Kathryn O'Reilly
Physician-scientist who, in Neal Rosen's lab at Memorial Sloan Kettering, showed that blocking mTORC1 with rapamycin-like drugs switches on the survival kinase Akt through a feedback loop, a main reason these drugs worked less well against cancer than hoped
Department of Dermatology, New York University School of Medicine (2009, at the time of the most recent PubMed paper) · Program in Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Center, Neal Rosen lab (2006)
Kathryn O'Reilly is the first author of ORE2006, one of the most cited papers on why rapamycin-like drugs disappointed as cancer treatments. Normally, when mTORC1 and its target S6K1 are active, they send a brake signal back up the pathway that dampens insulin and growth-factor receptors. O'Reilly and colleagues in Neal Rosen's lab showed that blocking mTORC1 takes that brake off. Signals from receptor tyrosine kinases then rise, and Akt, a kinase that helps cancer cells survive, becomes more active. They saw this in cancer cell lines and also in tumour samples from patients treated with everolimus (RAD001), so it is a real effect in people, not only in a dish. The finding pushed the field toward drugs that block both mTOR and the PI3K/Akt pathway, or mTOR together with growth-factor receptors.
PubMed lists O'Reilly on 11 papers. In 2009, at the Department of Dermatology of New York University School of Medicine and again with Neal Rosen among the co-authors, she was first author of a study of 72 patients with metastatic melanoma, which found that a high level of phosphorylated 4E-BP1, a sign that mTORC1 is driving protein synthesis, went with shorter survival.
A current position could not be confirmed, and the most recent confirmed affiliation (NYU, 2009) is given at the time of that study.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2006 | M | mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt ORE2006 First author: showed in cancer cells and in patient tumours treated with everolimus that mTORC1 inhibition removes a feedback brake and activates upstream receptor signalling and Akt. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Kathryn O'Reilly.
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- José Baselga Breast cancer oncologist who led the BOLERO-2 trial showing that the mTOR inhibitor everolimus added to hormone therapy lengthens progression-free survival
- Neal Rosen Showed that blocking mTORC1 releases a feedback brake on receptor tyrosine kinases and AKT, explaining how tumours escape mTOR and PI3K inhibitors and shaping how these drugs are combined in the clinic
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