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Salima Benbarche

As seen in: Nature, Science Magazine, Cell Press
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Articles

RAF-independent MEK mutations drive refractory histiocytic neoplasms but respond to ERK inhibition

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By Eli L. Diamond, Jean-François Emile, Takeshi Fujino, Julien Haroche, Maxim I. Maron, Alexander Lewis Verified, Jahan A. Rahman, Anne Reiner, Dana F. Bossert, Marc K. Rosenblum, Mariko Yabe, Kseniya Petrova-Drus, Jasmine H. Francis, Veronica Rotemberg, Raajit Rampal, Sarah Paiji Yoo, Anthony F. Daniyan, sonia mahajan, Vaios Hatzoglou, Robert Young, Gary A. Ulaner, Wiebke Rösler, Oshrat Hershkovitz-Rokah, Ofer Shpilberg, Roei D. Mazor, Michael Singer Verified, M. Adriana Cuibus, Salima Benbarche, Pu Zhang, Nina Fox, Cynthia Castro, Matthew Witkowski, Fleur Cohen-Aubart, Louis Terriou, Maher Hanoun, Nicolas Schleinitz, Gabriela Sosa, Timo Hautala, Neal Rosen, Omar Abdel-Wahab Verified, Benjamin H. Durham, Kenyon Weis, Steven Tittley
| Cell Press Verified
Keywords BRAF cobimetinib Erdheim-Chester disease histiocytoses Langerhans cell histiocytosis macrophage MEK ERK trametinib ulixertinib Introduction Histiocytic neoplasms (histiocytoses) are a diverse group of clonal hematopoietic disorders defined by the accumulation of macrophages, dendritic cells, or monocyte-derived cells in various tissues.1 Histiocytoses subtypes include Langerhans cell histiocytosis (LCH), Erdheim-Chester disease (ECD), juvenile xanthogranuloma (JXG),...
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GPATCH8 modulates mutant SF3B1 mis-splicing and pathogenicity in hematologic malignancies

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By Salima Benbarche, Laura Galvis, Jeetayu Biswas, Bo Liu
| Cell Press Verified
Highlights • GPATCH8 is required for mutant SF3B1-dependent splicing alterations • GPATCH8 is involved in quality control of intronic branchpoint selection • GPATCH8 opposes activity of SUGP1, and each competes for interaction with DHX15 • Deletion of GPATCH8 corrects aberrant differentiation of SF3B1-mutant MDS cells Summary Mutations in the RNA splicing factor gene SF3B1 are common across hematologic and solid cancers and result in widespread alterations in splicing, yet there is currently...
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High caspase 3 and vulnerability to dual BCL2 family inhibition define ETO2::GLIS2 pediatric leukemia - Leukemia

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By Julie Rivière, Salima Benbarche, Birgit Geoerger, Françoise Pflumio, Camille Lobry, Arnaud Petit
| Nature Verified
Abstract Pediatric acute myeloid leukemia expressing the ETO2::GLIS2 fusion oncogene is associated with dismal prognosis. Previous studies have shown that ETO2::GLIS2 can efficiently induce leukemia development associated with strong transcriptional changes but those amenable to pharmacological targeting remained to be identified.
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