Telomere Telomerase And Cancer

[mage lang=”en|es|fr|en” source=”flickr”]telomere telomerase and cancer[/mage]
If telomere shortening could be avoided (eg, telomerase), what do you think the benefits and risks would be?

Do you think cell senescence or slow or stop the aging increased cancer mechanical, such as longer life cells encourage such developments. Do you think you that any significant changes would occur?

A variety of syndromes of accelerated aging are associated with short telomeres. These include Werner syndrome syndrome, ataxia telangiectasia, Bloom, Fanconi anemia, Nijmegen breakage syndrome and ataxia telangiectasia, a disorder. The genes that are mutated in these diseases have a role in the repair of damage to DNA, and their precise roles in maintaining telomere length is an active area of ​​research. While it is unknown extent of erosion telomeres contributes to the normal aging process, maintenance of DNA, in general, and specifically to telomeric DNA, have emerged as key players. Dr. Michael Fossel has been suggested that telomerase therapy (see link) can be used not only to fight cancer, but to really get on aging and prolonging human life significantly. He believes that human trials of telomerase therapies based on extending the life occur in the next 10 years. This chronology is important because it coincides with the retirement of baby boomers United States and Europe. When cells are approaching the Hayflick limit in cell culture, the aging time can be extended by inactivation the tumor suppressor protein – TP53 and retinoblastoma protein (pRb). Cells that have been modified so eventually undergo an event called a "crisis" when the majority of cells in culture die. Sometimes a cell will stop dividing once they reach the crisis. Normally, the telomeres are lost, and the integrity of chromosomes is reduced at each subsequent cell division. Chromosome ends are exposed interpreted as a double-strand breaks (DSB) of DNA, this damage is usually repaired by reconnecting (religation) the broken ends together. When the cell is due to telomeres shortened, the ends of chromosomes may be set. This temporarily solves the problem of lack of telomeres, but during the anaphase of cell division the chromosomes fused randomly broken causing many mutations and chromosomal abnormalities. As this process continues, the genome of the cell becomes unstable. Over time, if enough damage will occur in the chromosomes of the cell so the cell dies (for programmed cell death (apoptosis or not), or an additional mutation with activities of telomerase. Intro: