Neal Rosen

Reveals the feedback loop that lets tumors dodge mTOR and PI3K inhibitors, reshaping how these drugs are used in the clinic

MD, PhD, Albert Einstein College of Medicine · residency, Brigham and Women's Hospital · fellowship, NCI · Member Emeritus, MSKCC

Rosen Lab (Member Emeritus), Memorial Sloan Kettering Cancer Center ↗

Neal Rosen Portrait: Memorial Sloan Kettering Cancer Center

In 2006 (ORE2006), showed mTOR inhibition paradoxically activates upstream RTK/Akt signaling via feedback release — foundational explanation for why single-agent mTOR inhibitors often fail. As senior author on ROD2011, extended this to mTOR-kinase inhibitors.

This 'feedback reactivation' framework became a central organizing principle of modern targeted-therapy combinations. NIH/NCI Outstanding Investigator Award (2016); AACR Academy Fellow (2022).

Milestones in the Atlas

Year	Evidence	Study
2006	M	mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt ORE2006 mTOR inhibition relieves feedback suppression of RTK signaling, paradoxically activating Akt.
2011	M	mTOR kinase inhibition causes feedback-dependent biphasic regulation of AKT signaling ROD2011 Senior author: mTOR-kinase inhibitors cause feedback-dependent biphasic AKT rebound.

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