You are leading a team of researchers at a pharmaceutical company. Your goal is to design drugs that help fight cancer. Specifically, you want to focus on drugs that bind to and inactivate certain proteins, thereby halting cell cycle progression. One of your team members suggests targeting the retinoblastoma (Rb) protein and inhibiting this protein. Will this approach be successful? Why or why not?

Question

A. This approach will be successful. Rb is tumor-suppressor protein, and functions to inhibit the action of a number of cell cycle regulatory proteins. A drug designed to inactivate the Rb protein would activate cell cycle inhibition. Lack of Rb activity would therefore inhibit the cell cycle regulatory proteins.
B. This approach will not be successful.  Rb is an oncogene, and functions to activate a number of cell cycle regulatory proteins.  A drug designed to inactivate the Rb protein would actually activate cell cycle progression.  As a result, this drug would likely make this situation worse for patients whose cancer cells contain mutant Rb.
C. This approach will be successful. Rb is an oncogene, and functions to activate a number of cell cycle regulatory proteins. A drug designed to inactivate the Rb protein would halt the cell cycle in cells that contain an active Rb.  As a result, cancer cells expressing a constitutively active Rb protein would be good targets for this type of therapeutic.
D. This approach will not be successful. Rb is tumor-suppressor protein, and functions to inhibit the action of a number of cell cycle regulatory proteins. A drug designed to inactivate the Rb protein would essentially create the same situation as in as a cell that lacks both copies of the Rb gene. Lack of Rb activity would release the inhibition of cell cycle regulatory proteins, thereby promoting cell cycle progression, rather than halting it.

Answer 1

Answer: D