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Nature, ISSN 0028-0836, 01/2012, Volume 481, Issue 7380, pp. 157 - 163
Journal Article
Nature, ISSN 0028-0836, 10/2011, Volume 478, Issue 7367, pp. 64 - 69
Journal Article
Blood, ISSN 0006-4971, 02/2017, Volume 129, Issue 6, pp. 667 - 679
The genetic landscape of classicalmyelopro-liferative neoplasm (MPN) is in large part elucidated. The MPN-restricted driver mutations, including those in JAK2,... 
POLYCYTHEMIA-VERA | ACTIVATING MUTATION | CLONAL HEMATOPOIESIS | ACQUIRED UNIPARENTAL DISOMY | JAK2 V617F MUTATION | ACUTE MYELOID-LEUKEMIA | ESSENTIAL THROMBOCYTHEMIA | HEMATOLOGY | CHRONIC MYELOMONOCYTIC LEUKEMIA | THROMBOPOIETIN RECEPTOR | DISEASE PROGRESSION | Thrombocythemia, Essential - physiopathology | Epigenesis, Genetic | Humans | Gene Expression Regulation, Neoplastic | STAT Transcription Factors - metabolism | Polycythemia Vera - genetics | Receptors, Granulocyte Colony-Stimulating Factor - genetics | Thrombocythemia, Essential - genetics | Calreticulin - genetics | Receptors, Erythropoietin - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | DNA-Binding Proteins - metabolism | Polycythemia Vera - metabolism | Janus Kinase 2 - metabolism | Calreticulin - metabolism | Receptors, Granulocyte Colony-Stimulating Factor - metabolism | Polycythemia Vera - physiopathology | Primary Myelofibrosis - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Primary Myelofibrosis - physiopathology | Janus Kinase 2 - genetics | Repressor Proteins - genetics | Proto-Oncogene Proteins - genetics | DNA-Binding Proteins - genetics | Receptors, Thrombopoietin - metabolism | Disease Progression | DNA (Cytosine-5-)-Methyltransferases - genetics | Receptors, Thrombopoietin - genetics | Primary Myelofibrosis - genetics | STAT Transcription Factors - genetics | Mutation | Receptors, Erythropoietin - metabolism | Thrombocythemia, Essential - metabolism
Journal Article
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 06/2013, Volume 210, Issue 6, pp. 1137 - 1151
Journal Article
Blood, ISSN 0006-4971, 02/2015, Volume 125, Issue 9, pp. 1367 - 1376
Journal Article
Journal Article
PLoS Medicine, ISSN 1549-1277, 2006, Volume 3, Issue 7, pp. 1140 - 1151
The JAK2V617F allele has recently been identified in patients with polycythemia vera (PV), essential thrombocytosis (ET), and myelofibrosis with myeloid... 
Recombinant Fusion Proteins - adverse effects | Humans | Myeloproliferative Disorders - pathology | Mutation, Missense | Primary Myelofibrosis - pathology | Receptors, Cytokine - physiology | Janus Kinases - physiology | Bone Marrow Transplantation | Hematopoiesis - physiology | Myeloid Cells - drug effects | Transcription, Genetic | Colony-Forming Units Assay | Phosphorylation - drug effects | mRNA Cleavage and Polyadenylation Factors - genetics | Hematologic Neoplasms - physiopathology | Disease Models, Animal | Cells, Cultured - drug effects | Bone Marrow Cells - pathology | Hematopoiesis - genetics | Signal Transduction - genetics | Thrombocytosis - etiology | Sequence Analysis, DNA | Cell Division - drug effects | mRNA Cleavage and Polyadenylation Factors - physiology | Receptor, Platelet-Derived Growth Factor alpha - physiology | Hematologic Neoplasms - drug therapy | Mice | Mice, Inbred BALB C | Myeloid Cells - pathology | Protein Processing, Post-Translational - genetics | Myeloproliferative Disorders - genetics | Oncogene Proteins, Fusion - physiology | STAT Transcription Factors - physiology | Protein Processing, Post-Translational - drug effects | Cells, Cultured - pathology | Bone Marrow Cells - drug effects | Spleen - pathology | Thrombocytosis - pathology | Gene Expression Regulation | Janus Kinases - antagonists & inhibitors | Point Mutation | Megakaryocytes - pathology | Primary Myelofibrosis - genetics | Animals | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Receptor, Platelet-Derived Growth Factor alpha - genetics | Myeloproliferative Disorders - etiology | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Genetic Vectors | Megakaryocytes - drug effects | Cytokines - pharmacology | Amino Acid Substitution | Thrombocytosis - genetics | Genetic aspects | Myelofibrosis | Research | Hematology | Gene Therapy | Genomics | Genetics | Oncology | Cancer Biology | Hematology (including Blood Transfusion)
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, p. e61807
The Notch pathway can have both oncogenic and tumor suppressor roles, depending on cell context. For example, Notch signaling promotes T cell differentiation... 
PROMOTER DNA METHYLATION | LYMPHOMAS | TUMOR-SUPPRESSOR FUNCTION | MULTIDISCIPLINARY SCIENCES | ACUTE LYMPHOCYTIC-LEUKEMIA | GROWTH | GENES | TRANSCRIPTION | MALIGNANCIES | CANCER | TUMORIGENESIS | Transcription, Genetic - drug effects | Apoptosis - drug effects | Receptors, Notch - metabolism | Humans | Apoptosis - genetics | Receptors, Notch - genetics | Gene Expression Profiling | Hematopoiesis - drug effects | Basic Helix-Loop-Helix Transcription Factors - metabolism | T-Lymphocytes - metabolism | Serrate-Jagged Proteins | T-Lymphocytes - drug effects | B-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - blood | B-Lymphocytes - metabolism | Repressor Proteins - metabolism | Bone Marrow - drug effects | Jagged-1 Protein | Basic Helix-Loop-Helix Transcription Factors - genetics | Membrane Proteins - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia, B-Cell - pathology | Repressor Proteins - genetics | Hematopoiesis - genetics | Signal Transduction - genetics | Azacitidine - pharmacology | Leukemia, B-Cell - blood | Leukemia, B-Cell - genetics | Signal Transduction - drug effects | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Cell Line, Tumor | Histones - metabolism | DNA Methylation - drug effects | Calcium-Binding Proteins - genetics | Gene Silencing - drug effects | Blood Cells - metabolism | Cell Lineage - drug effects | Intercellular Signaling Peptides and Proteins - metabolism | Epigenesis, Genetic - drug effects | Membrane Proteins - metabolism | T-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology | Blood Cells - drug effects | Hydroxamic Acids - pharmacology | Cell Lineage - genetics | Calcium-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Azacitidine - analogs & derivatives | DNA Methylation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | B-Lymphocytes - drug effects | Bone Marrow - pathology | Receptor, Notch3 | Cell Proliferation - drug effects | Sulfites | Epigenetic inheritance | DNA microarrays | Genes | Genetic aspects | Genetic engineering | Acute lymphocytic leukemia | B cells | T cells | Methylation | Cell differentiation | Biotechnology | Transcription factors | Bisulfite | Pathogenesis | Leukemia | Differentiation (biology) | Lymphocytes T | Kinases | Inactivation | Signal transduction | Restoration | Lymphocytes | DNA methylation | Bone marrow | Tumorigenesis | Acetylation | Deoxyribonucleic acid--DNA | CpG islands | Acute lymphatic leukemia | Deactivation | Lymphatic leukemia | Tumor cell lines | Gene silencing | Signaling | Lymphocytes B | Cell lines | Regulatory mechanisms (biology) | Stem cells | Epigenetics | Ligands | Tumor suppressor genes | Leukemogenesis | Lymphomas | Notch protein | Aberration | Apoptosis | Cancer | Deoxyribonucleic acid | DNA
Journal Article