Diabetes and Cancer: P110 Alpha controls the action of insulin and other hormonal signals that play roles in cancer, diabetes and obesity
- From: "GysdeJongh" <jongh711@xxxxxxxxx>
- Date: Thu, 13 Apr 2006 14:32:17 +0200
Wouw , this is a break through in our understanding of this condition I
think ....
http://www.licr.org/C_news/archive.php/2006/04/12/diabetes-and-cancer/
Diabetes and Cancer: Alpha Connection
Protein frequently mutated in cancer has a surprising alter-ego
(London, April 12) - A study published by Nature today has defined the
function of p110 alpha, the flag-ship molecule of the eight member PI3K
family, which is one of the most frequently activated pathways in cancer.
The function of p110 alpha in the body has eluded researchers for over a
decade but a new approach to generating mouse models, has allowed
investigators from the Ludwig Institute for Cancer Research's (LICR) UCL
Branch and the UCL Centre for Diabetes & Endocrinology to solve the mystery
and yield important information for planned clinical trials with PI3K
inhibitors.
The study showed that p110 alpha controls the action of insulin and other
key hormonal signals that play roles in growth, diabetes and obesity. p110
alpha is frequently mutated or overexpressed in cancer, and the results of
the present work imply that cancer cells hijack a key signalling pathway to
fuel their energy needs and drive their proliferation and survival. The
current work has far-reaching implications, given that several million of
people are affected by metabolic disorders, and every year, several hundreds
of thousand new cancer cases with mutations in p110 alpha are diagnosed.
Importantly, says LICR's Dr. Bart Vanhaesebroeck, the senior author of the
study, the findings have immediate implications for the testing of p110
alpha-specific inhibitors for human therapies. "Accurate information on the
specific role of p110 alpha is needed urgently by the pharmaceutical
industry, which is preparing to initiate clinical trials based on PI3K
inhibition, not only in cancer but also in inflammation, allergy and
auto-immunity. These mice mimic the effect of systemic administration with a
p110 alpha-specific drug,"
According to Dr. Vanhaesebroeck, traditional mouse models investigating the
function of PI3K proteins have been engineered to completely remove the p110
alpha gene. However the LICR and University College London team and
collaborators from the Universities of Edinburgh and Fribourg introduced a
single mutation into the p110 alpha gene that inactivates, but does not
remove, the protein. The scientists discovered that the mice were smaller,
but ate more and had increased levels of body fat. Additionally, the mice
had raised insulin levels and were glucose-intolerant. However, the mice did
not go on to develop full diabetes. "The finding that these mice, despite
having dampened insulin signalling, showed no signs of developing diabetes,
is welcome news, as this suggest that drugs that block p110 alpha function
in cancer cells may not have the severe metabolic disturbances first
expected."
For Dr. Dominic Withers from the UCL Centre for Diabetes & Endocrinology, a
senior co-author on the study, this work adds another important part to
solving the puzzle of how insulin works. "In order to be able to treat
diabetes and other metabolic disorders, such as obesity, we first have to
understand the normal regulation of this complex system, so that therapies
are targeted at the key players in this pathway."
Gys
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