The enzyme telomerase is used to extend the cancer cell's life span. Cancer cells become immortalized through telomere maintenance mechanisms, such as telomerase reverse transcriptase (TERT) activation. While telomerase does not drive the oncogenic process, it is permissive and required for the sustain growth of most advanced cancers. Researchers were surprised to discover a new way that an enzyme in cancer cells, telomerase, acts to keep cancer cells multiplying. The knowledge of the basic biology of telomeres and telomerase has yielded fundamental insights into both cancer prevention and cancer promotion.

The presence of telomerase in various human cancers and its absence in many normal cells mean the enzyme might serve as a good target for anticancer drugs. As such, TERT is an antigen of great relevance to develop widely applicable immunotherapies.

Increased telomerase expression produces vulnerability of cancer cells, distinguishing them from normal cells in the body, although normal cells do also have some active telomerase.

Telomerase reverse transcriptase (TERT) is a conserved self-tumor antigen which is overexpressed in most tumors and plays a critical role in tumor formation and progression. Telomerase is commonly expressed in human cancer cells. Its reactivation is associated with the acquisition of immortalization and malignancy.

Telomerase and Cancer - PubMed Telomerase, a eukaryotic ribonucleoprotein (RNP) complex, contains both an essential RNA and a protein reverse transcriptase subunit. Telomerase is an attractive cancer target as it appears to be required in essentially all tumours for immortalization of a subset of cells, including cancer stem cells.


Endometrial cancer is the fourth common cancer in women in the UK and is the commonest gynecological cancer (CRUK). Telomerase by necessity would have to be carefully regulated in large long-lived species to avoid the early onset of cancer, whereas in smaller mammals, such as mice, telomerase is known to be more promiscuous and most inbred strains of mice have very long telomeres compared with humans, but the reasons for this are not well understood. In addition, normal human cells including stem cells have lower telomerase activity and generally maintain telomeres at longer lengths compared to cancer cells. Telomerase by necessity would have to be carefully regulated in large long-lived species to avoid the early onset of cancer while in smaller mammals, such as mice, telomerase is known to be more promiscuous and most inbred strains of mice have very long telomeres compared to humans but the reasons for this are not well understood. The maintenance of telomeres by the cellular ribonucleoprotein enzyme telomerase is of well-documented importance for cancer. Recent studies also suggest that telomerase is implicated in tumor progression in unexpected ways. While every cell in the body has the genetic coding to produce telomerase, only certain cells actually need it.

However, telomerase-associated gene signatures in cancer remain elusive. This is a major reason that cancer cells can accumulate over time, creating tumors.
In addition to maintaining telomere length, TERT activates manifold cell survival signaling pathways. Targeting telomerase for cancer therapy Ideal cancer therapeutic targets are those that are specific for certain tumors and that pose a threat for maintaining its malignancy. Cancer cells make telomerase, however, preventing the telomeres from becoming so short that the cells can no longer survive. Telomerase and Cancer.

Telomerase, a eukaryotic ribonucleoprotein (RNP) complex, contains both an essential RNA and a protein reverse transcriptase subunit. Therefore, aging and cancer are two ends of the same spectrum.

On one hand, it is possible that having too … The telomerase holoenzyme, which has a highly conserved role in maintaining telomere length, has long been regarded as a high-profile target in cancer therapy due to the high dependency of the majority of cancer cells on constitutive and elevated telomerase activity for sustained proliferation and immortality. Moreover, differences in telomerase expression, telomere length and cell kinetics between normal and tumour tissues suggest that ta … This site needs JavaScript to work properly.


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