Question 1

Considering the clonal evolution of tumors,mutations in which kinds of genes would speed up the rate of mutations?
a.structural genes
b.metabolism genes
c.DNA-repair genes
d.nuclear-import genes

DNA - repair genes

Accepted Answer

Mutations in DNA-repair genes would speed up the rate of mutations in tumors as these genes are responsible for repairing any errors or damages in DNA. Therefore, mutations in these genes would mean that errors or damages are not being properly repaired, leading to more mutations accumulating at a faster rate.

Question 2

Which of the following is true of tumor-suppressor genes?
a.Their normal function is to promote cell proliferation.
b.Their mutant forms are typically dominant.
c.They were the first cancer-causing genes to be identified.
d.None of the above is true of tumor-suppressor genes.

Accepted Answer

Tumor-suppressor genes are genes whose normal function is to inhibit cell proliferation, and mutations in these genes can lead to the uncontrolled growth of cells, which is a hallmark of cancer. Mutations in tumor-suppressor genes are typically recessive, meaning that both copies of the gene (one inherited from each parent) must be mutated in order for the gene's function to be lost. Tumor-suppressor genes were discovered after the discovery of oncogenes, which are genes that promote cell proliferation and can also contribute to the development of cancer.

Question 3

In an experiment you mutate the retinoblastoma gene RBsuch that its gene product behaves as if hyperphosphorylated.The result would be a ______ association between RB and E2F,with _______ transcription of genes necessary for DNA replication.
a.stronger; unregulated
b.stronger; tightly regulated
c.weaker; unregulated
d.weaker; tightly regulated

weaker; unregulated

Accepted Answer

Hyperphosphorylation of the RB protein leads to a weaker association with E2F, allowing E2F to activate transcription of genes necessary for DNA replication in an unregulated manner.

Question 4

In cancer cells you notice that the chromosomes are not shortening,even after many cell divisions.A mutation in the expression of which gene might lead to this observation?
a.DNA-repair genes
b.retinoblastoma
c.palladin
d.telomerase
e.ras

Accepted Answer

Telomerase is responsible for maintaining the length of telomeres, which protect the ends of chromosomes during cell division. Cancer cells often have high levels of telomerase activity, which allows them to continue dividing without shortening their telomeres. A mutation in the expression of telomerase could lead to the observation that the chromosomes are not shortening.

Deck 15: Cancer Genetics