Telomeres, the beginning(s) of the end. On the Nobel Prize in Physiology or Medicine awarded to Elisabeth H. Blackburn, Carol W. Greider and Jack W. Szostak

The 2009 Nobel Prize for Physiology and Medicine
was awarded to Elizabeth H. Blackburn, Jack W. Szostak, and
Carol W. Greider for their work on telomeres and telomerase.
Telomeres are formed by short DNA sequences repeated in
tandem and associated with different proteins. These structures, which are found at the ends of chromosomes, are crucial
for maintaining genomic stability by preventing chromosomes
from joining with one another. In addition to this essential protective function, telomeres play a vital role in complete DNA
end replication. Telomere length is maintained by the enzyme
telomerase—a complex made up of RNA and proteins that in
humans is active is germinal and embryonic cells but inactive in
somatic cells. The absence of telomerase in proliferating cells
leads their telomeres to shorten with successive cell divisions.
Eventually, the telomeres reach a critically short length that in
turn causes massive chromosome instability. This may be the
mechanism through which a cell acquires the genetic alternations needed to become malignant. Normally, however, below
this critical length, the cells stop dividing and either enter a
phase of senescence or an irreversible state of arrest, or mechanisms are activated for programmed cell death. However,
some cells that also carry alterations in cell cycle checkpoint
proteins continue replicating, giving rise to uncapped chromosome ends and thus to a malignant potential.