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Tracy Hampton, PhD

JAMA. 2008;300(9):1016.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Researchers have blocked the development of prostate tumors in cancer-prone mice by disabling a molecule that is part of a cellular signaling network disrupted in several common cancers (Jia S et al. Nature. 10.1038/nature07091 [published online ahead of print June 25, 2008]). The molecule, p110beta, and a counterpart, p110alpha, are different forms of an enzyme called phosphatidylinositol-3-OH kinase PI(3)K. When activated by growth factor receptors, PI(3)K turns on a sequence of genes and proteins that causes cells to divide and grow.

Scientists at the Dana-Farber Cancer Institute in Boston knocked out the gene encoding p110beta protein in mice that also lacked the phosphatase and tensin homologue (PTEN) tumor suppressor protein. Because PTEN acts as a brake against the development of cancer, mice lacking this tumor suppressor are cancer-prone.

Mice that lacked PTEN but had functioning p110beta proteins all developed early prostate cancers by 12 weeks of . . . [Full Text of this Article]

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