Question

1) Only damaged cells will undergo apoptosis. Explain why this is true or false.

2) Describe 2 different ways that a gain of function in a receptor tyrosine kinase receptor could lead to increased growth and/or survival for a cancer cell.

3) Explain how cancer development be compared to evolution in terms of mutations? Relate this to why cancer is more prevalent with age.

4) Explain why p53 is referred to as “the guardian of the genome” in your own words. Be sure to discuss its normal function, it’s role in cell signaling, and the responses to DNA damage. Then what happens in cancer?

5) Why are targeted therapies more desirable than classical cancel treatments?

6) Predict what would happen to the cell cycle in a cell if the following mutations took place:

1. )       A mutation alters Cdk so that it doesn’t need cyclin to be active.
2. )       A mutation inactivates the kinase part of the cyclin-Cdk complex (no phosphorylation).

Answer 1

Answer 1. False. Because even undamaged cells undergo apoptosis to aid in proper development of the organism. Eg. during metamorphosis of tadpole to frog, the tail is reabsorbed by apoptosis of cells. Hence the answer is false.

Answer 2. Gain in function mutation refers to the activation of receptor tyrosine kinase(RTK) even in absence of ligand or growth signal. A mutation in the one of the exons of the conserved regions of RTK can cause the RTK to hyperactivate and further signal down to confer oncogenic properties. Another way is the overexpression of RTK on the cells caused mainly due to abnormal gene amplification enabling multiple growth signals confering oncogenic properties.