Genetics, PLEASE HELP Mutations that inhibit apoptosis are often found in tumors

Question

Genetics,

PLEASE HELP

Mutations that inhibit apoptosis are often found in tumors. Explain how this inhibition could contribute to tumor formation without an increase in the rate of cell division. You do gene therapy by introducing normal copies of a gene into a tumor cell. The mutated copy of that gene had caused the tumor by promoting cell division. If the mutation were in a tumor-suppressor gene, would you expect these normal genes to block the tumor-promoting activity of the mutation? Why or why not? If the mutation were in an oncogene, would you expect these normal genes to block their tumor-promoting activity? Why or why not? Exposed chromosome ends and double strand breaks can lead to the messed up and unstable genome that is characteristic of cancer cells. What are three ways exposed chromosome ends and double strand breaks happen? Be specific. How does the cell respond to exposed chromosome ends and double strand breaks (what happens)? What is an "unstable genome"? How does this make things worse? d. What are the genetic consequences of all of this (i.e., what is a "messed up" genome)? Why is angiogenesis necessary for

Explanation / Answer

1). Mutations that inhibit cellular apoptosis also contribute to tumour formation because there is no cell death, means as the cell divides continuously (though the division is not uncontrolled), all the cell mass accumulates, which causes tumour formation.

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