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Phaedra C. Ghazi
Researcher at Beth Israel Deaconess Medical Center
Publications - Â 5
Citations - Â 164
Phaedra C. Ghazi is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: KRAS & Cancer. The author has an hindex of 3, co-authored 3 publications receiving 108 citations. Previous affiliations of Phaedra C. Ghazi include Harvard University.
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Journal ArticleDOI
Tissue-Specific Oncogenic Activity of KRASA146T
Emily J. Poulin,Emily J. Poulin,Asim K. Bera,Jia Lu,Yi Jang Lin,Yi Jang Lin,Samantha Dale Strasser,Samantha Dale Strasser,Joao A. Paulo,Tannie Q. Huang,Carolina Morales,Wei Yan,Joshua Cook,Joshua Cook,Jonathan A. Nowak,Douglas K. Brubaker,Douglas K. Brubaker,Douglas K. Brubaker,Brian A. Joughin,Christian W. Johnson,Christian W. Johnson,Rebecca A. Destefanis,Rebecca A. Destefanis,Phaedra C. Ghazi,Phaedra C. Ghazi,Sudershan R. Gondi,Thomas E. Wales,Roxana E. Iacob,Lana Bogdanova,Jessica J. Gierut,Jessica J. Gierut,Yina Li,Yina Li,John R. Engen,Pedro A. Perez-Mancera,Benjamin S. Braun,Steven P. Gygi,Douglas A. Lauffenburger,Kenneth D. Westover,Kevin M. Haigis,Kevin M. Haigis +40 more
TL;DR: It is demonstrated that the selection for specific KRAS mutants in human cancers from different tissues is due to their distinct signaling properties, demonstrating that context-dependent variations in signaling downstream of differentKRAS mutants drive the KRAS mutational pattern seen in cancer.
Journal ArticleDOI
Integrated in vivo multiomics analysis identifies p21-activated kinase signaling as a driver of colitis
Jesse Lyons,Jesse Lyons,Douglas K. Brubaker,Douglas K. Brubaker,Phaedra C. Ghazi,Katherine R. Baldwin,Katherine R. Baldwin,Amanda L. Edwards,Myriam Boukhali,Samantha Dale Strasser,Samantha Dale Strasser,Lucia Suarez-Lopez,Lucia Suarez-Lopez,Yi-Jang Lin,Vijay Yajnik,Joseph L. Kissil,Wilhelm Haas,Douglas A. Lauffenburger,Kevin M. Haigis,Kevin M. Haigis +19 more
TL;DR: A multiomics analysis that integrated RNA microarray, total protein mass spectrometry, and phosphoproteomics analyses of tissues isolated from a mouse model of colitis identified Pak as a potential therapeutic target in IBD.
The colonic epithelium plays an active role in promoting colitis by shaping the tissue cytokine profile
Phaedra C. Ghazi,Alessio Tovaglieri,Katherine R. Baldwin,Emily J. Poulin,Jessica J. Gierut,Casie A. Genetti,Vijay Yajnik,David T. Breault,Kevin M. Haigis,Jesse Lyons,Alina Starchenko,Douglas A. Lauffenburger +11 more
TL;DR: In this paper, the authors identify the mammalian target of rapamycin (mTOR) signaling as a potential driver of inflammation in a mouse model of colitis and demonstrate that proper differentiation of epithelial cells is an important feature of colonic homeostasis because of its effect on the secretion of inflammatory cytokines.
Journal ArticleDOI
Abstract 3600: DCC-3116, a first-in-class selective inhibitor of ULK1/2 kinases and autophagy, synergizes with the KRASG12C inhibitor sotorasib resulting in tumor regression in KRAS mutant NSCLC xenograft models
Martin McMahon,M Bogdan,Mary Jane Timson,Hikmat Imad Al-Hashimi,Phaedra C. Ghazi,Yu Zhan,Bryan D. Smith,Conan G. Kinsey,Daniel L. Flynn +8 more
TL;DR: DCC-3116 is an investigational, potent and selective pharmacological inhibitor of the protein kinases ULK1 and ULK2, which are critical initiating components of the autophagy pathway and synergizes with the KRASG12C inhibitor sotorasib resulting in tumor regression in KRAS mutant NSCLC xenograft models.
Journal ArticleDOI
Abstract PR03: Cooperative anti-tumor effects of combined inhibition of KRASG12C plus autophagy in preclinical models of KRASG12C-driven lung cancer
TL;DR: Ghazi et al. as mentioned in this paper demonstrated that KRASG12C-driven lung cancer cells increase autophagic flux in response to treatment with sotorasib-induced autophagy, an intracellular recycling pathway.