Associate Professor, Medicine-Brigham and Women's Hospital, Harvard Medical School
Hematology
Dr. Benjamin L. Ebert, MD
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Benjamin Ebert practices Hematology. He graduated from Harvard Medical School. Harvard Medical School is a top medical university. Harvard Medical School is ranked 1 in research and 12 in primary care medicine He has 1 awards "Elected Member". Dr. Benjamin L. Ebert has written publications. He has 83 publications published with PubMed. The lastest publication is: 'Lenalidomide: deciphering mechanisms of action in myeloma, myelodysplastic syndrome and beyond.'
Publications
- Lenalidomide: deciphering mechanisms of action in myeloma, myelodysplastic syndrome and beyond.
- Niche-Based Screening in Multiple Myeloma Identifies a Kinesin-5 Inhibitor with Improved Selectivity over Hematopoietic Progenitors.
- Age-related clonal hematopoiesis associated with adverse outcomes.
- Mutations in G protein β subunits promote transformation and kinase inhibitor resistance.
- Perivascular Gli1(+) Progenitors Are Key Contributors to Injury-Induced Organ Fibrosis.
- L-Leucine improves the anaemia in models of Diamond Blackfan anaemia and the 5q- syndrome in a TP53-independent way.
- Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice combine to promote disease progression in Myeloproliferative neoplasms.
- Somatic mutations predict poor outcome in patients with myelodysplastic syndrome after hematopoietic stem-Cell transplantation.
- Rational design of highly active sgRNAs for CRISPR-Cas9-mediated gene inactivation.
- TET2 mutations predict response to hypomethylating agents in myelodysplastic syndrome patients.
- Role of Casein Kinase 1A1 in the Biology and Targeted Therapy of del(5q) MDS.
- National trends in hospitalizations for Sickle cell disease in the United States following the FDA approval of hydroxyurea, 1998-2008.
- MDS Is a Stem Cell Disorder After All.
- Generation of mouse models of myeloid malignancy with combinatorial genetic lesions using CRISPR-Cas9 genome editing.
- Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in Myeloproliferative neoplasm pathogenesis.
- Csnk1a1 inhibition has p53-dependent therapeutic efficacy in acute myeloid leukemia.
- The emerging importance of ribosomal dysfunction in the pathogenesis of hematologic Disorders.
- Genome-scale CRISPR-Cas9 knockout screening in human Cells.
- Musashi-2 controls Cell fate, lineage bias, and TGF-β signaling in HSCs.
- Niche-based screening identifies small-molecule inhibitors of leukemia stem Cells.
- Global H3K4me3 genome mapping reveals alterations of innate immunity signaling and overexpression of JMJD3 in human myelodysplastic syndrome CD34+ Cells.
- Lenalidomide Causes Selective Degradation of IKZF1 and IKZF3 in Multiple Myeloma Cells.
- Toll-like receptor alterations in myelodysplastic syndrome.
- Sinister Symbiosis: Pathological Hematopoietic-Stromal Interactions in CML.
- Diminutive somatic deletions in the 5q region lead to a phenotype atypical of classical 5q- syndrome.
- The biology and clinical impact of genetic lesions in myeloid malignancies.
- In Vivo RNAi Screening Identifies a Leukemia-Specific Dependence on Integrin Beta 3 Signaling.
- NRAS mutations with low allele burden have independent prognostic significance for patients with lower risk myelodysplastic syndromes.
- New strategies in myelodysplastic syndromes: application of molecular diagnostics to clinical practice.
- Macrophages support pathological erythropoiesis in Polycythemia vera and ?-thalassemia.
- Depletion of Jak2V617F MPN-propagating stem cells by interferon-alpha in a murine model of Polycythemia vera.
- (R)-2-Hydroxyglutarate Is Sufficient to Promote Leukemogenesis and Its Effects Are Reversible.
- miR-433 is aberrantly expressed in Myeloproliferative neoplasms and suppresses hematopoietic cell growth and differentiation.
- Implantable microenvironments to attract hematopoietic stem/cancer Cells.
- Mitochondrial Atpif1 regulates haem synthesis in developing erythroblasts.
- Myeloproliferative neoplasm animal models.
- Molecular Pathophysiology of Myelodysplastic Syndromes.
- Novel approaches to the treatment of Sickle cell disease: the potential of histone deacetylase inhibitors.
- Stress granules contribute to α-globin homeostasis in differentiating erythroid Cells.
- Power cut: inhibiting mitochondrial translation to target leukemia.
- Translational medicine: ribosomopathies.
- Correction of Sickle Cell Disease in Adult Mice by Interference with Fetal Hemoglobin Silencing.
- Molecular dissection of the 5q deletion in myelodysplastic syndrome.
- Coordinate loss of a microRNA and protein-coding gene cooperate in the pathogenesis of 5q- syndrome.
- Clinical effect of point mutations in myelodysplastic syndromes.
- Dexamethasone and lenalidomide have distinct functional effects on erythropoiesis.
- The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia Cells resistant to kinase inhibitors.
- Haploinsufficiency for ribosomal protein genes causes selective activation of p53 in human erythroid progenitor Cells.
- Unraveling the molecular pathophysiology of myelodysplastic syndromes.
- Human tumors instigate granulin-expressing hematopoietic Cells that promote malignancy by activating stromal fibroblasts in mice.
- Densely interconnected transcriptional circuits control Cell states in human hematopoiesis.
- Stem Cell gene expression programs influence clinical outcome in human leukemia.
- STATistical power of clonal analysis: differential STAT1 pathway activation downstream of the JAK2V617F mutation.
- NF1 inactivation revs up Ras in adult acute myelogenous leukemia.
- Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia.
- Chemical genetic strategy identifies histone deacetylase 1 (HDAC1) and HDAC2 as therapeutic targets in Sickle cell disease.
- Physiological Jak2V617F expression causes a lethal Myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells.
- The Apc(min) mouse has altered hematopoietic stem Cell function and provides a model for MPD/MDS.
- Ribosomopathies: human Disorders of ribosome dysfunction.
- The connectivity map links iron regulatory protein-1-mediated inhibition of hypoxia-inducible factor-2a translation to the anti-inflammatory 15-deoxy-delta12,14-prosta...
- Preface. The biology and treatment of myelodysplastic syndrome.
- The genetic basis of myelodysplastic syndromes.
- Therapeutic potential of targeting haploinsufficient genes in cancer.
- Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies.
- Deletion 5q in myelodysplastic syndrome: a paradigm for the study of hemizygous deletions in cancer.
- A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive Myeloproliferative neoplasms.
- Small-molecule inhibitors of HIF-2a translation link its 5'UTR iron-responsive element to oxygen sensing.
- Identification of an evolutionarily conserved transcriptional signature of CD8 memory differentiation that is shared by T and B Cells.
- MicroRNA-mediated control of Cell fate in megakaryocyte-erythrocyte progenitors.
- An erythroid differentiation signature predicts response to lenalidomide in myelodysplastic syndrome.
- Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles.
- pVHL acts as an adaptor to promote the inhibitory phosphorylation of the NF-kappaB agonist Card9 by CK2.
- Metagene projection for cross-platform, cross-species characterization of global transcriptional states.
- MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.
- Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.
- An RNA interference model of RPS19 deficiency in Diamond-Blackfan Anemia recapitulates defective hematopoiesis and rescue by dexamethasone: identification of dexametha...
- Activating mutation in the tyrosine kinase JAK2 in Polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
- Genomic approaches to hematologic malignancies.
- Use of temozolomide with other cytotoxic chemotherapy in the treatment of patients with recurrent brain metastases from lung cancer.
- Lenalidomide induces degradation of IKZF1 and IKZF3.
- Loss of Function of TET2 Cooperates with Constitutively Active KIT in Murine and Human Models of Mastocytosis.
- Mutations in epigenetic regulators including SETD2 are gained during relapse in paediatric acute lymphoblastic leukaemia.
Schools
Harvard Medical School
Massachusetts General Hospital
Dana Farber Cancer Institute
Conditions Treated
- Anemia
- Coagulation Disorders (incl. Hemophilia)
- Hemophilia
- Leukocytosis
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Doctors Specialties
- Hematology
- Medical Oncology
- Oncology
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- Blue Card PPO
- BlueConnect HMO
- Blue with Managed Care Behavioral Health HMO
- Preferred Blue PPO
- Cigna HMO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- Commercial Insurance Company
- First Health (Coventry Health Care) PPO
- Choice Care PPO
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- Tufts PPO
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
Awards
- Elected Member
Education
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Brigham and Women's Hospital -
Massachusetts General Hospital -
Harvard Medical School
Hospital
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Brigham and Women's Hospital -
Massachusetts General Hospital -
Dana-Farber Cancer Institute
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1104933605 |
| Last Name Of The Provider | EBERT |
| First Name Of The Provider | BENJAMIN |
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