Anatomy and Cell Biology 4411B Lecture Notes - Cytostasis, E2F, Proteasome

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tanhippopotamus305

23 May 2012

School

Western University

Department

Anatomy and Cell Biology

Course

Anatomy and Cell Biology 4411B

Professor

Gannareddy

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Document Summary

Fasl: altered gene expression (increase the expression of p16 and p21, de- creased expression of c-fos and cyclins, causes of cellular senescence. Senescence: telomere-dependent senescence - stretches of repetitive dna and associated proteins that cap the ends of linear chromosomes and protect them from degradation or fusion by dna-repair processes. Cell lose 50-200 base pairs of telomeric dna during each s-phase. The end-replication problem will eventu- ally render the telomeres too short and critically non-functional. This causes cells to not proliferation indefinitely because the lack of telomeres will cause. Dna damage and the cell will senesce: dna damage will also cause senescence. This depends on p53, p16 and p21: senescence caused by chromatin perturbation - chromatin state determines the extent to which genes are active (euchromatin) or silent (heterochro- matin). Histone deacetylase inhibition (hdai) is thought to induce senes- cence. Decrements in neurogenesis, haematopoesis and pancreatic function due to a decrease in progenitor and stem cells.

Related Questions

Match:

( ) The ability to degrade the extracellular matrix and basal membrane in order to migrate throughout normal tissue, enter and exit vessels, and colonize a new site in the body.

( )Altering growth factors, receptors, signaling cascades, and transcription factors in order to stimulate the expression of growth promoting genes and the cell cycle.

( ) Increasing expression of proteins such as VEGF that stimulate the production of new vasculature to supply oxygen and nutrients to the tumor.

( ) Loss of function mutations in or deletion of gatekeeper and caretaker genes altering cell cycle progression and DNA damage repair pathways.

( )Altering expression of proteins and enzymes that lengthen telomeres and avoid cellular senescence.

( ) Bypassing normal cellular mechanisms that help to eliminate faulty or infected cells.

A. Enabling Replicative Immortality B. Avoiding Immune Destruction C. Deregulating Cellular Energetics D. Evading Cell Death E. Evading Growth Suppressors F. Activating Invasion and Metastasis G. Sustaining Proliferative Signaling H. Inducing Angiogenesis I. Tumor-Promoting Inflammation

rubypig988

What role do telomeres and telomerase play in cancer progression?

	A.	Telomeres are needed for the chromosome fusions that often occur in cancer cells, so telomerase must be reactivated for cancer to progress.
	B.	Telomerase is usually turned off in cancer cells, allowing the cell to lose its telomeres and enter apoptosis.
	C.	Telomerase activity causes cells to avoid the process of apoptosis, so most healthy cells keep telomerase on. When telomerase is turned off, a cell can progress into a precancerous state.
	D.	Telomere shortening is a natural process that limits the number of divisions a cell can undergo, but if telomerase becomes active in a cell, then the cell can reenter a proliferative phase.

I am trying to understand the importance of proliferation limitsand cell senescence. In particular, I would like to compare theproliferation limit of Embryonic Stem cells (ES) and fibroblasts(which would be trans-differentiated) and describe how thisdifference plays a role when thinking about engineering organs, forexample a heart transplant.

How do ES cells and fibroblasts compare with regards to theHayflick limit?

Anatomy and Cell Biology 4411B Lecture Notes - Cytostasis, E2F, Proteasome

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