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Nature Medicine, ISSN 1078-8956, 01/2017, Volume 23, Issue 1, pp. 69 - 78
In acute myeloid leukemia (AML), therapy resistance frequently occurs, leading to high mortality among patients. However, the mechanisms that render leukemic... 
TRANSFORMATION | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | SOMATIC MUTATIONS | CELL BIOLOGY | THERAPY | GENE EZH2 | DIFFERENTIATION | INHIBITOR | EXPRESSION | Immunohistochemistry | CDC2 Protein Kinase | Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors | Neoplasm Transplantation | Cyclin-Dependent Kinases - metabolism | Cytarabine - pharmacology | Immunoprecipitation | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Bortezomib - pharmacology | Gene Knockdown Techniques | Young Adult | Flow Cytometry | Mass Spectrometry | Aged, 80 and over | Leukemia, Myeloid, Acute - drug therapy | Adult | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Blotting, Western | Homeodomain Proteins - genetics | Drug Resistance, Neoplasm - genetics | Protein Kinase Inhibitors | Animals | Proteomics | Cell Line, Tumor | HSP90 Heat-Shock Proteins - metabolism | Aged | Mice | Protein Processing, Post-Translational | Histones - metabolism | Proteasome Endopeptidase Complex - metabolism | Pyridones - pharmacology | Leukemia, Myeloid, Acute - genetics | Genetic aspects | Methyltransferases | Drug resistance | Health aspects | Antimitotic agents | Prognosis | Mortality | Heat shock proteins | Histones | Drug therapy | Antineoplastic agents | Gene expression | Drugs | Therapy | Hsp90 protein | Phosphorylation | Leukemia | Chemoresistance | Cytotoxicity | Kinases | Degradation | Proteins | Cytarabine | Restoration | Histone methyltransferase | HOX gene | Protein-tyrosine kinase | Tyrosine | Bortezomib | Myeloid leukemia | Patients | Sensitivity | Inhibitors | Derepression | Cell lines | Proteasomes | Blast resistance | Methylation | Acute myeloid leukemia | Heat shock
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 12/2017, Volume 143, Issue 6, pp. 671 - 683
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 11/2016, Volume 291, Issue 47, pp. 24594 - 24606
Journal Article
Cancer Cell, ISSN 1535-6108, 10/2016, Volume 30, Issue 4, pp. 563 - 577
The transition from castration-resistant prostate adenocarcinoma (CRPC) to neuroendocrine prostate cancer (NEPC) has emerged as an important mechanism of... 
castration-resistant prostate adenocarcinoma | prostate cancer organoid | N-Myc | genetically engineered mouse | neuroendocrine prostate cancer | Aurora kinase A | EZH2 | REARRANGEMENT | INACTIVATION | GENOMICS | PROTEIN | ONCOLOGY | ADENOCARCINOMA | MOUSE MODEL | SMALL-CELL CARCINOMA | PTEN | DIFFERENTIATION | IDENTIFICATION | CELL BIOLOGY | Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors | Prostatic Neoplasms - metabolism | Humans | N-Myc Proto-Oncogene Protein - genetics | Male | Genes, myc | Prostatic Neoplasms, Castration-Resistant - genetics | Prostatic Neoplasms, Castration-Resistant - pathology | Heterografts | Prostatic Neoplasms - genetics | Transcription, Genetic | N-Myc Proto-Oncogene Protein - biosynthesis | Prostatic Neoplasms - drug therapy | Neuroendocrine Tumors - pathology | Prostatic Neoplasms - pathology | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Signal Transduction | Neuroendocrine Tumors - metabolism | Mice, Transgenic | Prostatic Neoplasms, Castration-Resistant - drug therapy | Pyrimidines - pharmacology | Prostatic Neoplasms, Castration-Resistant - metabolism | Neuroendocrine Tumors - genetics | Azepines - pharmacology | Animals | N-Myc Proto-Oncogene Protein - metabolism | Neuroendocrine Tumors - drug therapy | Mice | Protein Kinase Inhibitors - pharmacology | Development and progression | Genetic aspects | Genetic engineering | Genetic transcription | Prostate cancer | Genetically modified organisms
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 05/2017, Volume 24, Issue 5, pp. 889 - 902
Hepatocellular carcinoma (HCC) is the most common type of liver cancer in humans. The focal adhesion tyrosine kinase (FAK) is often over-expressed in human HCC... 
OVEREXPRESSION | METHYLATION | PROTEIN | INHIBITION | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | NUCLEAR FAK | MECHANISMS | HISTONE METHYLTRANSFERASE EZH2 | CANCER | EXPRESSION | CELL BIOLOGY | Focal Adhesion Kinase 1 - genetics | Neoplasm Transplantation | RNA, Small Interfering - genetics | E2F2 Transcription Factor - genetics | Apoptosis - drug effects | Humans | Gene Expression Regulation, Neoplastic | Apoptosis - genetics | Male | Receptor, Notch2 - genetics | E2F2 Transcription Factor - metabolism | Tumor Suppressor Protein p53 - genetics | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Focal Adhesion Kinase 1 - metabolism | Promoter Regions, Genetic | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Liver Neoplasms - genetics | Signal Transduction | Receptor, Notch2 - metabolism | Tumor Suppressor Protein p53 - metabolism | E2F3 Transcription Factor - genetics | G2 Phase Cell Cycle Checkpoints | Hep G2 Cells | Animals | Histones - genetics | Mice, Nude | Aminopyridines - pharmacology | Carcinoma, Hepatocellular - pathology | E2F3 Transcription Factor - metabolism | Liver Neoplasms - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Histones - metabolism | Focal Adhesion Kinase 1 - antagonists & inhibitors | Carcinoma, Hepatocellular - metabolism | RNA, Small Interfering - metabolism | Original Paper
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
STEM CELLS, ISSN 1066-5099, 08/2016, Volume 34, Issue 8, pp. 2183 - 2193
Journal Article