Cancer-Causing Proteins Winston Salem NC

The drugs, called thiazole antibiotics, appear to block a cellular protein called FoxM1, one of the most over-produced proteins in cancer cells, according to researchers at the University of Illinois at Chicago College of Medicine. FoxM1 is believed to play an important role in causing cells to become cancerous and may present a promising target for future anti-cancer treatments.

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Edward Gus Shaw
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Medical School: Bowman Gray Sch Of Med Of Wake Forest Univ, Winston-Salem Nc 27157
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Cancer-Causing Proteins

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Scientists are closer to understanding how a recently approved class of antibiotics may work against cancer.

The drugs, called thiazole antibiotics, appear to block a cellular protein called FoxM1, one of the most over-produced proteins in cancer cells, according to researchers at the University of Illinois at Chicago College of Medicine. FoxM1 is believed to play an important role in causing cells to become cancerous and may present a promising target for future anti-cancer treatments.

The researchers also found that thiazoles may inhibit proteasomes, a molecular complex within cells that disposes of old proteins marked for destruction. Recently, a number of proteasome inhibitors have shown promise against cancer. One of these inhibitors, bortezomib (Velcade), has proven effective against a number of cancers, including myeloma and certain forms of lymphoma.

The new research, which appears in the online journal PLoS ONE, points to the possible anti-cancer use of thiazoles in the future. In a university news release, study author Andrei Gartel, an associate professor of molecular genetics, said that by using thiazole antibiotics in combination with well-known proteasome inhibitors, "we may see a synergy that allows us to markedly reduce the dose of any one of these drugs and still effectively kill the cancer cells."

More information

Read more about cancer treatments at the U.S. National Cancer Institute.

SOURCE: University of Illinois at Chicago, news release, Aug. 11, 2009

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