Conference Proceedings

Inhibiton of mTOR by RAD001 restores normal B cell differentiation and prevents B cell lymphomas in E mu-MYC mice.

Meaghan Wall, Gretchen Poortinga, Daniela Cardozo, Ricky W Johnstone, Grant A McArthur

BLOOD | AMER SOC HEMATOLOGY | Published : 2006


Abstract The c-Myc proto-oncogene encodes a bHLH-LZ transcription factor that regulates proliferation, differentiation and apoptosis. Deregulated expression of c-MYC is a frequent finding in a wide variety of human cancers, including B cell lymphoma. One emerging function of c-MYC is the regulation of ribosome biogenesis, protein synthesis and metabolism i.e. cell growth. mTOR, a key downstream signal transduction molecule in the PI3K/AKT growth regulatory pathway, is amenable to pharmacological inhibition by rapamycin analogues such as RAD001. We hypothesized that control of cell growth by c-MYC is important for its ability to regulate differentiation and act as an oncogene a..

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