TELOMERASE : SENESCENCE AND CANCER
Evidence is now forthcoming that telomerase is not active in all the mammalian cells. This is mainly
because cells that have undergone differentiation no longer divide or divide only to a limited extent.
Telomerase is highly active in the early embryo, and after birth it is active in the reproductive and
stem cells. Stem cells divide continuously throughout the lifetime of an organism to produce new
cells. These cells in turn are responsible to tissues and organs in the functional state e.g.
hematopoietic stem cells of bone marrow. Many biologists limit the process of telomere shortening
with cell senescence (i.e. cell death). This is mainly based on the observations made in the in vitro
mammalian cell cultures. However, some researchers question this relation between telomere
shortening and senescence Cancerous cells are able to divide continuously. There is a strong
evidence to suggest that the absence of senescence in cancer cells is linked to the activation of the
enzyme telomerase. Thus, telomere length is maintained throughout multiple cell divisions. lt is
however, not clear whether telomerase activation is a cause or an effect of cancer. There is
however, evidence to suggest that telomerase activation is in fact the cause of certain cancers e.g.
dyskeratosis congenita due to a mutation in the gene responsible for the RNA component of
telomerase. The enzyme telomerase is an attractive target for cancer chemotherapy. The drugs have
been designed to inactivate telomerase, and consequently induce senescence in the cancer cells.
This in turn prevents the rapid cell proliferation.
