Whether BRCA1 or BRCA2 mutation is more dangerous in breast cancer cases based on the given study. Introduction: Cancer is a disease in which there is an abnormal growth of cells due to unlimited cell division. It is a genetic disease which is characterized by the changes in the genes due to certain mutations. The abnormal cells are called tumor or cancer cells. Tumor suppressor genes inhibit the growth and cell division of the abnormal cells. When inactivated by mutations, these genes lose their inhibitory properties causing an increase in the cell division leading to cancer.

Question

p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). Armed with your knowledge about the different mechanisms which govern transcription and translation, what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?

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Question

Chapter 16, Problem 3ITD

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Whether BRCA1or BRCA2 mutation is more dangerous in breast cancer cases based on the given study.

Introduction:

Cancer is a disease in which there is an abnormal growth of cells due to unlimited cell division. It is a genetic disease which is characterized by the changes in the genes due to certain mutations. The abnormal cells are called tumor or cancer cells. Tumor suppressor genes inhibit the growth and cell division of the abnormal cells. When inactivated by mutations, these genes lose their inhibitory properties causing an increase in the cell division leading to cancer.

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p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). Armed with your knowledge about the different mechanisms which govern transcription and translation, what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?

p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?

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