Pradip K. Majumder
Cancer biologist who, in William Sellers's lab at Dana-Farber, showed that mTOR inhibitors reverse AKT-driven early prostate cancer in mice
Department of Medical Oncology, Dana-Farber Cancer Institute, and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (at the time of the study, 2004)
AKT is a growth kinase that is often overactive in prostate cancer, usually because the brake PTEN is lost. In MAJ2004, Pradip Majumder and colleagues in William Sellers's lab used mice that make active AKT in the prostate. These mice develop prostatic intraepithelial neoplasia (PIN), an early, pre-invasive stage of prostate cancer. Treating them with the mTOR inhibitor RAD001 (everolimus) reversed the PIN. The authors traced the effect to two routes: the drug caused the abnormal cells to die by apoptosis, and it switched off a set of genes controlled by HIF-1, a transcription factor that drives growth and blood vessel formation. The study, done in mice, helped make the case that tumours driven by AKT depend on mTOR and could respond to mTOR inhibitors.
No current institutional page was found. The affiliation shown is the one on the Atlas paper.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2004 | A | mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways MAJ2004 First author: showed in AKT-transgenic mice that the mTOR inhibitor RAD001 reverses prostatic intraepithelial neoplasia through apoptosis and HIF-1-dependent pathways. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Pradip K. Majumder.
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- James Brugarolas First author of the 2004 study showing that hypoxia switches off mTOR through REDD1 and the TSC1/TSC2 complex; now directs a kidney cancer research program studying signalling and resistance to targeted drugs.
- William R. Sellers Cancer biologist and physician-scientist whose work spans cancer genomics and cancer therapeutics, including how the PI3K/AKT/mTOR pathway drives tumours and how to target it.
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