M
Margaret E. Torrence
Researcher at Harvard University
Publications - 12
Citations - 1553
Margaret E. Torrence is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & KRAS. The author has an hindex of 8, co-authored 12 publications receiving 1148 citations. Previous affiliations of Margaret E. Torrence include Massachusetts Institute of Technology.
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Journal ArticleDOI
Elevation of circulating branched-chain amino acids is an early event in human pancreatic adenocarcinoma development
Jared R. Mayers,Chen Wu,Chen Wu,Clary B. Clish,Peter Kraft,Margaret E. Torrence,Brian P. Fiske,Chen Yuan,Ying Bao,Mary K. Townsend,Shelley S. Tworoger,Shawn M. Davidson,Thales Papagiannakopoulos,Annan Yang,Talya L. Dayton,Shuji Ogino,Shuji Ogino,Meir J. Stampfer,Edward Giovannucci,Zhi Rong Qian,Douglas A. Rubinson,Jing Ma,Howard D. Sesso,John Michael Gaziano,John Michael Gaziano,Barbara B. Cochrane,Simin Liu,Jean Wactawski-Wende,JoAnn E. Manson,Michael Pollak,Alec C. Kimmelman,Amanda Souza,Kerry A. Pierce,Thomas J. Wang,Robert E. Gerszten,Charles S. Fuchs,Charles S. Fuchs,Matthew G. Vander Heiden,Brian M. Wolpin,Brian M. Wolpin +39 more
TL;DR: It is suggested that increased whole-body protein breakdown is an early event in development of PDAC, and elevated plasma levels of branched-chain amino acids (BCAAs) are associated with a greater than twofold increased risk of future pancreatic cancer diagnosis.
Journal ArticleDOI
Tissue of origin dictates branched-chain amino acid metabolism in mutant Kras-driven cancers
Jared R. Mayers,Margaret E. Torrence,Laura V. Danai,Thales Papagiannakopoulos,Shawn M. Davidson,Matthew R. Bauer,Allison N. Lau,Brian W. Ji,Purushottam D. Dixit,Aaron M. Hosios,Alexander Muir,Christopher R. Chin,Elizaveta Freinkman,Tyler Jacks,Brian M. Wolpin,Dennis Vitkup,Matthew G. Vander Heiden +16 more
TL;DR: In this article, the authors argue that tissue of origin is an important determinant of how cancers satisfy their metabolic requirements, and that tissue context defines cancer dependence on specific metabolic pathways is unknown, but despite the same initiating events, these tumors use branched chain amino acids (BCAAs) differently.
Journal ArticleDOI
Collagen-derived proline promotes pancreatic ductal adenocarcinoma cell survival under nutrient limited conditions.
Orianne Olivares,Jared R. Mayers,Victoire Gouirand,Margaret E. Torrence,Tristan Gicquel,Laurence Borge,Sophie Lac,Julie Roques,Marie-Noëlle Lavaut,Patrice Berthezene,Marion Rubis,Véronique Secq,Stéphane Garcia,Vincent Moutardier,Dominique Lombardo,Juan L. Iovanna,Richard Tomasini,Fabienne Guillaumond,Matthew G. Vander Heiden,Matthew G. Vander Heiden,Sophie Vasseur +20 more
TL;DR: It is demonstrated that collagen serves as a proline reservoir for PDAC cells to use as a nutrient source when other fuels are limited and that proline oxidase (PRODH1) is required forPDAC cell proliferation in vitro and in vivo.
Tissue of origin dictates branched-chain amino acid metabolism in mutant Kras-driven cancers
Jared R. Mayers,Margaret E. Torrence,Laura V. Danai,Thales Papagiannakopoulos,Shawn M. Davidson,Matthew R. Bauer,Allison N. Lau,Brian W. Ji,Purushottam D. Dixit,Aaron M. Hosios,Alexander Muir,Christopher R. Chin,Elizaveta Freinkman,Tyler Jacks,Brian M. Wolpin,Dennis Vitkup,M. G. Vander Heiden +16 more
TL;DR: Loss of Bcat1 and Bcat2, the enzymes responsible for BCAA use, impairs NSCLC tumor formation, but these enzymes are not required for PDAC tumorformation, arguing that tissue of origin is an important determinant of how cancers satisfy their metabolic requirements.
Journal ArticleDOI
The mTORC1-mediated activation of ATF4 promotes protein and glutathione synthesis downstream of growth signals
Margaret E. Torrence,Michael R MacArthur,Michael R MacArthur,Aaron M. Hosios,Alexander J. Valvezan,John M. Asara,James R. Mitchell,James R. Mitchell,Brendan D. Manning +8 more
TL;DR: Torrence et al. as discussed by the authors found that less than 10% of the genes activated by ATF4 during cellular stress are also activated in response to mTORC1-driven growth.