Tumor-suppressor genes includes p53 and Rb. How would a "gain-of-function" mutation likely affect the cell?
|A)||The cell would divide constantly because of the loss of cell cycle repression.|
|B)||The cell would divide much less frequently because of the extra cell cycle repression.|
|C)||The cell would divide normally because these genes have no effect on cell cycle control.|
|D)||The cell would commit suicide by apoptosis.|
In lab, you are studying cell cycle control in the fission yeast, S. pombe. A student finds a new mutant that she wants to call "giant" because the cells are much larger than normal (suggesting that it is not dividing normally.) What type of mutation do you think your student has isolated?
|A)||a loss-of-function mutation in a tumor-suppressor gene|
|B)||a loss-of-function mutation in a cellular proto-oncogene|
|C)||a gain-of-function mutation in a tumor-suppressor gene|
|D)||a gain-of-function mutation in a cellular proto-oncogene|
|E)||Both a and d are possible.|
|F)||Both b and c are possible.|
Which of the following would be an effective approach to a new cancer therapy?
|A)||finding a way to stabilize p53 specifically in tumor cells|
|B)||preventing nucleotide synthesis in tumor cells|
|C)||inactivating the HER2 receptor on tumor cells|
|D)||inhibiting growth of new blood vessels with endostatin|
|E)||All of the above would help to fight cancer.|
How would the cell cycle be affected if you removed the phosphorylation sites in the Rb protein?
|A)||The cell cycle would not be affected because pRb is not phosphorylated normally.|
|B)||The cell cycle would be blocked in G1.|
|C)||The cell cycle would be blocked in G2.|
|D)||The cell cycle would be shorter.|
Embryonic stem (ES) cells are an attractive source of material for therapeutic cloning because
|A)||they can be induced to assume any cell fate.|
|B)||ES cells are not targets for the host immune response, so tissue rejection is not an issue.|
|C)||there are no other sources of stem cells to use for therapeutic cloning, so ES cells are the only solution.|
|D)||ES cells will not work as a source of tissue for cloning.|
How would growing cells in the presence of methyladenosine affect the mismatch repair system?
|A)||The repair system would only repair half of the errors introduced by DNA polymerase.|
|B)||There would be no repair of mismatched DNA.|
|C)||Mismatch repair would be normal, but excision repair would fail.|
|D)||Methyladenosine would prevent DNA replication, so there would be no need for mismatch repair.|
Too much time in a tanning booth probably causes DNA damage to epithelial cells. The most likely effect would be
|D)||single-stranded nicks in the phosphodiester backbone.|
Using a "car and driver" analogy, which of the following accurately describes the role of tumor-suppressor genes and proto-oncogenes in normal cells?
|A)||Tumor-suppressor genes are the gas pedal, while proto-oncogenes are the brakes.|
|B)||Tumor-suppressor genes are the brakes while proto-oncogenes are the gas.|
|C)||Both tumor-suppressor genes and proto-oncogenes are like the gas, but tumor-suppressors are like turbo and proto-oncogenes are like a regular carburetor.|
|D)||Tumor-suppressor genes are like the steering wheel, and proto-oncogenes are like the turn signals.|
During the early years of cancer research, there were two schools of thought regarding the causes of cancer: 1) that cancer was caused entirely by environmental factors, and 2) that cancer was caused by genetic factors. Which was correct?
|A)||#1 because we have identified many potential carcinogens|
|B)||#2 because we know of many proto-oncogenes|
|C)||#2 because we know of many tumor-suppressor genes|
|D)||Both were correct; most chemical carcinogens function by altering genes.|
If you found a specific chromosomal deletion in the genome from a tumor, what could be the cause of this specific cancer?
|A)||The deletion likely affected a tumor-suppressor gene, leading to a loss of function in the tumor cells.|
|B)||The deletion likely affected a proto-oncogene, leading to a loss of function in the tumor cells.|
|C)||The deletion likely affected a tumor-suppressor gene, leading to a gain of function in the tumor cells.|
|D)||The deletion likely affected a proto-oncogene, leading to a gain of function in the tumor cells.|