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Long story short: Absolutely. Short story long: While your intuition that growing a lot of cells can increase the risk of damage that might cause cancer is spot on, your specifics are a little off. It's not the telomeres themselves that are the problem, but broad spectrum DNA damage and transcriptional changes. The condition of the telomeres doesn't ...


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In a normal cell, during each replication the telomere is shortened slightly due to the end replication problem, as you probably know. As mutations occur and a normal cell begins to exhibit cancerous characteristics, it needs a way to stop the self-destruction which happens when the telomeres become too short. In fact it is the cancer cells themselves which ...


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Different cancers divide at different rates. One way to qualitatively visualize this is observe hair loss in patients who are undergoing chemotherapy. Commonly, a drug like cisplatin will be administered which will cross-link DNA, inhibiting cell division by activating apoptosis. Tissues which are killed most readily by cisplatin are those which are dividing ...


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Short-wave UV light (UVB and UVC) causes transition mutations at dipyrmidine sequences (ref.). In the work presented on KNSTRN quoted by the OP the authors report that 19 from a panel of 100 squamous cell carcinomas (SCC) contained a mutation in KNSTRN (and furthermore three of these contained no other mutation across the six genes that were analysed (Fig. ...


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This is actually a bad idea for severeal reasons: First it is not a good idea to tamper with genes, especially not with ones which are involved in the regulation of mitosis and the correct segregation of sister chromatids. Remember that a one amino acid exchange because of a C to T transition causes the problems with SCC? Into what do you want to change the ...



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