BIO120H1 Lecture : Notes taken during lecture

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redtermite204

30 Mar 2011

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C-cadherin and integrin feed into cell cell to cell contact cell know if other cells around, modifying cell proliferation. Myc = growth factors through receptor tyrosine kinases regulating myc expression, which regulates cell cycle. Cyclin b brings cell up to dna synthesis. All human cancers have rb misregulation and p53, especially rb misregulation or mutation. There are ~10 to the power of 14 cells in the human body . small percentage of these cells divide, make two daughter cells. every time cell divides, dna replication is imperfect. body can recognize that and cell undergoes programmed cell death, and its removed from system. get too big and push on something important, cut off circulation of something important: 24 hours in cell cycle at maximum rate of division. how long would it take the tumour to be too big. uncontrolled proliferation -> mass of abnormal cells .

Related Questions

Her2 is an EGF receptor family member that drives proliferation of cells including in the breast. Too much Her2 signaling can contribute to Her2 positive breast cancer. Mutations can be generated in different proteins in the Her2 signaling pathway. The following are 5 different possible mutations.

Mutant a: Ras protein that cannot exchange GDP for GTP.

Mutant b: RAF protein with a mutation in the active site such that ATP does not bind.

Mutant c: Her2 receptor that lacks tyrosines in its intracellular domain.

Mutant d: MAPK that is constitutively active.

Mutant e: Myc expressed 10X higher than normal.

The following cell lines with mutations in Her2, Ras/MAPK pathway are treated with the ligand for the Her2 receptor and compared to normal cells treated with ligand. For each Her2 mutant pathway cell line, describe whether myc synthesis is higher or lower compared to normal cells and if proliferation (cell division) is higher or lower compared to normal cells treated with ligand

A. Cell line with mutations a and b.

B. Cell line with mutations c and e

C. Cell line with mutations d and e

D. Rb is also important for regulation of the cell cycle at the restriction point or start. What would be the effect on myc and cell proliferation of a mutation that switched all the serines and threonines that are phosphorylated to alanine?

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

You are interested in studying the origins of cancer and join a research lab to do so. You find that many cancer cell lines have mutations in the gene DRG1. You further investigate the mutations to DRG1 and find that some of the cell lines have mutations that affect expression of DRG1, so that no DRG1 mRNA is made in these cells, while other cell lines have mutations that lead the cells to produce a non-functional DRG1 protein.

a) Is DRG1 a proto-oncogene or a tumor suppressor? Explain your reasoning.

b) Your labmates propose several hypotheses about the possible role for DRG1 in normal cells. For each hypothesis, state whether or not you think it makes sense and explain your reasoning. a. DRG1 normally acts to repair DNA damage. b. DRG1 is a receptor for a mitogen (a signaling molecule that promotes cell division)

c. DRG1 is a receptor for a signaling molecule that causes apoptosis (programmed cell death).

BIO120H1 Lecture : Notes taken during lecture

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