PCL477H1-Lecture 12 to post [Compatibility Mode]

PCL477H1-Lecture 12 to post [Compatibility Mode] - Lecture...

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Lecture 12 overview what is cancer cancer as a genetic disease sequential genetic changes on road to cancer relationship of DNA damage to cancer carcinogenesis DNA damage as an instigator of neoplastic transformation: t ti l di t ti ti -mutations leading to oncogene activation genomic instability as a cause of cancer susceptibility chromosomal instability and aneuploidy mutator phenotype and microsatellite instability
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Cancer: What is it? Cancer : applied to diseases with abnormal accumulation and inappropriate dissemination of cells Hyperplasia : increased capacity for proliferation Metastatic potential : ability of cells to invade, migrate and grow in an inappropriate region of the body Heterogeneity: from cell to cell within same cancer/tumour from tumour to tumour within the same cancer type Compared to normal cells, cancer cells display defects in regulatory circuits that govern proliferation and homeostasis
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The Hallmarks of Cancer 1. Self-sufficiency in growth signals (Hanahan and Weinberg, Cell 70: 57-70, 2000) Normal cells : require external stimulatory signals to proliferate: growth factors and receptors extracellular matrix components ll ll dh i /i i l l cell-to-cell adhesion/interaction molecules Cancer cells : reduced or loss of dependence on these external signals 2 Insensitivity to growth inhibitory signals 2. Insensitivity to growth-inhibitory signals -most cells in our tissues are instructed not to divide and remain in differentiated states (except stem cells) -many cancer cells display features of de-differentiation: dysplasia many cancer cells display features of de differentiation: dysplasia 3. Evasion of programmed cell death (apoptosis) Steady state cell numbers = cell proliferation + cell death Normal cells have a programmed lifespan Cancer cells nonresponsive to death signals, forgotten how to die
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The Hallmarks of Cancer 4 limitless replication potential . Normal cells typically have a limited ability to replicate themselves i.e. a cell population doubles so many times, then stops growing (enters a state known as senescence) (enters a state known as senescence ) The replication ability of most cancer cells is limitless –immortalization 5 sustained angiogenesis (the growth of new blood vessels) 5. sustained angiogenesis Normal cells need to be within 100 mm of a capillary blood vessel Advanced cancers acquire the ability to stimulate the growth of new blood vessels within the tumour 6. tissue invasion and metastasis Primary tumours spawn ‘pioneer’ cells -move out into adjacent tissues and into bloodstream or lymphatic system whereupon they continue growth in a new location -the major cause of cancer deaths benign tumour = no metastasis malignant tumour = evidence of metastasis
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Cancer as a Genetic Disease oncogenes: ‘over-activated’ versions of proto-oncogenes i i ll di d i i h i i l -originally discovered in viruses that cause cancer in animals (jun, fos, myc) Overactivity: transformation of normal cell to a cancer cell tumour suppressor genes:
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