Search results
Results from the WOW.Com Content Network
The lack of telomerase does not affect cell growth until the telomeres are short enough to cause cells to "die or undergo growth arrest". However, inhibiting telomerase alone is not enough to destroy large tumors. It must be combined with surgery, radiation, chemotherapy or immunotherapy. [57]
This occurs through telomerase activation or the activation of a telomere-recombination pathway (i.e., the ALT pathway). [ 22 ] [ 25 ] Thus, cancer cells have short telomeres because they progress through an intermediate stage of telomere shortening—caused by division after DNA damage checkpoint inactivation—before enabling mechanisms for ...
If increased telomerase activity is associated with malignancy, then possible cancer treatments could involve inhibiting its catalytic component, hTERT, to reduce the enzyme's activity and cause cell death. Since normal somatic cells do not express TERT, telomerase inhibition in cancer cells can cause senescence and apoptosis without affecting ...
The steady shortening of telomeres with each replication in somatic (body) cells may have a role in senescence [19] and in the prevention of cancer. [ 20 ] [ 21 ] This is because the telomeres act as a sort of time-delay "fuse", eventually running out after a certain number of cell divisions and resulting in the eventual loss of vital genetic ...
Alternative Lengthening of Telomeres (also known as "ALT") is a telomerase-independent mechanism by which cancer cells avoid the degradation of telomeres.. At each end of the chromosomes of most eukaryotic cells, there is a telomere: a region of repetitive nucleotide sequences which protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes.
This could not have been demonstrated until he had demonstrated that normal cells are mortal. [3] [4] Cellular senescence does not occur in most cancer cells due to expression of an enzyme called telomerase. This enzyme extends telomeres, preventing the telomeres of cancer cells from shortening and giving them infinite replicative potential. [14]
Whether inflammation is present in the body before or after a cancer diagnosis, it affects all life stages of cancer—part of what Ravella calls the “tumor microenvironment” — “from the ...
The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).