BIOLOGY 172 Lecture Notes - Lecture 28: Tumor Suppressor Gene, Angiogenesis, Metastasis

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taupecod750

20 Dec 2018

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We have many types of cells & many ways to disrupt the cell cycle, so there are many types of cancer. Multiple mutations that promote the cancer phenotype accumulate over time in one cell. Tissue invasion & metastasis - spread of cancer - tumors break off and spread. Sustained angiogenesis - growth of new blood vessels - don"t run out of nutrients. Mutations in cell growth & division, apoptosis, metastasis, angiogenesis. Hereditary retinoblastoma - mutation in tumor suppressor gene - predisposition to cancer ( runs in the family ) The other one mutates, then you get retinoblastoma. If p53 cannot bind to dna, it cannot activate its target genes to arrest cell division or trigger apoptosis. Over 50% of human cancer cells have p53 mutations. Oncogenes - promotes cell growth, hyperactivity causes cancer. Deletion or point mutation in coding sequence. Gene amplification - more copies of gene more protein. Proto-oncogene could be placed next to highly active enhancer.

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

1. The RAS proteinacquires a mutation that prevents release of GTP. Which of thefollowing characteristics are these cells likely toacquire?

A. Self-Sufficiency in growth signals
B. Insensitivity to anti-growth signals
C. Metastasis

2. Which of the following genes would you suspect to bea tumor supressor?
A. MSH2
B. CDK2
C. c-myc

3. A gene that is involved in a normal cellular processesbut when mutated contribute to cancer developmentis:
A. a proto-oncogene
B. a housekeeping gene

4. When a person carries a mutation in a tumor suppressorgene on one-chromosome and subsequently loses function of theirwildtype tumor suppressor allele, this describes:
A. gene conversion to an oncogene
B. loss of heterozygosity
C. haploinsufficiency

5. The mechanism by which alterations in DNA methylationcould promote carcinogenesis is:
A. by lengthening telomeres
B. by interacting with reactive oxygen species and thereforebecoming a potent mutagen
C. by either repressing or enhacing gene expression

6. When anaylzing a cell you find that it has aninactivating mutation in p53 and a mutation in the VEGF receptorthat makes activation independent of ligand binding. Which of thefollowing hallmarks would you expect the cell toexhibit?
I. self-sufficiency in growth
II. insensitivit to anti-growith signals
III. limitless replicative potential
IV. evading apoptosis
V. sustained angiogenesis

A. IV and V only
B. II, III, VI
C. I and III only

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BIOLOGY 172 Lecture Notes - Lecture 28: Tumor Suppressor Gene, Angiogenesis, Metastasis

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