Biology 2581B Lecture Notes - Lecture 12: Tumor Suppressor Gene, Oncogene, Chromosome Instability

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1 Mar 2019

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Tumor suppressor gene: growth inhibitory: mutations in tumor suppressor genes contribute to the development of cancer by inactivating that inhibitory function = loss-of-function mutations, mutations in tumor suppressor genes are recessive. Many are located in introns + in other dna that isn"t transcribed and translate. Epigenetic changes: alterations to chromatin structure that affect gene expression. Cancer cells have significant alterations to their dna methylation patterns and histone structure: dna methylation is often associated with repression of transcription, hypomethylation leads to transcription of oncogenes, stimulates cancer. Some cpg islands are hypermethylated, which may inhibit transcription of tumor- suppressor genes + stimulate the development of cancer. Histone proteins in nucleosomes are often abnormally modified in cancer cells. Example of how epigenetic changes can be associated with tumor growth. Some types of tumors are consistently associated with specific chromosome mutations, yet many cancers are not (have individual gene mutations)

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Classify the statements below as describing proto-oncogenes or tumor suppressor genes.

1. Some products of these genes normally function in repairing damaged DNA.

2. These genes code for proteins that normally promote cell division.

3. Mutations that increase activity of these genes may lead to cancer.

4. These genes code for proteins that normally prevent uncontrolled cell division.

5. Loss-of-function mutations in these genes may lead to cancer.

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B__1) Driver mutations provide a growth advantage to a tumor cell. Which type of mutation is known to accumulate in cancer cells but has no direct contribution to the cancer phenotype?

A) alteration mutations B) passenger mutations C) carrier mutations

D) indirect mutations E) insignificant mutations

_A__2) Which of the following general mechanisms appear to be involved in the formation of cancer cells?

A) genomic instability, DNA repair failure, chromatin modifications

B) inversions, operon formation, methylation

C) RNA failure, DNA phosphorylation, phosphorylation of adenyl cyclase

D) transdetermination, mutation, allosteric interactions

E) suppression, tabulation, projection

_A__3) What is the name of the protein that combines with cyclins to exert local control of the cell cycle?

A) cyclin-dependent kinase B) phosphatase C) ATPase D) integrase E) hexokinase

_D__4) A protein functions as a cell-cycle regulator that causes cell death (apoptosis) to a damaged cell. What is the symbol given to this protein?

A) p34 B) p102 C) cyclin D) p53 E) phosphokinase

_A__5) The retinoblastoma protein (pRB), like p53, serves as a(n) ________ in regulating the cell cycle.

A) tumor suppressor B) tumor enhancer C) up regulator D) oncogene E) pseudooncogene

_C__6) Mutant versions of genes that are normally involved in promoting the cell cycle are known as ________.

A) tumor suppressors B) proto-oncogenes C) oncogenes D) malignant genes E) attenuators

_B__7) In sporadic cases of retinoblastoma, how many gene mutations are thought to be necessary in the same cell for a tumor to develop?

A) one B) two C) four D) six

__D_8) What is the name of the protein that appears to regulate the entry of cells into an S phase? This protein is also known as the "guardian of the genome."

A) p34 B) p102 C) cyclin D) p53 E) phosphokinase

1.) You are studying a particular type of cancer. You observe that the cells are expressing higher than normal levels of the activated version of the G protein Ras (ie, they contain more Ras-GTP than normal).

a.(2 pts) Further study shows that the one of the Ras genes has been mutated, would you classify this as the mutation of a tumor-suppressor gene or an oncogene?

b.(2 pts) Given your knowledge of the regulation of G proteins, suggest an explanation for how this mutant Ras protein results in more Ras-GTP than normal.

c.(2 pts) In a different cancer you also observe an increase in the activated form of Ras, however, in this case, the mutation has occurred in both copies of a gene encoding a protein that normally interacts with Ras. The mutant forms of the protein no longer interact with Ras and this leads to inappropriate growth. Since the mutation leads to cancer, would this loss of function be an example of an oncogene or a tumor-suppressor? Can you suggest a function for this protein?

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Biology 2581B Lecture Notes - Lecture 12: Tumor Suppressor Gene, Oncogene, Chromosome Instability

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