RNA Tumor Virus (Herschman)

Question 1

RNA Tumor Viruses

Many growth factor receptors are what type of receptor?

Answer 1

ligand-dependent kinases

Question 2

RNA Tumor Viruses

T/F: Tumor cells divide more rapidly/traverse the cell cycle more rapidly than normal cells when in the cell cycle

Answer 2

FALSE: Tumor cells do not divide more rapidly/traverse the cell cycle more rapidly than normal cells when in the cell cycle.

Question 3

RNA Tumor Viruses

Name 2 ways that normal cells might lose growth control and become cancer cells.

Answer 3

The Go to G1 transition might become autonomous to Growth Factor control. Cells might loose their response to signals to exit the cell cycle.

Question 4

Define: Dominant Oncogene

Answer 4

genes that gain an autonomous function and can drive the cell into division even in the presence of a normal copy of the gene.

Question 5

Define: Tumor Suppressor Genes

Answer 5

Genes whose loss of function results in the ability of cells to express the cancer phenotype.

Both copies of gene must be mutated in order to get cancer.

Question 6

What are the gene components of a non tumorigenic virus?

Answer 6

2 LTR’s (Long Terminal Repeats), gag (glycosaminoglycan), pol (polymerase), env (envelope)

Question 7

What is the v-src gene?

Answer 7

v-src is an oncogene found in the Rous sarcoma virus that codes for pp60(v-src). pp60 is a tyrosine kinase. Causes sarcoma in chickens.

Question 8

Where did the v-src gene come from?

Answer 8

It likely originated as the human form, c-src. Recombination with the viral DNA introduced it into viruses, and subsequent mutations make it oncogenic.

Question 9

Can “defective” RNA tumor viruses that do not have either env, pol, or gag cause cancer?

Answer 9

Yes, if they exist in a cell that contains a wild-type virus that DOES have env, pol, gag, the “defective” RNA tumor virus can be packaged and infect surrounding cells

Question 10

What does a mitogen do?

(Hint: in relation to pathways we’ve studied before…)

Answer 10

Mitogen stimulation activates pathway that results in phosphorylation of restriction boundary (RB) protein. Phosphorylation of RB causes RB to dissociate from E2F and now E2F can stimulatio transcription of genes critical to G1/S transition.