706_F06pset6_key - Problem Set#6 1 You are studying the...

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Problem Set #6 1. You are studying the effects of the TSG1 tumor suppressor gene in mice. You knockout one copy of the TSG1 gene in mice and you derive cells from these animals (They are now heterozygotes, +/-). As expected, the tsg1-knockout mutation is fully recessive at the cellular level. You examine tumor formation in mice and observe the following: % of mice w/ no tumors time WT tsg1 +/- A. If the tsg +/- mutation is recessive in cells, why do you observe an effect on tumor development in the animals? tsg+/- mutation is recessive in cells, but in the organ- ism, it appears dominant due to loss of heterozygos- ity (LOH). Next you add some suspected cancer-causing chemicals, PCBs, to their food. You watch for tumor formation in all mice and see the following: time B. Explain why the tsg +/- animals developed tumors more rapidly than WT animals when ex- posed to PCBs. PCB appears to be a mutagen, which acceler- ate the accumulation of mutations, leading eventually to cancer. Cancer is a multistep process, and tsg1 +/- mice are one step closer to cancer due to their inherent muta- tion. Therefore, we observe tsg +/- animals to develop tumors more rapidly when exposed to PCBs. C. You breed two tsg +/- mice before they develop tumors. Six months later, both of the parent mice have developed tumors. You breed the parent mice again to see the effect of the parental tumors on tumor formation in the progeny. Do you expect that these progeny mice will develop tumors at an ear- lier, later, or similar age as compared to the progeny bred before the parent mice developed tumors? The progeny would develop tumors at a similar rate as the first set of progeny. Cancerous cells are almost always derived froma single cell that was able to acquire the additional muta- tions needed for malignancy. The mutations in the somatic tumor cells are not passed onto
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706_F06pset6_key - Problem Set#6 1 You are studying the...

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