In addition to potential preventative therapies that may offset or prevent cancer by repairing telomeres, Telomolecular is focused on the discovery of inducible genes and enzymes that may reactivate p53 DNA damage checkpoint control activator, pRB tumor suppressor, and other tumor suppressors. Special agreements have been reached with partners in this area. Inactivation of the p53 tumor suppressor protein, by mutation or by viruses, has been identified in over one-half of all human tumors. The inactivated protein usually has reduced DNA-binding capacity, which renders it ineffective in regulating cell division and cell growth. Delivery of the p53 gene to tumor cells has led to the elimination of the tumor in both animal models and some early clinical studies. The retinoblastoma protein (pRb)/cyclin/cyclin-dependent kinase (Cdk)/p16 tumor-suppressor pathway participates in the regulation of cellular proliferation and undergoes mutational or epigenetic inactivation in essentially 100% of selected human malignancies. Since this pathway is frequently altered by inactivation of either the RB gene or the upstream Cdk4/6-inhibitor gene, Cdkn2a/p16ink4a, it is commonly referred to as the RB/p16 tumor-suppressor pathway. Reactivating this pathway delimits human cancers.

Telomolecular is developing a pipeline of cutting edge technologies that may effectively address many forms of cancer including:

1. hTert mediated putative therapy (HMPT)
2. Reactivation of tumor suppressor genes (RTSG)
3. Reactivation of DNA damage checkpoint control (RDDCC)

Telomeres and cancer are interdependent subjects. More than 90% of all cancer is caused by critical telomere shortening, for example, in 97% of premalignant endothelial lesions critical telomere shortening is observed (Meeker, John Hopkins University 2005). These "destabilized" cells have a tendency to transform as a result of end-to-end chromosomal fusions or as a result of a generally high metastatic potential due to down regulated protein production. After the accumulation of critical errors a cell may immortalize. Immortal cells express high levels of telomerase, which stimulates cell proliferation and permits cancer cells to grow without limitation. When p53 DNA damage checkpoint control and pRB tumor suppressor pathways have been deactivated, immortalization in normal somatic cells is dangerous. Paradoxically, p53 and p16 pathways do not tend to inactivate when chromosomal telomeres are healthy, even if immortalized. In the laboratory, immortalization of normal somatic cells does not lead to the development of cancer and generally prohibits "cell crisis", a fundamental process that is required in the development of most cancer. In hundreds of parallel experiments, when immortalized cell lines are pushed beyond their traditional replicative capacities cancer has never been observed.