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    Breast Cancer is one of the Most common cancers in women. HER2 expression is a poor prognostic factor. Treatment includes surgery, radiotherapy and chemotherapy.

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    c2f Pres

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    Breast Cancer is one of the Most common cancers in women. HER2 expression is a poor prognostic factor. Treatment includes surgery, radiotherapy and chemotherapy.

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    Breast Cancer is one of the Most common cancers in women. HER2 expression is a poor prognostic factor. Treatment includes surgery, radiotherapy and chemotherapy.

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    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    146 views25 pages

    c2f Pres

    Uploaded by

    api-195799092
    Breast Cancer is one of the Most common cancers in women. HER2 expression is a poor prognostic factor. Treatment includes surgery, radiotherapy and chemotherapy.

    Copyright:

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    of 25

    Oncology

    Dr Marina Milic, FY1 LTHT

    Reminder
    Cancer and theFather of Medicine: Hippocrates carcinos and carcinoma (crab)
    2 Cancer features: unregulated cell growth and invasion Ca cells: deregulated proliferation, loss of differentiation, loss of normal apoptotic pathways, genetic instability, invasion, metastasis,evasion of immune system Multistep process

    Breast Cancer
    Incidence 48 000/year (1.3 M annually ww)

    Leading cause of death in women


    5-10% hereditary (BRCA1,2 mutations),rest NH

    NON-INVASIVE : Ductal Ca in situ


    INVASIVE: Ductal breast Ca (80%)

    Breast Ca
    Pathogenesis / series of molecular alterations at cellular level : outgrowth and spread of epithelial breast cells 4 main subtypes: luminal A, luminal B,basal, HER-2 caused by different genetic and epigenetic alterations Prognostic factors: lymph node status, Tm size,lymphatic/vascular invasion, histologic grade/subtype, HER2 amplification/overexpression, ER/PR status

    Pathogenesis
    Driven by activation of steroid hormones which bind to their Rec (ER/PR) in breast epithelial cells inducing cell growth,differentiation and survival Signal transduction by RTKs (epith c) specifically ErbB family (EGFR,HER2(ErbB2),ErbB3,ErbB4) in response to growth factor stimulation and activation of downstream signaling pathways

    HER2 expression in Breast Ca


    Tm : HER2+ (25%) and HER2-

    Cellular expression of HER2 at high levels a/w aggressive disease and is poor prognostic factor
    HER2 Rec doesnt bind an own ligand,activated by homo/heterodimerization with another Rec ErbB family initiating oncogenic signal--> angiogenesis,proliferation,decreased apoptosis

    Management
    Tx : Surgery primary Tx

    Histology, PR/ER status, HER guide prognosis


    Evaluation on LN inv by sentinel node biopsy or axillary lymph node dissection Hormone Pos Tm(ER+PR+)more indolent course, respond to hormonal Tx

    HER-2 pos predictive of response to certain chemo agents (Doxorubicin, Trastuzumab...)


    Adjuvant chemo/RT for micrometastatic Ca

    1) NSCLC 80% : adenoCa, squamous cell, large c Ca


    --> AdenoCa +subtype, peripheral location, non-smokers +

    Lung Cancer

    2) SCLC :25-30% central parts of lungs (cavitary lesion in proximal bronchus), a/w hyperCa ++

    At dg 20% have localized disease, 25% regional and 55% distant metastatic disease
    Most common sy: cough, SOB, chest pain, haemoptysis, hoarsness, fatigue, weight loss, recurrent bronchitis/pneumonia Metastatic sy: bone pain, spinal cord compression, neurological sy

    NCSLC

    Diagnosis
    CXR : nodule, mass, infiltrates, wide mediastinum,atelectasis, hilar enlargement,pleural effusions

    Dg confirmation : bronchoscopy, sputum cytology, transthoracic needle biopsy, CT


    TNM staging system: except for SCLC T (primary Tm involvement):T0, T1

    TNM staging system


    T (primary Tm involvement): Tx cannot be assessed, T0 no evidence of Tm, Tis : in situ -->T1,2,3,4: size/extension of primary Tm L (Lymph node involvement) : Nx, N0 -->N1 : ipsilateral -->N2 : met in ipsilateral mediastinal/subcarinal node -->N3 : met contralateral mediastinal, hilar, ipsi/contralateral scalene node, supraclavicular node M (Metastatic involvement): M0 no mets, M1 distant mets

    Management
    Surgery Tx of choice grade I and II NSCLC: lobectomy, pneumonectomy, wedge resection Chemotherapy 80% pts at some stage (Cisplatin, Carboplatin) Radiotherapy : stage I and II only if nonresectable 5-year survival 8%, : 49% local disease, 16% for regional, 2% distant metastatic disease

    Prostate Cancer
    Clinical presentation Symptoms: urinary retention,hematuria, back pain (non specific) Diagnosis: - Physical examination alone (DRE) cannot differentiate from BPH - Elevated PSA (Prostate Specific Antigen) : no level rules out Ca but risk of disease increases with PSA elevation

    Prostate Ca Diagnosis
    Physical examination alone (DRE) cannot differentiate from BPH - Elevated PSA (Prostate Specific Antigen) : no level rules out Ca but risk of disease increases with PSA elevation Biopsy establishes the diagnosis Gleason score

    Management
    Radical prostatectomy

    Radiotherapy
    Active surveillance Androgen deprivation therapy (surgical or medical castration LHRH analogues or antagonists, antiandrogens) Metastatic disease : rise in PSA postop>0.2 or 3 consecutive PSA increases after RT signal impending progression Risk of metastatic disease depend on patients Gleason score, PSA doubling time, onset of PSA rise

    BPH (Benign Prostatic hypertrophy)

    Histologic diagnosis: epithelial/stromal proliferation +/- apoptotic failure-->gland enlargement

    Hyperplasia results in gland enlargement restricting urine outflow


    Part of the ageing process, hormonally dependent on Testosterone and DHT production (50% of men by age 60, 90% by 85)

    Clinical manifestations
    Voiding dysfunction-lower UT symptoms: frequency,urgency,hesitancy,nocturia, incomplete emptying,dribbling
    Complications: acute urinary retention, renal failure, UTIs ,hematuria, bladder stones Asymptomatic/mild sy pts: watch and wait/medical Tx Sy pts with bladder outlet obstructiontransurethral radical prostatectomy (TURP)

    Physical Examination
    Physical examination : DRE estimate gland size: nb of fingerbreadth wide (115-20g of tissue) pelvic floor tone,fluctuance, pain sensitivity(protatodynia,prostatitis)

    Colorectal cancer
    98% adenocarcinomas 20% develop in cecum,20% in rectum, 10% rectosigmoid junction, 25% in sigmoid colon 3 pathways to Ca:

    1) Adenomateous polyposis coli (APC) gene (inactivation


    2) hereditary nonpolyposis 3) ulcerative colitis dysplasia

    History
    Bleeding (60%)/occult bleeding (fecal occult blood test)

    Change in bowel habit


    Abdominal pain (20%)

    Malaise

    Physical examination
    DRE : rectal Tm assessed for size,ulceration, presence of pararectal LN, sphincter function

    Rigid proctoscopy for rectal Ca


    Colonoscopy/biopsy/histopathologic Dg

    Metastatic evaluation: CT chest/abdo/pelvis

    Etiology: environmental and genetic factors


    75% sporadic
    25% in pts with risk factors: - familial/pt Hx of polyps - genetic predisposition : hereditary nonpolyposis colorectal Ca (HNPCC), familial adenomateous polyposis (FAP) both autosomal dominant inherited syndromes - inflammatory bowel disease (risk of Ca increases with disease duration, Incidence of Colorectal Ca in Crohns disease 4-20 higher than in general pop, UC incidence of 1% per year after 10 years)

    Investigations/Mx
    Colonoscopy for pts with no major comorbidity

    Flexi sigmoidoscopy for those with major Cb


    CEA(Carcinoembryonic Ag), Ca 19-9 assay

    Staging
    Surgery for resectable Tm/radiochemotherapy

    Thank you

    ANY QUESTIONS ???

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