O
Ophélia Maertens
Researcher at Brigham and Women's Hospital
Publications - 8
Citations - 856
Ophélia Maertens is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Germline mutation & Kinase. The author has an hindex of 7, co-authored 8 publications receiving 728 citations.
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Journal ArticleDOI
Drug-Induced Death Signaling Strategy Rapidly Predicts Cancer Response to Chemotherapy
Joan Montero,Kristopher A. Sarosiek,Joseph D. DeAngelo,Ophélia Maertens,Jeremy Ryan,Dalia Ercan,Huiying Piao,Neil S. Horowitz,Ross S. Berkowitz,Ross S. Berkowitz,Ursula A. Matulonis,Pasi A. Jänne,Pasi A. Jänne,Philip C. Amrein,Karen Cichowski,Ronny Drapkin,Ronny Drapkin,Anthony Letai +17 more
TL;DR: It is proposed that Dynamic BH3 Profiling can be used as a broadly applicable predictive biomarker to predict cytotoxic response of cancers to chemotherapeutic agents in vivo.
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Reactivation of ERK Signaling Causes Resistance to EGFR Kinase Inhibitors
Dalia Ercan,Chunxiao Xu,Masahiko Yanagita,Calixte S. Monast,Christine A. Pratilas,Joan Montero,Mohit Butaney,Takeshi Shimamura,Lynette M. Sholl,Elena Ivanova,Madhavi Tadi,Andrew H. Rogers,Claire E. Repellin,Marzia Capelletti,Ophélia Maertens,Eva M. Goetz,Anthony Letai,Levi A. Garraway,Matthew J. Lazzara,Neal Rosen,Nathanael S. Gray,Kwok-Kin Wong,Pasi A. Jänne +22 more
TL;DR: It is shown, in multiple complementary models, that resistance to WZ4002 develops through aberrant activation of extracellular signal-regulated kinase (ERK) signaling caused by either an amplification of mitogen-activated protein kinase 1 (MAPK1) or by downregulation of negative regulators of ERK signaling.
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An expanding role for RAS GTPase activating proteins (RAS GAPs) in cancer
TL;DR: This review will focus on the current understanding of RAS GAPs in human disease and will highlight important outstanding questions about their potential role(s) in human cancer.
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Defining Key Signaling Nodes and Therapeutic Biomarkers in NF1-Mutant Cancers
Clare F. Malone,Jody A. Fromm,Ophélia Maertens,Thomas Deraedt,Rachel Ingraham,Karen Cichowski +5 more
TL;DR: It is demonstrated that mTORC1 and MEK are key therapeutic targets in NF1-mutant cancers and establishes a noninvasive biomarker of effective, combined target inhibition that can be evaluated in clinical trials.
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Mutations in RABL3 alter KRAS prenylation and are associated with hereditary pancreatic cancer.
Sahar Nissim,Ignaty Leshchiner,Ignaty Leshchiner,Joseph D. Mancias,Matthew B. Greenblatt,Ophélia Maertens,Christopher A. Cassa,Jill A. Rosenfeld,Andrew G. Cox,Andrew G. Cox,John Hedgepeth,Julia Wucherpfennig,Andrew J. Kim,Jake Henderson,Patrick Gonyo,Anthony Brandt,Ellen L. Lorimer,Bethany Unger,Jeremy W. Prokop,Jerry R. Heidel,Xiaoxu Wang,Chinedu Ukaegbu,Benjamin C. Jennings,Joao A. Paulo,Sebastian Gableske,Carol A. Fierke,Gad Getz,Gad Getz,Shamil R. Sunyaev,Shamil R. Sunyaev,J. Wade Harper,Karen Cichowski,Karen Cichowski,Alec C. Kimmelman,Yariv Houvras,Sapna Syngal,Sapna Syngal,Carol L. Williams,Wolfram Goessling +38 more
TL;DR: Zebrafish modeling and biochemical approaches suggest that truncated RABL3 elevates KRAS activity via accelerated prenylation and uncover a mechanism for dysregulated RAS activity in development and cancer.