"There are rare mutations that strongly predispose people to getting a type of cancer, but most cancers are caused by a combination of environmental influences and moderately influential differences in the DNA that an individual is born with. The kinds of changes we are studying are not instant tickets to cancer but are predispositions. This is something that is much harder to track but could be very useful in the future realm of personalized medicine," says David Quigley, MA, the first author on the paper and the lead computational expert on the project.
Significantly, the UCSF researchers used only a personal computer to map out the relevant gene networks. Previous studies using this technique have required supercomputers or other forms of high-powered computing. Reducing computing requirements should allow many more laboratories to use genetic network analysis techniques.
In their study, the researchers bred together laboratory mice of the species Mus Musculus with wild mice of the species Mus Spretus. M. Musculus has strong susceptibility to skin cancer and M. Spretus has strong resistance to skin cancer.
The researchers attempted to induce skin cancer in the mixed offspring of these mice and then examined how genetic control of gene expression affected their tumor susceptibility. By examining genetic differences between mice who did and did not develop skin cancer, the researchers identified the Vitamin D Receptor as a candidate master regulator for skin cancer in the mice.
Vitamin D levels in the blood have long been recognized as having an influence on skin functions and susceptibility to inflammatory diseases in humans and mice. Diminished Vitamin D levels or a faulty Vitamin D Receptor gene have also been associated with the propensity for various types of cancer in people an
'/>"/>
| Source: PRWeb Copyright©2009 Vocus, Inc. All rights reserved |