Chapter_20_Solutions

Chapter_20_Solutions - Chapter 20 Cancer CANCER AS A...

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CANCER AS A MICROEVOLUTIONARY PROCESS DEFINITIONS 20–1 Carcinogenesis 20–2 Malignant 20–3 Cancer stem cells 20–4 Sarcoma 20–5 Primary tumor 20–6 Tumor progression 20–7 Genetically unstable 20–8 Benign 20–9 Replicative cell senescence 20–10 Carcinoma TRUE/FALSE 20–11 False. A carcinoma consists of a variety of normal cells, along with the can- cer cells. The fibroblasts in the supporting connective tissue, the associated inflammatory cells, and the cells of the newly formed blood vessels all are normal cells that are present because they are in contact with the cancer cell mass or have been recruited into the tumor. These normal cells do not evolve from the cancer cell population. 20–12 True. Genes can be shut off, for example, by changes in chromatin structure; specific covalent modifications of histones can attract complexes of chro- matin-binding proteins that are stably maintained following DNA replica- tion. Gene transcription can also be eliminated by methylation of CpG din- ucleotides in the promoter region. Specific histone modifications and DNA methylation are often linked. 20–13 False. There is an optimum level of genetic instability for the development of cancer. A cell must be mutable enough to evolve rapidly, but not so mutable that it accumulates too many harmful changes and dies. 20–14 True. Many cancers appear to be maintained by a small population of stem cells. These cancer stem cells usually divide more slowly than the cells in the bulk of the tumor, and they are less sensitive to treatments aimed at rapidly dividing cells. If the stem cells are not killed, the cancer is likely to return. In This Chapter CANCER AS A A457 MICROEVOLUTIONARY PROCESS THE PREVENTABLE A460 CAUSES OF CANCER FINDING THE CANCER- A461 CRITICAL GENES THE MOLECULAR BASIS A464 OF CANCER-CELL BEHAVIOR CANCER TREATMENT: A469 PRESENT AND FUTURE A457 Chapter 20 20 Cancer
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A458 Chapter 20: Cancer THOUGHT PROBLEMS 20–15 The incidence of cancer increases dramatically with age because it takes mutations in several critical genes to disable a cell’s normal mechanisms for controlling its growth. Since growing cells continually accumulate muta- tions, which they pass on to their progeny cells, the chance that a cell will accumulate a critical set of mutations increases with age. The steep rise in cancer incidence in older women seen in Figure 20–1 reveals that colon can- cer increases as the sixth power of age, suggesting that it arises only after mutations have occurred in six or so genes that regulate cell growth in the colon. 20–16 The key difference in the incidences of colon cancer and osteosarcomas is the size of the population of cells at risk for the disease. Colon cancer arises from the population of proliferating cells in the colon, which are present in roughly the same number throughout life. This population can accumulate mutations over time, giving rise to the age dependence seen in Figure 20–1.
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This note was uploaded on 01/07/2011 for the course BIOLOGY 7.012 taught by Professor Ericlander during the Spring '04 term at MIT.

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Chapter_20_Solutions - Chapter 20 Cancer CANCER AS A...

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