freshmen+2008-2.Bernard

freshmen+2008-2.Bernard - What kind of phenotypic changes...

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Continuous divisions : de-repressed cell cycle Autonomous growth stimulation : oncogenes Immortalization (1) : no apoptosis (no programmed cell death) Immortalization(2) : no decrease of telomeres Accumulate more mutations : loss of mismatch repair, excision repair Growth beyond small size : get blood vessels (angiogenesis) Exit tissue of origin, enter new tissue : Invasion (by proteases) Survive in the blood stream : overcome anoikis (death in suspension) What kind of phenotypic changes are necessary to get from a normal to a cancer cell?
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Molecular causes of cancer development - loss of function through deletions, mutations: tumor suppressors, no apoptosis - gain of function, point mutations, fusions: oncogenes, telomerase - inherited point mutations in APC: loss of structure, adhesion - epigenetic changes: similar consequences as mutations - chromosomal aberrations: creation of new genes - mutational landscapes: the whole “symphony of changes” leading to any cancer - infections: HPV, HBV, Helicobacter
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Molecular causes of cancer development: The cell cycle (1) The cell cycle is a concept that the same sequence of reactions has to be repeated each time to have one cell divide into two cells. Cell cycle
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Molecular causes of cancer development: The cell cycle (2) The G1/S checkpoint is crucial to arrest the cell cycle, i.e. stop further divisions. G1/S checkpoint
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skin cancer normal skin QuickTime and a Photo - JPEG decompressor are needed to see this picture. Molecular causes of cancer development: The cell cycle (3) These cells are arrested in G1 These cells go through the cell cycle and divide All cells go through the cell cycle and divide
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The cell cycle (4) G1/S checkpoint - what is the nature of the G1/S block ? -
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freshmen+2008-2.Bernard - What kind of phenotypic changes...

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