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CSHL scientists identify new drug target against virulent type of breast cancer
Date:8/25/2008

ce cancerous proliferation on its own, it enhances the proliferation of cells that also express ErbB2 by speeding up their entry into the cell cycle. Proliferation in cancer is the result of the cell cycle gone out of control -- beyond limits that healthy cells impose on their own multiplication.

Dr. Muthuswamy likened the cooperation between the Brk and ErbB2 proteins to that between factors that propel a car. "If ErbB2 is the accelerator that makes the car move, Brk helps shift the gear to gain more speed," he explained.

How Brk is implicated in drug resistance

Aside from hurrying along tumor progression, Brk was also found to diminish the effectiveness of ErbB2-inhibiting drugs on tumor growth. This finding reinforces the need for combination therapies. "We might need to hit ErbB2-expressing cancers with drugs against both ErbB2 and Brk," said Muthuswamy.

Brk-inhibitors might also be useful on their own. The CSHL scientists speculate that these drugs might fight tumors that never react to or become resistant to ErbB2-inhibitors.

Targeting Brk is also a safe strategy, according to the scientists, because "Brk does not promote the proliferation of normal cells, and its expression in normal tissues is restricted to non-proliferating cells." Inhibiting this protein might thus "produce fewer unwanted side effects than (targeting) other cancer-promoting proteins" which may be present in larger numbers.

The scientists have also thought up other ways of putting their discovery of the role of Brk in cancer progression to good use. "We also think that Brk would be an ideal clinical marker than could be used to provide both a diagnosis and prognosis for breast cancer," said Dr. Muthuswamy.


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Contact: Peter Tarr
tarr123@gmail.com
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert

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