syndrome Left-sided varicocele Paraneoplastic syndromes: polycythemia (EPO overproduction), hypercalcemia, fever, HTN, Cushing’s, femininization or masculinization, SAA amyloidosis 5  PRESENTATION NOT In Charlotte Eikaas 2023/24 PENILE CANCER EPIDEMIOLOGY: rare in Europe- MC in Brazil and central TREATMENT Africa Penile carcinoma in situ → circumcision (#1), topical imiquimod or 5-FU, laser ablation RISK FACTORS & ETIOLOGY T1/T2 → wide local excision, partial or total glansectomy; possibly RT Caused by HPV 16, 18, 31 and 33 (HPV 6 +11 = warts) T3/T4 → partial penectomy + radical inguinal Risk factors: poor hygiene, not being circumcised, lymphadenectomy phimosis, lichen sclerosis, smoking (verrucous PC), UVA exposure PROGRESSION & PROGNOSIS: Sentinel nodes = inguinal nodes SUBTYPES Risk of perineural invasion Very poor prognosis- a very aggressive type of cancer Penile carcinoma in situ Bowen disease: single lesion, old males, becomes invasive in 10% Bowenoid papulosis: multiple lesions, sexually active adults, virtually never becomes invasive Invasive SCC: MC subtype of penile cancer PRESENTATION: mass on penis; very variable morphology- may be lump, ulcer, sore, crust, wart, etc; may also produce inguinal lymphadenopathy DIAGNOSIS: biopsy confirms cancerous state; other modalities may be used to determine stage Pelvic USG/MRI- to examine penis and nearby structures Lymph nodes If palpable → biopsy of affected node If non-palpable → sentinel node biopsy TNM T1= only glans T2 = invading spongiosum T3 = invading corpus cavernosum T4 = anything beyond 6  Charlotte Eikaas 2023/24 TESTICULAR CANCER EPIDEMIOLOGY DIAGNOSIS: mainly based on enzymes and USG; note that the enzymes are not diagnostic, and cannot be used for screening MC malignant cancer in young males- AA 20-35 y/old Adult males → usually seminoma USG = gold standard for diagnosis Children → usually yolk sac tumors Biopsy CANNOT be done; biopsy = orchidectomy LDH = serum marker for all GCT, but also many other cancers RISK FACTORS & ETIOLOGY AFP = marker for yolk sac tumors Cryptorchidism- only known etiology; other are RF B-HCG = marker for seminoma + choriocarcinoma Testicular dysgenesis syndrome Abdominal CT + chest RTG/CT Klinefelter syndrome Staging using Royal Marsden Hospital classification; limited to… Neoplasia in contralateral testis 7 a) < 2 ou 1. Testes only Genetic- mutations of KIT (CD117) or BAK ↳ 2. 3) 25 am a ( > 5 Sub - diaphragmatic lymph nodes ↳ 3. Supra - diaphragmatic lymph nodes (e.g., mediastinal) SUBTYPES: 95% are germ cell tumors, listed below. The remaining are sex-chord/stromal tumors or mixed ↳ 4. Hematogenous metastasis Seminoma: MC testicular cancer in adults; average age 40-50 TREATMENT: mainly based on orchidectomy + chemo y/old, best prognosis. May grow very big. Extremely Seminoma stage I: radical orchidectomy + surveillance radiosensitive and chemosensitive Seminoma stage II: surgery + RT (non-bulky) or chemo Non-seminomas: metastasize earlier- both via lymph and (bulky tumor) blood to liver and lungs. 90% achieve full remission with Non-seminoma stage II: surgery + chemo aggressive chemo Seminoma/non-seminoma stage III+IV: surgery + chemo +/- resection OR RT of residual mass Embryonal carcinoma: 2nd MC in adults, 20-30 y/old, aggressive High chemosensitivity AND radiosensitivity Yolk sac tumor: MC in children, AFP+, good prognosis Complications of treatment: infertility, secondary tumors- Teratoma stomach, bladder, colon Choriocarcinoma: rare, but highly malignant, extensive hematogenous metastasis in most cases- very poor No hormonal therapy! prognosis PROGRESSION & PROGNOSIS: strongly depends on subtype; very good in most cases, since its usually seminoma PRESENTATION Spread (seminoma) Visible/palpable tumor in scrotum- testicular cancer is 1. Lymphatic- paraaortic nodes- comes first the most common cause of PAINLESS testicular 2. Hematogenous- germ cell tumor most likely to give bone swelling metastasis; occurs late Gynecomastia Highly curable malignancy, even in advanced stage! Epididymitis Recurrence is not uncommon; usually within 2 years 7