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In cancer research, we never talk about "curing" cancer because, as others have pointed out, there is no way of being sure that all of the cancer has been eradicated. You may be interested to consider "Recurrence" statistics which describe the amount of time from when a cancer was treated to when it was detected to have returned. If you are willing to do ...


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Apoptosis is very tightly controlled for obvious reasons. Setting it off without proper control would result in the uncontrolled loss of cells. Apoptosis is one of the major pathways which are either mutated or shut-off in cancers, preventing the body from eliminating malingnant cells. These two papers are interesting in this context: Apoptosis: A Review ...


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It is both, a and b. The JAK-STAT-Pathway sits below the Erb-receptor and is therefore giving the signal from mutated Erb down the signalling cascade. Besides that a permanent active version of Jak2 has been found which also permanently activates this pathway. Both are contributing to cancer. See this two articles: Molecular Pathways: JAK/STAT Pathway: ...


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i thnk it is MAP Kinase pathway b'coz RAS is a protein involved in this pathway and mutation in it lead to permanent attachment of GTP leading to cell proliferation causing carcer


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There's this database of genetic/drug interactions, which I think is pretty much exactly what you're looking for. Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent ...



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