Lewis C. Cantley
Discovered PI3K, the pathway that feeds into mTOR from growth factors
PhD, Cornell · discovered PI3K at Tufts University School of Medicine (1984) · director of the Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine (2012–2022) · now Professor of Cell Biology, Dana-Farber Cancer Institute & Harvard Medical School
Lewis Cantley discovered and characterized phosphoinositide 3-kinase (PI3K) in the 1980s, a lipid-signalling enzyme that turned out to sit at the top of one of the most frequently mutated pathways in human cancer. PI3K activation, through Akt, is a principal route by which growth factors and insulin switch on mTORC1, directly linking Cantley's discovery to the biology this Atlas documents.
Over a career spanning Harvard, Tufts, Beth Israel Deaconess, and now Weill Cornell Medicine, where he directs the Meyer Cancer Center, Cantley's lab has continued to map how PI3K signalling controls cell growth and metabolism, including work connecting LKB1, AMPK and TSC2 to the PI3K–mTOR network. He has received the Breakthrough Prize and the Wolf Prize in Medicine, among many other honours.
The timeline below follows Cantley's contributions gathered in this Atlas.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2002 | R | The phosphoinositide 3-kinase pathway CAN2002 Reviews the phosphoinositide 3-kinase (PI3K) pathway that Cantley discovered, and its role in growth-factor signalling to mTOR. |
| 2003 | M | Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb TEE2003 TSC1-TSC2 acts as a GTPase-activating protein (GAP) for Rheb; when TSC is inactive, Rheb accumulates in its active GTP-bound form and directly activates mTORC1. |
| 2004 | M | The tumor suppressor LKB1 kinase directly activates AMP-activated kinase and regulates apoptosis in response to energy stress SHW2004 Co-authors the discovery that the LKB1 tumour suppressor directly activates AMPK, connecting energy stress to mTOR. |
| 2015 | R | Regulation of mTORC1 by PI3K signaling DIB2015 Review of mTORC1 regulation by PI3K signalling. |