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Neoplasia

Epidemiology = study of cancer patterns in populations (not on individual basis)Cancer incidence Geographic and environmental factors Age Genetic predisposition to cancer Nonhereditary predisposing conditions1. Cancer incidence 2nd MCC of all the deaths in USAMC cancers in men:Prostate - 3

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Neoplasia

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    1. Neoplasia

    2. Epidemiology = study of cancer patterns in populations (not on individual basis) Cancer incidence Geographic and environmental factors Age Genetic predisposition to cancer Nonhereditary predisposing conditions 1. Cancer incidence 2nd MCC of all the deaths in USA MC cancers in men: Prostate - 33% Lung - 14.0% Colon and rectum - 11% MC cancers in women : Breast - 25% Lung -12% Colon and rectum - 11% MC cancer causing deaths among both sexes ? LUNG CANCER

    3. Epidemiology Incidence

    5. Epidemiology = study of cancer patterns in populations (not on individual basis) 2. Geographic and environmental factors Geographic Stomach Cancer – Japan (7-8 times high) Lung Cancers – USA ( 2 times) Skin cancers – New Zealand Environmental immigration ?Stomach carcinoma of Japanese's immigrants to USA sun exposure Skin cancers & Ultraviolet rays Occupational –Asbestos, Vinyl chloride, 2-naphthylamine Obesity – 52% & 62% ? risk of cancers in Males & Females respectively Alcohol ? GIT cancers Cigarette smoking ? Lung cancers Sexual Practices ? Cervical Cancers

    6. Epidemiology Environmental factors

    7. Epidemiology = study of cancer patterns in populations (not on individual basis) 3. Age Incidence of cancers = ?? with age MC cancer age group = 50 yrs. MC cancers in Infants & Children - Blastomas MC cancers in Older Children (± 15 years) =Acute leukemia & CNS neoplasms (2nd MCC of deaths) 4. Genetic predisposition to cancer MC predisposing factors? Environmental (acquired) + Hereditary (Familial) Hereditary Predisposition ? 10% Three categories Environmental ? proliferations ? possible origins of malignant neoplasms: Regenerative (Cirrhosis ) Hyperplastic (Endometrial) Dysplastic ( cervical)

    8. Molecular basis of cancer

    9. Molecular basis of cancer 1. Fundamental Principles Non lethal genetic damage =Most important Monoclonal origin –Leukemia, Lymphoma Certain regulatory genes are principal 1.Protooncogenes ?growth promoting & normal Mutations in Proto-oncogene ? Oncogenes (abnormal) 2.Anti-oncogenes (growth-inhibiting/ Tumor-suppressor genes (TSG) =p53 & Rb. normally suppress cell proliferation. Mutations of TSG ? release cells from growth suppression & lead to hyper-proliferation. 3.Apoptotic genes (regulate programmed cell death) ?Act as dominant or TS genes 4. Genes regulating damaged DNA

    10. Molecular basis of cancer 2. Essential Alterations Self sufficiency in growth signals? no need of external stimuli Insensitivity of growth inhibitory signals? TGFß Evasion of Apoptosis? Ca. cells resistant apoptosis ( inactivation of p53) Defects in DNA repair ? NER Limitless replication potential ? telomerase reactivation Sustained angiogenesis? VEGF Ability to invade & metastasis ? ?cancer deaths 3. Normal Cell cycle

    11. Molecular basis of cancer 3. Normal Cell cycle Cell-Cycle Checkpoints Two main checkpoints 1. G1/S transition S phase ?point of no return ?checks for DNA damage (if yes) ?arrest the cell cycle (??p53)?if damage is not repairable ?apoptotic pathways 2. G2/M ?monitors the completion of DNA replication ?arrest in G2 ?important in cells exposed to ionizing radiation? chromosomal abnormalities G0 stage ?resting (nondividing) cells Cyclins and cyclin -dependent kinases (CDKs), and inhibitors ? control orderly progression of cells

    12. Molecular basis of cancer 3. Normal Cell cycle Cyclins ?synthesized during specific phases ?activate the CDKs ?decline rapidly CDKs ?phosphorylating critical target proteins ?cause progression of cells to the next phase of the cell cycle ?bind to cyclins Cyclin D and RB Phosphorylation Cyclin D ? first cyclin to increase in the cell cycle (mainly mid G1 ) Cyclin D binds to and activates CDK4 in G1 phase ? cyclin D-CDK4 complex ? Phosphorylation of RB ? ON-OFF switch for the cell cycle Cell-Cycle Progression beyond the G1/S Restriction Point Need active complex between cyclin E and CDK2 next decision point ?G2/M transition Absence of cyclin E ? prevent G0 cells from entering cell cycle

    13. Molecular basis of cancer 3. Normal Cell cycle Cell-Cycle Inhibitors Function as tumor suppressors Altered in tumors 1. Cip/Kip ? p21, p27, and p57 ?activation of p21 is under the control of p53) 2. INK4/ARF families ? p16INK4a and p14ARF ?block the cell cycle and act as tumor suppressors

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