Assistant Professor of Medicine, Dana-Farber Cancer Institute
Hematology
Dr. James E. Bradner, MD
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James Bradner practices Hematology. He graduated from University of Chicago Pritzker School of Medicine. University of Chicago Pritzker School of Medicine is ranked 10 in research and 19 in primary care medicine He received 1 awards: "Elected Member". James Bradner is a published doctor and has 88 publications published. The lastest was: 'MTAP deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in cancer cells.'
Publications
- MTAP deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in Cancer cells.
- Identification of bromodomain-containing protein-4 as a novel marker and epigenetic target in mast cell Leukemia.
- Harnessing Connectivity in a Large-Scale Small-Molecule Sensitivity Dataset.
- Comparative pharmacokinetic properties and antitumor activity of the marine HDACi Largazole and Largazole peptide isostere.
- Chromatin proteomic profiling reveals novel proteins associated with histone-marked genomic regions.
- The SWI/SNF ATPases Are Required for Triple Negative Breast Cancer Cell Proliferation.
- DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged Leukemia.
- Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers.
- Targeting the MYC and PI3K Pathways Eliminates Leukemia-Initiating Cells in T-cell Acute Lymphoblastic Leukemia.
- Convergent Transcription at Intragenic Super-Enhancers Targets AID-Initiated Genomic Instability.
- An in-tumor genetic screen reveals that the BET bromodomain protein, BRD4, is a potential therapeutic target in ovarian carcinoma.
- AF10 Regulates Progressive H3K79 Methylation and HOX Gene Expression in Diverse AML Subtypes.
- Syntheses and discovery of a novel class of cinnamic hydroxamates as histone deacetylase inhibitors by multimodality molecular imaging in living subjects.
- Targeting Transcriptional Addictions in Small Cell Lung Cancer with a Covalent CDK7 Inhibitor.
- Quantitative ChIP-Seq Normalization Reveals Global Modulation of the Epigenome.
- Biased multicomponent reactions to develop novel bromodomain inhibitors.
- BET Protein Antagonist JQ1 Is Synergistically Lethal with FLT3 Tyrosine Kinase Inhibitor (TKI) and Overcomes Resistance to FLT3-TKI in AML Cells Expressing FLT-ITD.
- Identification of ATR-Chk1 pathway inhibitors that selectively target p53-deficient Cells without directly suppressing ATR catalytic activity.
- PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies.
- NF-κB Directs Dynamic Super Enhancer Formation in Inflammation and Atherogenesis.
- Inhibition of bromodomain proteins for the treatment of human diffuse large B-cell Lymphoma.
- Epigenetic targeting of Hedgehog pathway transcriptional output through BET bromodomain inhibition.
- 7,9-Diaryl-1,6,8-trioxaspiro[4.5]dec-3-en-2-ones: Readily accessible and highly potent antiCancer compounds.
- Notch inhibition allows oncogene-independent generation of iPS Cells.
- MLL3 Is a Haploinsufficient 7q Tumor Suppressor in Acute Myeloid Leukemia.
- An epigenomic approach to therapy for tamoxifen-resistant breast Cancer.
- Targeting STAT5 in Hematologic Malignancies through Inhibition of the Bromodomain and Extra-Terminal (BET) Bromodomain Protein BRD2.
- Combined autophagy and proteasome inhibition: A phase 1 trial of hydroxychloroquine and bortezomib in patients with relapsed/refractory Myeloma.
- Triplication of a 21q22 region contributes to B Cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation.
- Activation of SOX2 expression by BRD4-NUT oncogenic fusion drives neoplastic transformation in NUT midline carcinoma.
- Highly Active Combination of BRD4 Antagonist and Histone Deacetylase Inhibitor against Human Acute Myelogenous Leukemia Cells.
- An epigenetic mechanism of resistance to targeted therapy in T cell Acute lymphoblastic leukemia.
- RapidCaP, a Novel GEM Model for Metastatic Prostate Cancer Analysis and Therapy, Reveals Myc as a Driver of Pten-Mutant Metastasis.
- Repression of BIM mediates survival signaling by MYC and AKT in high-risk T-cell Acute lymphoblastic leukemia.
- c-Myc inhibition prevents Leukemia initiation in mice and impairs the growth of relapsed and induction failure pediatric T-ALL cells.
- Improved targeting of JAK2 leads to increased therapeutic efficacy in Myeloproliferative neoplasms.
- Genome-wide localization of small molecules.
- Discovery and characterization of super-enhancer-associated dependencies in diffuse large B cell Lymphoma.
- BCL2-specific inhibitor ABT-199 synergizes strongly with cytarabine against the early immature LOUCY Cell line but not more differentiated T-ALL Cell lines.
- The Myeloma Drug Lenalidomide Promotes the Cereblon-Dependent Destruction of Ikaros Proteins.
- Bromodomain and extra-terminal (BET) protein inhibition suppresses HTLV-1 Tax-mediated tumorigenesis by inhibiting NF-κB signaling.
- Efficacy of BET Bromodomain Inhibition in Kras-Mutant Non-Small Cell Lung Cancer.
- The use of small molecules in somatic-Cell reprogramming.
- Cancer-associated IDH2 mutants drive an Acute myeloid leukemia that is susceptible to Brd4 inhibition.
- C-terminal binding protein-2 regulates response of epithelial ovarian Cancer cells to histone deacetylase inhibitors.
- BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure.
- BET acetyl-lysine binding proteins control pathological cardiac hypertrophy.
- Interview: interview with james bradner.
- New targets for hematologic Malignancies.
- Synthesis and HDAC inhibitory activity of isosteric thiazoline-oxazole largazole analogs.
- The bromodomain protein Brd4 insulates chromatin from DNA damage signalling.
- Selective HDAC1/HDAC2 Inhibitors Induce Neuroblastoma Differentiation.
- MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma.
- Selective inhibition of tumor oncogenes by disruption of super-enhancers.
- BET bromodomain-targeting compounds reactivate HIV from latency via a Tat-independent mechanism.
- Targeting transcription factor SALL4 in Acute myeloid leukemia by interrupting its interaction with an epigenetic complex.
- BET bromodomain inhibition as a novel strategy for reactivation of HIV-1.
- Transcriptional Amplification in Tumor Cells with Elevated c-Myc.
- Chromatin modifications as therapeutic targets in MLL-rearranged Leukemia.
- BET bromodomain inhibition as a therapeutic strategy to target c-Myc.
- Protection from UV-induced skin carcinogenesis by genetic inhibition of the ataxia telangiectasia and Rad3-related (ATR) kinase.
- RNAi screen identifies Brd4 as a therapeutic target in Acute myeloid leukaemia.
- Synthesis and Biological Evaluation of JAHAs: Ferrocene-Based Histone Deacetylase Inhibitors.
- Histone deacetylase 6 and heat shock protein 90 control the functions of foxp3+ T-regulatory Cells.
- Differentiation of NUT midline carcinoma by epigenomic reprogramming.
- HSP90 is a therapeutic target in JAK2-dependent Myeloproliferative neoplasms in mice and humans.
- Chemical genetic strategy identifies histone deacetylase 1 (HDAC1) and HDAC2 as therapeutic targets in sickle cell Disease.
- Chemical phylogenetics of histone deacetylases.
- Functional screening identifies CRLF2 in precursor B-cell Acute lymphoblastic leukemia.
- Donor-recipient mismatch for common gene deletion polymorphisms in Graft-versus-host disease.
- Tubacin kills Epstein-Barr virus (EBV)-Burkitt Lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis.
- In vivo pharmacodynamic imaging of proteasome inhibition.
- Identification and characterization of small molecule inhibitors of a class I histone deacetylase from Plasmodium falciparum.
- Synthesis and histone deacetylase inhibitory activity of largazole analogs: alteration of the zinc-binding domain and macrocyclic scaffold.
- Synthesis and conformation-activity relationships of the peptide isosteres of FK228 and largazole.
- A pulse at the heart of targeted therapy.
- HDAC6 inhibition enhances 17-AAG--mediated abrogation of hsp90 chaperone function in human Leukemia cells.
- Total synthesis and biological mode of action of largazole: a potent class I histone deacetylase inhibitor.
- Structural origin of selectivity in class II-selective histone deacetylase inhibitors.
- Effect of thrombocytopenia on outcomes following treatment with either enoxaparin or unfractionated heparin in patients presenting with Acute coronary syndromes.
- PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung Cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib.
- Coactivation of receptor tyrosine kinases affects the response of tumor Cells to targeted therapies.
- SD-1029 inhibits signal transducer and activator of transcription 3 nuclear translocation.
- Lymphocyte chemotaxis is regulated by histone deacetylase 6, independently of its deacetylase activity.
- IntraCellular protein degradation and its therapeutic implications.
- Small-molecule inhibition of proteasome and aggresome function induces synergistic antitumor activity in multiple Myeloma.
- Therapeutic Strategies to Inhibit MYC.
Schools
Pritzker School Of Med University Of Chicago
Brigham and Women39s Hospital
Dana Farber Cancer Institute
Procedures Preformed
- HPC Transplantation (Stem Cell Transplant)
- Plasmapheresis
- Thoracentesis
Conditions Treated
- Acute Leukemia
- Adrenal Gland Cancer
- Anemia
- Coagulation Disorders (incl. Hemophilia)
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Doctors Specialties
- Hematology
- Medical Oncology
- Oncology
Accepted Insurances
Awards
- Elected Member
Education
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Brigham and Women's Hospital -
University of Chicago Pritzker School of Medicine
Hospital
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Brigham and Women's Faulkner Hospital -
Brigham and Women's Hospital -
Massachusetts General Hospital -
Dana-Farber Cancer Institute -
South Shore Hospital
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1518920867 |
| Last Name Of The Provider | BRADNER |
| First Name Of The Provider | JAMES |
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