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New Molecular Pathway Identified For The Treatment Of A Wide Variety Of Human Cancers

by Aruna on July 22, 2009 at 4:54 PM
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New Molecular Pathway Identified For The Treatment Of A Wide Variety Of Human Cancers

University of California scientists have identified a new molecular pathway that may lead to new treatments and targeted drugs for cancer and other diseases.

The research team has found a way to turn off a key-signaling pathway involved in physiological processes that can also stimulate the development of cancer and other diseases.

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By activating a receptor in cells called the liver X receptor (LXR), they were able to inhibit the hedgehog (Hh) signaling pathway, which is involved in the maintenance of tissue integrity and stem cell generation.

When stimulated in an unregulated manner, however, the Hh pathway can also cause cancers of the brain, lung, blood, prostate, skin and other tissues.
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"Our finding shows that activation of LXR signaling is a novel strategy for inhibiting Hh pathway activity and for targeting various cell types, including cancer cells, which may provide important clues as to how we might be able to intervene with tumor formation," said Farhad Parhami, a professor of medicine at the David Geffen School of Medicine at UCLA and the study's principal investigator.

During the study, researchers performed various tests activating LXR receptors in cells and found that specific gene expression induced by the Hh pathway could be inhibited. This finding was also confirmed in mice.

"Since Hh signaling plays a major role in other physiological and pathological processes, we may be able to impact other diseases as well," Parhami said.

"The hedgehog Hh signaling pathway is an important regulator of tumor formation, and these findings suggest that LXR agonists may be novel treatments for a wide variety of human cancers," added Dr. William Matsui of Johns Hopkins Medical Institute, an expert on Hh signaling in cancer development.

The study appears in the journal Molecular Endocrinology.

Source: ANI
ARU
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