Research in the field of molecular processes of aging in the
last decade can be described as enormous, with many surprises that explain many
basic biological processes of multicellular organisms. Blasco and her team make
much of the progress occurring in this area of research. The concepts with which
they work (cancer, aging, stem cells, telomere length and amount of telomerase)
are woven together to shed light on the possible link between stem cells in
cancer development and aging.

Among their findings, highlights the relationship between telomere shortening
and advancement of aging and its acceleration in the context of human diseases
associated with mutations in telomerase. 1 These patients suffer a premature
loss of tissue renewal; a phenomenon which suggests that telomerase and its
mutations may affect tissue homeostasis and survival of the individual.
Moreover, this altered telomerase activity is related to the ability of stem
cells to regenerate tissues.

Next to envececimiento and cancer, embryonic development is another stage in
that telomeres play a role. While the oocytes show a very low telomerase
activity and a short telomeres, the embryo rapidly retrieves this activity and
telomere length, although not yet sure how. 2 The recent work of Telomeres and
Telomerase have shown that this telomere elongation in the embryo is independent
of telomerase and could depend on DNA recombination protein RAD50 or as TRF1.
From the blastocyst stage, the length of telomeres being maintained, then yes,
of telomerase activity. In relation to these particular mechanisms, has also
identified a novel function of the machinery of DNA repair errors in mediating
the cellular response of the presence of short telomeres (telomere dysfunction).
3