an important gene to investigate in terms of cancer and tumorigenesis. The hTERT gene has been examined for mutations and their association with the risk of contracting cancer. Over two hundred combinations of hTERT polymorphisms and cancer development have been found. There were several different types of cancer involved, and the strength of the correlation between the polymorphism and developing cancer varied from weak to strong. The regulation of hTERT has also been researched to determine possible mechanisms of telomerase activation in cancer cells. Importantly, mutations in the hTERT promoter were first identified in melanoma and have subsequently been shown to be the most common noncoding mutations in cancer. Glycogen synthase kinase 3 (GSK3) seems to be over-expressed in most cancer cells. GSK3 is involved in promoter activation through controlling a network of transcription factors. Leptin is also involved in increasing mRNA expression of hTERT via signal transducer and activation of transcription 3 (STAT3), proposing a mechanism for increased cancer incidence in obese individuals. There are several other regulatory mechanisms that are altered or aberrant in cancer cells, including the Ras signaling pathway and other transcriptional regulators. Phosphorylation is also a key process of post-transcriptional modification that regulates mRNA expression and cellular localization. Clearly, there are many regulatory mechanisms of activation and repression of hTERT and telomerase activity in the cell, providing methods of immortalization in cancer cells. Therapeutic potential 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 normal human cells. It has been found that dominant-negative mutants of hTERT could reduce telomerase activity within the cell. This led to apoptosis and cell death in cells with short telomere lengths, a promising result for cancer treatment. Although cells with long telomeres did not experience apoptosis, they developed mortal characteristics and underwent telomere shortening. Telomerase activity has also been found to be inhibited by phytochemicals such as isoprenoids, genistein, curcumin, etc. These chemicals play a role in inhibiting the mTOR pathway via down-regulation of phosphorylation. The mTOR pathway is very important in regulating protein synthesis and it interacts with telomerase to increase its expression. Several other chemicals have been found to inhibit telomerase activity and are currently being tested as potential