LA JOLLA, CAA collaborative study by researchers at the Salk Institute for Biological Studies uncovered that the tumor suppressor p53, which made its name as "guardian of the genome", not only stops cells that could become cancerous in their tracks but also controls somatic cell reprogramming.
Although scientists have learned how to reprogram adult human cells such as skin cells into so-called induced pluripotent stem cells (iPSCs), the reprogramming efficiency is still woefully low. The Salk study, published in the Aug. 9 advance online edition of Nature, gives new insight why only a few cells out of many can be persuaded to turn back the clock.
"Although we have been able to reprogram specialized cells for a while now, there had been nothing known about the control mechanisms that prevent it from happening spontaneously in the body and why it has been so hard to change their fate in a Petri dish," says Juan-Carlos Izpisa Belmonte, Ph.D., a professors in the Gene Expression Laboratory, who worked closely with Geoffrey M. Wahl, Ph.D., also a professor in the Gene Expression Laboratory.
Their findings bring iPSCs technology a step closer to fulfilling its promise as source of patient-specific stem cells but also force scientists to rethink the development of cancer.
"There's been a decade-old idea that cancer arises through the de-differentiation of fully committed and specialized cells but eventually it was discarded in favor of the currently fashionable cancer stem cell theory," says Wahl. "Now, that we know that p53 prevents de-differentiation, I believe it is time to reconsider the possibility that reprogramming plays a role in the development of cancer since virtually all cancer cells lose p53 function in one way or another."
As mammalian embryos transition through a series of developmental stages, the choices of embryonic stem cells, which enjoy almost limitless prospects, are progressively limited
|Contact: Gina Kirchweger|