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TORgeting oncogene addiction for cancer therapy. | LitMetric

TORgeting oncogene addiction for cancer therapy.

Cancer Cell

Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Published: February 2006

AI Article Synopsis

Article Abstract

The PI3K-Akt-mTOR growth-regulating pathway is conserved from mammals to flies and hyperactivated in many cancers. Accordingly, rapamycin analogs, which are inhibitors of mTOR-Raptor signaling, have recently garnered much interest as potential therapeutic agents against cancer. However, due to the heterogeneity of tumors, prior knowledge of the genetic and biochemical background of cancer cells will be required for effective targeted therapy. Thus, the identification of biological markers against activated oncogenic pathways is needed. In the January issue of Nature Medicine, Thomas et al. identify the loss of VHL tumor suppressor gene as a potential determining factor in tumor sensitivity to rapamycin.

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http://dx.doi.org/10.1016/j.ccr.2006.01.021DOI Listing

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TORgeting oncogene addiction for cancer therapy.

Cancer Cell

February 2006

Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

The PI3K-Akt-mTOR growth-regulating pathway is conserved from mammals to flies and hyperactivated in many cancers. Accordingly, rapamycin analogs, which are inhibitors of mTOR-Raptor signaling, have recently garnered much interest as potential therapeutic agents against cancer. However, due to the heterogeneity of tumors, prior knowledge of the genetic and biochemical background of cancer cells will be required for effective targeted therapy.

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