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Reviving a foe of cancer
Date:4/25/2013

nificantly suppressed tumor growth in mice.

"These results demonstrate that functional p53 in melanoma is normally inhibited by two different factors, instead of one, as previously thought. They also provide a proof of principle that both of those factors need to be blocked if p53 is to be successfully reactivated in cancer cells," said Lu.

Since multiple signaling pathways drive the growth of tumor cells, Lu and her colleagues wondered if the restoration of p53 function could be used as a strategy to enhance existing cancer therapies that target parallel signaling pathways. To find out, they treated advanced melanomas with JNJ, Nutlin-3 and a chemotherapeutic drug used in the clinic today named vemurafenib. This drug specifically inhibits BRAFV600E, a mutated protein that drives cancer cell proliferation. With such treatment, advanced melanoma tumors in preclinical mouse models shrank by a full 75 percent after 28 days of treatment. This has notable implications for the treatment of cancers in which p53 is not mutated but is instead functionally silencedroughly half of all cancer cases.

Based on their results, Lu and her colleagues argue that the best strategy in such cases might be to use drug combinations that target multiple, parallel pathways involved in tumor development and maintenance. Such combinations of drugs that normally have short-term efficacy could achieve an additive, if not a long-term synergistic effect.


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Contact: Rachel Steinhardt
rsteinhardt@licr.org
212-450-1582
Ludwig Institute for Cancer Research
Source:Eurekalert

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