Ross L. Levine mainly investigates Cancer research, Immunology, Myeloid, Mutation and Myelofibrosis. His Cancer research research includes elements of Myeloproliferative neoplasm, Somatic cell, Myeloproliferative Disorders, Erythropoietin receptor and Leukemia. His research integrates issues of Myeloid leukemia and IDH1 in his study of Leukemia.
In his work, Oncology is strongly intertwined with Internal medicine, which is a subfield of Immunology. His Myeloid research integrates issues from IDH2, Haematopoiesis and Bone marrow. His research investigates the connection between Myelofibrosis and topics such as Polycythemia vera that intersect with problems in Janus kinase 2 and Extramedullary hematopoiesis.
His primary areas of study are Cancer research, Myeloid leukemia, Immunology, Internal medicine and Myeloid. His Cancer research study combines topics from a wide range of disciplines, such as Haematopoiesis, Signal transduction, Janus kinase 2, Mutation and Leukemia. While the research belongs to areas of Haematopoiesis, he spends his time largely on the problem of Molecular biology, intersecting his research to questions surrounding DNA methylation.
His Myeloid leukemia study combines topics in areas such as IDH2 and Epigenetics. Immunology is represented through his Myelofibrosis, Pathogenesis and Myelodysplastic syndromes research. His studies deal with areas such as Essential thrombocythemia, Myeloproliferative Disorders and Thrombopoietin receptor as well as Myelofibrosis.
Ross L. Levine mostly deals with Cancer research, Internal medicine, Leukemia, Myeloid leukemia and Oncology. His study in Cancer research focuses on Myeloid in particular. His Leukemia research is multidisciplinary, incorporating perspectives in Kinase and Somatic evolution in cancer.
His biological study deals with issues like IDH2, which deal with fields such as Enasidenib. The concepts of his Oncology study are interwoven with issues in Myelofibrosis, Ruxolitinib, Decitabine and Transplantation. His biological study spans a wide range of topics, including Essential thrombocythemia and Polycythemia vera.
Ross L. Levine focuses on Cancer research, Leukemia, Myeloid leukemia, Myeloid and Haematopoiesis. Ross L. Levine has included themes like Cancer, Myeloproliferative neoplasm, Mutation and Progenitor cell, Stem cell in his Cancer research study. His work deals with themes such as Survival rate, Kinase, Gastroenterology and Somatic evolution in cancer, which intersect with Leukemia.
His Myeloid leukemia research is multidisciplinary, relying on both Epigenetic therapy, Epigenetics and NPM1. His Myeloid research incorporates elements of Enasidenib and Oncology. Much of his study explores Myelofibrosis relationship to Essential thrombocythemia.
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Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel
Hartmut Döhner;Elihu Estey;David Grimwade;Sergio Amadori.
The landscape of somatic copy-number alteration across human cancers
Rameen Beroukhim;Craig H. Mermel;Craig H. Mermel;Dale Porter;Guo Wei.
Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
Ross L. Levine;Ross L. Levine;Martha Wadleigh;Jan Cools;Benjamin L. Ebert;Benjamin L. Ebert.
Cancer Cell (2005)
Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation.
Maria E. Figueroa;Omar Abdel-Wahab;Chao Lu;Patrick S. Ward.
Cancer Cell (2010)
Prognostic relevance of integrated genetic profiling in acute myeloid leukemia
Jay P. Patel;Mithat Gönen;Maria E. Figueroa;Hugo Fernandez.
The New England Journal of Medicine (2012)
The Common Feature of Leukemia-Associated IDH1 and IDH2 Mutations Is a Neomorphic Enzyme Activity Converting α-Ketoglutarate to 2-Hydroxyglutarate
Patrick S. Ward;Jay Patel;David R. Wise;Omar Abdel-Wahab.
Cancer Cell (2010)
IDH mutation impairs histone demethylation and results in a block to cell differentiation
Chao Lu;Patrick S. Ward;Patrick S. Ward;Gurpreet S. Kapoor;Dan Rohle;Dan Rohle.
IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype
Sevin Turcan;Daniel Rohle;Daniel Rohle;Anuj Goenka;Logan A. Walsh.
Clinical effect of point mutations in myelodysplastic syndromes.
Rafael Bejar;Kristen Stevenson;Omar Abdel-Wahab;Naomi Galili.
The New England Journal of Medicine (2011)
MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.
Yana Pikman;Benjamin H Lee;Thomas Mercher;Elizabeth McDowell.
PLOS Medicine (2006)
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