Peggy P. Hsu
Identifies Grb10 as mTORC1's own brake on growth-factor signaling and now hunts the first cells that turn into lung cancer
BA, Princeton · PhD, MIT (Sabatini Lab) · MD, Harvard · residency, Brigham and Women's · oncology fellowship, Dana-Farber & MGH · postdoc, Vander Heiden Lab, MIT · now at University of Michigan
Hsu Lab, University of Michigan Rogel Cancer Center ↗
Portrait: American Society for Clinical Investigation (ASCI)
Used quantitative phosphoproteomics (HSU2011) to map mTOR's substrates directly, identifying Grb10 — mTORC1 phosphorylates/stabilizes it, and Grb10 suppresses PI3K/growth-factor signaling, explaining mTORC1-hyperactivation-causes-insulin-resistance. (Independently confirmed same year by Yonghao Yu's group.)
Physician-scientist path through MIT/Harvard/Dana-Farber/MGH; now thoracic oncologist and stem cell biologist studying how airway basal cells give rise to never-smoking, ALK-fusion lung cancer. NCI K08, Burroughs Wellcome Fund Career Award (2025), 2026 ASCI Young Physician-Scientist.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2006 | M | Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB SAR2006 Co-authored the mTORC2-disassembly/rapamycin insulin-resistance finding. |
| 2011 | M | The mTOR-regulated phosphoproteome reveals a mechanism of mTORC1-mediated inhibition of growth factor signaling HSU2011 Mapped the mTOR phosphoproteome, identifying Grb10 as a direct mTORC1 substrate feeding back on PI3K. |