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Previous Volume 351:2337-2338 November 25, 2004 Number 22 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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PTEN, the lipid phosphatase and tensin homologue, is a key tumor suppressor. Mutations resulting in the loss of PTEN or the loss of its function are common and functionally relevant in tumors of different histologic origins, including breast cancer.¹ A recent study by Nagata and colleagues² shows that PTEN not only antagonizes tumorigenesis but also sensitizes breast cancers to targeted therapy with trastuzumab (Herceptin), a humanized monoclonal antibody against ErbB2 (also referred to as HER2/neu), a membrane-receptor tyrosine kinase in the epidermal growth factor receptor family.³

PTEN normally opposes the activation of the proto-oncogenic phosphatidylinositol 3' kinase (PI3K)–Akt signaling pathway . . . [Full Text of this Article]

Source Information

From the Cancer Biology and Genetics Program, Memorial-Sloan Kettering Cancer Center, New York.

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