SENS3 Report: the GIFT Versus Cancer

From the Methuselah Foundation Blog:

Here is a second report from Michael Rae on the third Strategies for Engineered Negligible Senescence conference (SENS3):

Attendees at SENS3 heard first-hand about an extremely exciting approach to cancer treatment that has not yet hit the scientific literature or the press. In 2003, Dr. Zheng Cui and his colleagues at the Comprehensive Cancer Center of Wake Forest University reported the discovery of mice with immune cells that rendered them invulnerable to cancer: they had been intentionally giving mice cancer by injecting them with virulent cancer cells as part of a separate study, when they discovered a single mouse in the colony that was completely immune to the invasive cells.

His curiosity piqued, Dr. Cui went on to show that it could resist multiple rounds of such injections, and were so impressed that they used him to father a whole colony of mice, all of whom shared this remarkable invulnerability to cancer. Based on that ability, he calls them spontaneous regression/complete resistance (SR/CR) mice.

For the complete article please visit: http://blog.methuselahfoundation.org/2007/09/sens3_report_the_gift_versus_c_1.html

SENS3 Report: Towards Mitochondrial Repair

From: The Methuselah Foundation Blog

Michael Rae reports from the proceedings at SENS3:

Among the most exciting presentations at the third conference on Strategies for Engineered Negligible Senescence (SENS3) were those in Friday's session on the rescue of mitochondrial mutations. This is a subject to which Conference organizer and Methuselah Foundation Chief Science Officer Dr. Aubrey de Grey has made widely-recognized contributions.

Unlike most other parts of the cell, mitochondria house many of the genes encoding their essential proteins within themselves. These genes are vulnerable to the constant assault of free radicals produced by the mitochondria as a side-effect of their role as cellular power plants. When mitochondrial DNA is damaged, it cannot make the proteins needed to carry on the essential business of generating energy for the cell; the ensuing metabolic damage is the driver of age-related rise in oxidative stress. This oxidative stress fuels free radical damage and interferes with essential signaling pathways in cells far from the original site of the damage.

For the complete article please visit http://blog.methuselahfoundation.org/2007/09/sens3_report_the_gift_versus_c_1.html