Which of these events do you think is likely to promote tumorigenesis in affected cells? Group of answer choices DNA methylation of the promoter region of a tumor suppressor gene Hypermethylation of transcription factors that antagonize Wntsignaling Open chromatin in the region of of DNA harboring an activating mutation of beta-catenin All of these

Which of the following chromosomal changes would be LEAST likely to cause the development of cancer? a chromosomal deletion of a region containing the tumor suppressor gene duplication of a tumor suppressor gene a loss-of-function mutation in a tumor suppressor gene DNA methylation of the promoter of a tumor suppressor gene a mutation in a regulatory element that disrupts transcription of a tumor suppressor gene

There are three broad categories of cancer-related genes: proto-oncogenes, tumor suppressor genes, and DNA repair/stability genes. Distinguish between these three groups, then indicate which you think RB1 belongs to.

Mutations that increase the creation of blood vessels and turn on expression of telomerase are.... Group of answer choices not involved in tumor development. often seen in the very beginning of tumor development. important to help the tumor to continue growing after the cancer has started.

In your own words, explain how cancer cells differ from normal cells in regard to the following: Telomeres, which are products of telomerase enzyme

Which of the following could be classified as an oncogene? None are possible oncogenes A mutant of MAP kinase that was active with or without being phosphorylated All are possible oncogenes A mutant of MEK with significantly reduced enzyme activity A mutant cAMP phosphodiesterase that made it super-active

Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth.        the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.

How does p53 induce apoptosis?  How does the cell determine what "too much" damage is? Meaning, how can it tell if the damage to the DNA is too severe to fix in order for the cell to move on to S phase? Thank you.

Which of the following types of mutations would be most likely to cause cells to undergo apoptosis (programmed cell death)?     One that increases the affinity of p21 for Cdks     One that decreases the affinity of Rb for the transcription factor E2F     One that decreases the ability of p53 to bind to DNA     One that causes p53 to be constitutively phosphorylated

Artificially induced apoptosis (controlled cellular death) is found to be an effective treat- ment for some forms of cancer. Which of the following describes the most likely mechanism by which apoptosis might be induced? A B с D by causing ribosomes to increase the rate of protein synthesis by triggering the division of mitochondria in the cell to increase ATP production by increasing the expression of membrane-bound glucose protein channels by causing lysosomes to release digestive enzymes into the cytosol