Biology 1002B Lecture Notes - Lecture 17: Tumor Suppressor Gene, Oncogene, Microrna

15 views4 pages

pinkserval403

27 Jan 2020

School

Western University

Department

Biology

Course

Biology 1002B

Professor

Tom Haffie Denis Maxwell

For unlimited access to Class Notes, a Class+ subscription is required.

Document Summary

Lecture 17-outcomes: general role of cyclin/cdk complexes in regulation of cell cycle checkpoints (not the specific. In cancer cells, the proto-oncogenes are deregulated and become oncogenes, genes that stimulate the cell to progress to the cancerous state of the unregulated cell cycle. The incidence of cancers increases upon exposure to mutagens, agents that cause mutations in dna. Particular chemicals and certain kinds of radiation are effective mutagens: 4. Particular chromosomal mutations are associated with specific forms of cancer. In these cases, chromosomal breakage affects the expression of genes associated with the regulation of cell division: 5. Some viruses carry cancer genes with them, while others contain viral genes that disrupt normal cell cycle control of host cells: explanation for why cancer incidence tends to increase with age. 0. 27-0. 42, relatively little: role of proto-oncogenes, tumor suppressor genes and oncomirs in normal organismal metabolism/development expression of proto-oncogenes promotes cell cycling, ex.

Related Questions

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

The Myc gene is a very important proto-oncogene that encodes the Myc transcription factor. The Myc gene is normally only expressed in response to the presence of growth factors, and once expressed the Myc protein promotes passage through the restriction point by activating the transcription of early cell cycle genes. As an indication of the importance of Myc, overexpression of the Myc protein is sufficient to cause tumorigenesis in many cell types. For example, Burkittâs lymphoma is the result of a chromosomal translocation that leads to increased myc expression in B-lymphocytes.

(A) (3 pts) What is the restriction point, and which CDK complex is most directly activated by passage through the restriction point?

(B) (10 pts) Describe how activation of the CDK complex from part (A) leads to entry of cells into S-phase. Your answer must indicate the protein(s) that this CDK directly acts on, the proteins that directly stimulate S-phase entry, and the mechanism that prevents premature entry into S-phase.

(C) (8 pts) Indicate whether each protein you mention in part (B) is a proto-oncoprotein (e.g. a protein encoded by a proto-oncogene) or a tumor suppressor. You can incorporate this into your answer to part (B) if you choose.

(D) (4 pts) Why does the overexpression of Myc lead to cancer, for example Burkittâs lymphoma?

The survival, __________________, and size of each cell in an animal are controlled by extracellular signal molecules secreted by neighboring and distant cells. Many of these signal molecules bind to a cell-surface __________________ and trigger various intracellular signaling pathways. One class of signal molecules, called __________________, stimulates cell division by releasing the molecular brakes that keep cells in the __________________ or __________________ phase of the cell cycle. Members of a second class of signal molecules are called __________________, because they stimulate cell growth and an increase in cell mass. The third class of signal molecules, called __________________, inhibits __________________ by regulating members of the __________________ family of proteins. In addition to such stimulatory factors, some signal proteins such as __________________ act negatively on other cells, inhibiting their survival, growth, or proliferation.

anaphase differentiation myostatin

annihilation G₀ nourishment

apoptosis G₁ nutrition

arrestase G₂ phosphatases

Bcl2 growth factors proliferation

biosynthetic interphase receptor

cascades ligand S

caspase M survival factors

Cdk mitogens transcription

cyclin

blushbeaver438

Biology 1002B Lecture Notes - Lecture 17: Tumor Suppressor Gene, Oncogene, Microrna

Document Summary

Get access

Related Documents

Biology 1002B Lecture Notes - Tumor Suppressor Gene, Synonymous Substitution, Open Reading Frame

Biology 1002B Lecture Notes - Lecture 18: Cyclin-Dependent Kinase, Post-Translational Modification, Tumor Suppressor Gene

Biology 1002B Lecture Notes - Lecture 18: Tumor Suppressor Gene, Colorectal Cancer, Prostate Cancer

Related Questions