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Human Telomerase Reverse Transcriptase Essay

1309 words - 5 pages

The naked mole-rate (NMR) is a mammal that can live up to three decades while the common household mouse lives up to 4 years. While NMR have died of natural age related causes, death because of cancer hasn't been observed (Liang, et al., 2010). Human telomerase reverse transcriptase (hTERT) role in tumorigenesis is important in the understanding of how cancer develops and grows. Figuring out how and why the NMR is cancer resistance could model how future anti- cancer drugs be more direct and effective in recognizing and destroy cancerous tumors.
For cancer to develop a normal cell requires many changes. An important barrier that is needed for a normal cell to become cancerous is overcoming the replicative senescence barrier ( Sun, t. al., 2004). Replicative senescence is the process that limits the growth of human cells. An important part of replicative senescence are telomeres. Telomeres are located at the ends of eukaryotic chromosomes, and consist of repeat GC sequences (Zhou, et. al., 2014). Whenever a cell undergoes replication, the cell’s telomeres are shortened. Telomerase is a ribonucleoprotein that is essential for the maintenance of telomeres. Cancer cells continue to replicate and with hTERT the cancer cells are immortal because of the continued lengthening of telomeres cancer cells can continue to replicate without entering crisis (when cells cease to exist or die).
There are two models that show how replicative senescence/crisis act as a mechanism for tumor suppression. the first model shows that without telomerase or other telomere lengthening mechanism cells would not be able to have tumorigenic properties. The second model shows that telomere shortening or the absence of telomerase does not prevent tumorigenic properties from existing but instead limits the number of replications. This was tested on human and bovine adrenocortical cells who were retrovirally infected with Simian virus 40 large T antigen (SV40 TAg) and Rat Sarcoma G12V (Ras), known oncogenes. A small period after infection; the infected cells were introduced into immunodeficient mice. Both the human and bovine cells entered tumorigenic state. the cells became fully malignant with evidence of tumours distant from the point of infection. The formation of malignant tumors in cells only expressing SV40 TAg and Ras was unexpected since the same oncogenic combination was found previously not tumorigenic without the presence of hTERT and SV40 small T antigen in other human cell types (Sun, et. al., 2004). However, there was a decrease in malignant properties found in tumours formed from SV40 TAg and Ras expressing cells because the cells appeared to enter crisis. This was a result of telomere shortening that is evidenced by anaphase bridges (end to end fusion of chromosomes). This is consistent with the second model hypothesized earlier since the continued shortening of telomeres reduced the tumorigenicity of the adrenocortical cells. Since the problem with the cells...

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