Professor of Medicine, Beth Israel Deaconess Medical Center
Hematology
Dr. Daniel G. Tenen, MD
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Daniel Tenen practices Hematology. He attended Harvard Medical School. Harvard Medical School is a top medical college. Harvard Medical School is ranked 1 in research and 12 in primary care medicine Daniel Tenen is a published MD. He has 101 papers published. The most current publication "SALL4, the missing link between stem cells, development and cancer."
Publications
- Hematopoietic Differentiation Is Required for Initiation of Acute Myeloid Leukemia.
- The Runx-PU.1 pathway preserves normal and AML/ETO9a leukemic stem cells.
- Runx1 exon 6 related alternative splicing isoforms differentially regulate hematopoiesis in mice.
- The gene signature in CCAAT-enhancer-binding protein α dysfunctional acute myeloid leukemia predicts responsiveness to histone deacetylase inhibitors.
- RNA editome imbalance in hepatocellular carcinoma.
- NOTCH2 and FLT3 gene mis-splicing are common events in patients with acute myeloid leukemia (AML): new potential targets in AML.
- Down-regulation of RUNX1/CBFβ by MLL fusion proteins enhances HSC self-renewal.
- SALL4 is a new target in endometrial cancer.
- Sox4 Is a Key Oncogenic Target in C/EBPα Mutant Acute Myeloid Leukemia.
- DNMT1-interacting RNAs block gene-specific DNA methylation.
- C/EBP? is required for development of dendritic cell progenitors.
- C/EBPa controls acquisition and maintenance of adult haematopoietic stem cell quiescence.
- In vivo generation of transplantable human hematopoietic cells from induced pluripotent stem cells.
- Sustained PU.1 Levels Balance Cell-Cycle Regulators to Prevent Exhaustion of Adult Hematopoietic Stem Cells.
- Targeting transcription factor SALL4 in acute myeloid leukemia by interrupting its interaction with an epigenetic complex.
- SALL4 is a key transcription regulator in normal human hematopoiesis.
- The ability of MLL to bind RUNX1 and methylate H3K4 at PU.1 regulatory regions is impaired by MDS/AML-associated RUNX1/AML1 mutations.
- RUNX1 regulates the CD34 gene in haematopoietic stem cells by mediating interactions with a distal regulatory element.
- DLK1-DIO3 genomic imprinted microRNA cluster at 14q32.2 defines a stem-like subtype of hepatocellular carcinoma associated with poor survival.
- CD34 is required for Dendritic Cell Trafficking and Pathology in Murine Hypersensitivity Pneumonitis.
- Two distinct auto-regulatory loops operate at the PU.1 locus in B cells and myeloid cells.
- Cannabinoid receptor 2 and its agonists mediate hematopoiesis and hematopoietic stem and progenitor cell mobilization.
- C/EBPα regulated microRNA-34a targets E2F3 during granulopoiesis and is down-regulated in AML with CEBPA mutations.
- Erlotinib at a dose of 25 mg daily for non-small cell lung cancers with EGFR mutations.
- PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
- BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells.
- Apoptosis induced by JAK2 inhibition is mediated by Bim and enhanced by the BH3 mimetic ABT-737 in JAK2 mutant human erythroid cells.
- Use of bicistronic vectors in combination with flow cytometry to screen for effective small interfering RNA target sequences.
- Cell-cycle regulator E2F1 and microRNA-223 comprise an autoregulatory negative feedback loop in acute myeloid leukemia.
- Identification of a myeloid committed progenitor as the cancer-initiating cell in acute promyelocytic leukemia.
- PML-RARalpha initiates leukemia by conferring properties of self-renewal to committed promyelocytic progenitors.
- Early chromatin unfolding by RUNX1: a molecular explanation for differential requirements during specification versus maintenance of the hematopoietic gene expression ...
- Dysregulation of the C/EBPalpha differentiation pathway in human cancer.
- Effects of erlotinib in EGFR mutated non-small cell lung cancers with resistance to gefitinib.
- PU.1 expression is modulated by the balance of functional sense and antisense RNAs regulated by a shared cis-regulatory element.
- Hsp90 inhibition suppresses mutant EGFR-T790M signaling and overcomes kinase inhibitor resistance.
- 15-Hydroxyprostaglandin dehydrogenase is a target of hepatocyte nuclear factor 3beta and a tumor suppressor in lung cancer.
- Phosphorylation of CCAAT/enhancer-binding protein alpha regulates GLUT4 expression and glucose transport in adipocytes.
- Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells.
- Differential responses to erlotinib in epidermal growth factor receptor (EGFR)-mutated lung cancers with acquired resistance to gefitinib carrying the L747S or T790M s...
- Gene transactivation without direct DNA binding defines a novel gain-of-function for PML-RARalpha.
- PU.1 is a major downstream target of AML1 (RUNX1) in adult mouse hematopoiesis.
- Distinct gene expression profiles of acute myeloid/T-lymphoid leukemia with silenced CEBPA and mutations in NOTCH1.
- CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alpha.
- C/EBPalpha binds and activates the PU.1 distal enhancer to induce monocyte lineage commitment.
- Target proteins of C/EBPalphap30 in AML: C/EBPalphap30 enhances sumoylation of C/EBPalphap42 via up-regulation of Ubc9.
- The Pu.1 locus is differentially regulated at the level of chromatin structure and noncoding transcription by alternate mechanisms at distinct developmental stages of ...
- Resistance to an irreversible epidermal growth factor receptor (EGFR) inhibitor in EGFR-mutant lung cancer reveals novel treatment strategies.
- BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with oncogenic EGFR mutations.
- A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia.
- Down-regulation of PU.1 by methylation of distal regulatory elements and the promoter is required for myeloma cell growth.
- c-Jun homodimers can function as a context-specific coactivator.
- Transcriptional profiling identifies cyclin D1 as a critical downstream effector of mutant epidermal growth factor receptor signaling.
- Essential role of Jun family transcription factors in PU.1 knockdown-induced leukemic stem cells.
- The order of expression of transcription factors directs hierarchical specification of hematopoietic lineages.
- CCAAT/enhancer binding proteins alpha and epsilon cooperate with all-trans retinoic acid in therapy but differ in their antileukemic activities.
- Hematopoietic stem cell and multilineage defects generated by constitutive beta-catenin activation.
- Three-dimensional magnetic resonance microscopy of pulmonary solitary tumors in transgenic mice.
- C/EBPbeta is required for 'emergency' granulopoiesis.
- Absence of the transcription factor CCAAT enhancer binding protein alpha results in loss of myeloid identity in bcr/abl-induced malignancy.
- ATRA resolves the differentiation block in t(15;17) acute myeloid leukemia by restoring PU.1 expression.
- Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.
- Respiratory failure due to differentiation arrest and expansion of alveolar cells following lung-specific loss of the transcription factor C/EBPalpha in mice.
- Lymphoid cell growth and transformation are suppressed by a key regulatory element of the gene encoding PU.1.
- Developmental checkpoints of the basophil/mast cell lineages in adult murine hematopoiesis.
- The hematopoietic transcription factor AML1 (RUNX1) is negatively regulated by the cell cycle protein cyclin D3.
- Metabolic response of mice to a postnatal ablation of CCAAT/enhancer-binding protein alpha.
- Distinctive and indispensable roles of PU.1 in maintenance of hematopoietic stem cells and their differentiation.
- Effect of transcription-factor concentrations on leukemic stem cells.
- CD34 expression by mast cells: of mice and men.
- Differential effects of gefitinib and cetuximab on non-small-cell lung cancers bearing epidermal growth factor receptor mutations.
- An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptor.
- Role of transcription factors C/EBPalpha and PU.1 in normal hematopoiesis and leukemia.
- Potential autoregulation of transcription factor PU.1 by an upstream regulatory element.
- EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.
- Inducible chronic phase of myeloid leukemia with expansion of hematopoietic stem cells in a transgenic model of BCR-ABL leukemogenesis.
- Unusual cases in multiple myeloma and a dramatic response in metastatic lung cancer: case 4. Mutation of the epidermal growth factor receptor in an elderly man with ad...
- Enhancement of hematopoietic stem cell repopulating capacity and self-renewal in the absence of the transcription factor C/EBP alpha.
- Biolistic expression of the macrophage colony stimulating factor receptor in organotypic cultures induces an inflammatory response.
- Primary human CD34+ hematopoietic stem and progenitor cells express functionally active receptors of neuromediators.
- A transcriptional profiling study of CCAAT/enhancer binding protein targets identifies hepatocyte nuclear factor 3 beta as a novel tumor suppressor in lung cancer.
- pDP4, a novel glycoprotein secreted by mature granulocytes, is regulated by transcription factor PU.1.
- Acute myeloid leukemia induced by graded reduction of a lineage-specific transcription factor, PU.1.
- A dominant-negative mutant of C/EBPalpha, associated with acute myeloid leukemias, inhibits differentiation of myeloid and erythroid progenitors of man but not mouse.
- Phosphorylation of C/EBPalpha inhibits granulopoiesis.
- Inducible expression of BCR/ABL using human CD34 regulatory elements results in a megakaryocytic myeloproliferative syndrome.
- The amino terminal and E2F interaction domains are critical for C/EBP alpha-mediated induction of granulopoietic development of hematopoietic cells.
- Paired activating and inhibitory immunoglobulin-like receptors, MAIR-I and MAIR-II, regulate mast cell and macrophage activation.
- Heterozygous PU.1 mutations are associated with acute myeloid leukemia.
- CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia.
- The myeloid master regulator transcription factor PU.1 is inactivated by AML1-ETO in t(8;21) myeloid leukemia.
- Distal elements are critical for human CD34 expression in vivo.
- Transgenic targeting with regulatory elements of the human CD34 gene.
- Downregulation of c-Jun expression by transcription factor C/EBPalpha is critical for granulocytic lineage commitment.
- C/EBPalpha is required for proteolytic cleavage of cyclin A by calpain 3 in myeloid precursor cells.
- Ras signaling enhances the activity of C/EBP alpha to induce granulocytic differentiation by phosphorylation of serine 248.
- Granulocyte inducer C/EBPalpha inactivates the myeloid master regulator PU.1: possible role in lineage commitment decisions.
- Induction of granulocytic differentiation by 2 pathways.
- Differential regulation of the human and murine CD34 genes in hematopoietic stem cells.
- SALL4, the missing link between stem cells, development and cancer.
Schools
Harvard Medical School
Doctors Specialties
- Medical Oncology
- Oncology
- Hematology
Accepted Insurances
Education
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Brigham and Women's Hospital -
Harvard Medical School
Hospital
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Beth Israel Deaconess Medical Center
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