2063 true tamoxifen is an estrogen receptor

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20–63 True. Tamoxifen is an estrogen receptor antagonist. By preventing the bind- ing of estrogen to the receptor, tamoxifen prevents the proliferation of breast cancer cells, which is dependent on estrogen binding. 20–64 False. Although there are likely to be some cancer cells in a hypermutable population that are resistant to a single drug, it is unlikely that cells will be resistant to multiple drugs. For such a combination therapy to work, the drugs must be designed so that a single mutation cannot render cells resis- tant. For example, if the multiple drugs in a cocktail can all be pumped out of the cell by an amplified ABC transporter, then treatment of a cancer cell population will select for cells that have amplified that gene…and the treat- ment will fail. If, on the other hand, a single mutation cannot render a cell resistant to all of the drugs in the cocktail, the treatment has the potential for eliminating all the cancer cells and producing a cure. CANCER TREATMENT: PRESENT AND FUTURE A469
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THOUGHT PROBLEMS 20–65 Technological advances in our ability to detect cancers since 1970 means that we can diagnose them at earlier stages in the course of the disease. Thus, even in the absence of better treatment regimes, a patient might be expected to survive somewhat longer now than in the past because they will be at a slightly earlier stage of the disease at the 5-year mark. Reference: Weinberg RA (2006) The Biology of Cancer, p726. New York: Gar- land Science. 20–66 The promyelocytes of APL are blocked at an intermediate stage in their development, at a point where they still divide and increase in number. It is this unchecked increase in number that causes problems for the cancer patient. Normally, such precursor cells divide only a few times before they terminally differentiate into a nondividing blood cell. By triggering the dif- ferentiation of promyelocytes into terminally differentiated neutrophils, which no longer divide, treatment with all- trans -retinoic acid eliminates the problems caused by unchecked proliferation. APL arises by one of a few types of translocation that fuses the retinoic acid receptor (RAR) gene on chromosome 17 with a gene on another chromo- some to make a hybrid protein that interferes with the normal developmen- tal program. It is not yet clear how the fusion protein blocks development, although it likely does so by interfering with the function of the normal RAR receptor. In some way, treatment with all- trans -retinoic acid allows APL cells to move through the block. Reference: Warrell RP Jr, de The H, Wang Z-Y & Degos L (1993) Acute prom- yelocytic leukemia. N. Engl. J. Med. 329, 177–189. 20–67 The products of oncogenes are the only feasible targets for such small molecules. The product of an oncogene has a dominant, growth-promoting effect on the cell. Thus, if the growth-promoting oncogene product were inhibited, the cell might return to a more normal state. This is the underly- ing rationale for searching for drugs that inhibit oncoproteins.
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