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Brittany Woods
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 10
Citations - 1041
Brittany Woods is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Myeloid & Haematopoiesis. The author has an hindex of 7, co-authored 10 publications receiving 863 citations. Previous affiliations of Brittany Woods include Harvard University & Kettering University.
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Journal ArticleDOI
Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Peter S. Hammerman,Martin L. Sos,Alex H. Ramos,Chunxiao Xu,Amit Dutt,Wenjun Zhou,Lear E. Brace,Brittany Woods,Wenchu Lin,Jianming Zhang,Xianming Deng,Sang Min Lim,Stefanie Heynck,Martin Peifer,Jeffrey R. Simard,Michael S. Lawrence,Robert C. Onofrio,Helga B. Salvesen,Danila Seidel,Thomas Zander,Johannes M. Heuckmann,Alex Soltermann,Holger Moch,Mirjam Koker,Frauke Leenders,Frauke Leenders,Franziska Gabler,Silvia Querings,Sascha Ansén,Elisabeth Brambilla,Christian Brambilla,Philippe Lorimier,Odd Terje Brustugun,Åslaug Helland,Iver Petersen,Joachim H. Clement,Harry J.M. Groen,Wim Timens,Hannie Sietsma,Erich Stoelben,Juergen Wolf,David G. Beer,Ming-Sound Tsao,Megan Hanna,Megan Hanna,Charlie Hatton,Charlie Hatton,Michael J. Eck,Pasi A. Jänne,Bruce E. Johnson,Wendy Winckler,Heidi Greulich,Heidi Greulich,Adam J. Bass,Jeonghee Cho,Daniel Rauh,Nathanael S. Gray,Kwok-Kin Wong,Eric B. Haura,Roman K. Thomas,Matthew Meyerson,Matthew Meyerson +61 more
TL;DR: Findings suggest that gain-of-function mutations in DDR2 are important oncogenic events and are amenable to therapy with dasatinib, and provide a rationale for designing clinical trials with the FDA-approved drug d asatinib in patients with lung SCCs.
Journal ArticleDOI
Mutational cooperativity linked to combinatorial epigenetic gain of function in acute myeloid leukemia.
Alan H. Shih,Yanwen Jiang,Cem Meydan,Kaitlyn Shank,Suveg Pandey,Laura Barreyro,Iléana Antony-Debré,Agnes Viale,Nicholas D. Socci,Yongming Sun,Alexander Robertson,Magali Cavatore,Elisa de Stanchina,Todd Hricik,Franck Rapaport,Brittany Woods,Chen Wei,Megan A. Hatlen,Muhamed Baljevic,Stephen D. Nimer,Martin S. Tallman,Elisabeth Paietta,Luisa Cimmino,Iannis Aifantis,Ulrich Steidl,Christopher E. Mason,Ari Melnick,Ross L. Levine +27 more
TL;DR: Mice generated with mutations in Tet2 and Flt3 resulted in fully penetrant, lethal AML, with a defined leukemia stem cell population characterized by site-specific changes in DNA methylation and gene expression.
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Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice.
Wei Wang,Wenli Liu,Wenli Liu,Trevor P. Fidler,Ying Wang,Yang Tang,Brittany Woods,Carrie L. Welch,Bishuang Cai,Carlos Silvestre-Roig,Ding Ai,Yong-Guang Yang,Andrés Hidalgo,Andrés Hidalgo,Oliver Soehnlein,Oliver Soehnlein,Ira Tabas,Ross L. Levine,Alan R. Tall,Nan Wang +19 more
TL;DR: Hematopoietic Jak2VF expression promotes early lesion formation and increased complexity in advanced atherosclerosis, likely contributing to plaque instability.
Journal ArticleDOI
Genetic studies reveal an unexpected negative regulatory role for Jak2 in thrombopoiesis
Sara C. Meyer,Matthew D. Keller,Brittany Woods,Lindsay M. LaFave,Lennart Bastian,Maria Kleppe,Neha Bhagwat,Sachie Marubayashi,Ross L. Levine,Ross L. Levine +9 more
TL;DR: It is demonstrated that Jak2 in terminal megakaryopoiesis is not required for PLT production, and that Jak 2 loss in PLTs and MKs results in non-autonomous expansion of stem/progenitors and of MKs and PLTs via dysregulated TPO turnover.
Journal ArticleDOI
Acquired Resistance to Dasatinib in Lung Cancer Cell Lines Conferred by DDR2 Gatekeeper Mutation and NF1 Loss
Ellen M. Beauchamp,Brittany Woods,Austin M. Dulak,Li Tan,Chunxiao Xu,Nathanael S. Gray,Adam J. Bass,Kwok-Kin Wong,Matthew Meyerson,Peter S. Hammerman +9 more
TL;DR: It is shown that NF1 loss activates a bypass pathway, which confers ERK dependency downstream of RAS activation, and this results indicate that acquired resistance to dasatinib can occur via both second-site mutations in DDR2 and by activation of bypass pathways.