Question 1
How do proto-oncogenes contribute to cancer when mutated?
Question 2
What role do proto-oncogenes play in normal cell cycles?
Question 3
What role does p21 have in relation to p53 and cell division?
Question 4
What effect does a faulty receptor have on cell division when proto-oncogenes mutate?
Question 5
What is the outcome if the p53 gene is mutated in both alleles?
Question 6
What is the significance of cyclin-dependent kinase inhibition in cell cycle control?
Question 7
What is required for a proto-oncogene to become an oncogene under the one-hit hypothesis?
Question 8
Which type of gene is known for creating proteins that act as a check on the cell cycle?
Question 9
Which hypothesis explains the necessity of a single mutation in proto-oncogenes for cancer risk?
Question 10
How can a growth factor binding influence a proto-oncogene's function?
Question 11
What type of mutation is most significant for p53's role in cancer prevention?
Question 12
In the two-hit hypothesis, what is required for tumor suppressor genes to promote cancer?
Question 13
What is the primary consequence of proto-oncogene mutation without external growth factors?
Question 14
What is the function of the p53 gene?
Question 15
What happens to a cell cycle when tumor suppressor genes are fully inactivated?