Professor, Pathology and Laboratory Medicine, Perelman School of Medicine

Pathology

Doctor Warren S. Pear, MD is an expert in the field of Pathology. He went to University of Rochester School of Medicine and Dentistry. He received awards:"Elected Member". Warren Pear is a published physician. He published 84 publications, including: 'Tribbles in normal and malignant haematopoiesis.' He accepts Medicare payments and is registered with Medicare.gov.

Publications

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• Tribbles at the cross-roads….
• Tribbles in normal and malignant haematopoiesis.
• Discovery of Biomarkers Predictive of GSI Response in Triple-Negative Breast Cancer and Adenoid Cystic Carcinoma.
• Loss of oncogenic Notch1 with resistance to a PI3K inhibitor in T-cell leukaemia.
• The Notch1 transcriptional activation domain is required for development and reveals a novel role for Notch1 signaling in fetal hematopoietic stem cells.
• NOTCH1-RBPJ complexes drive target gene expression through dynamic interactions with superenhancers.
• T cell development requires constraint of the myeloid regulator C/EBP-α by the Notch target and transcriptional repressor Hes1.
• Notch simultaneously orchestrates multiple helper T cell programs independently of cytokine signals.
• T cell factor 1 is required for group 2 innate lymphoid cell generation.
• Complementary Genomic Screens Identify SERCA as a Therapeutic Target in NOTCH1 Mutated Cancer.
• Divergent effects of supraphysiological Notch signals on leukemia stem cells and hematopoietic stem cells.
• Blockade of notch signaling in muscle stem cells causes muscular dystrophic phenotype and impaired muscle regeneration.
• Notch and PI3K: how is the road traveled?
• Identification of Flt3⁺CD150⁻ myeloid progenitors in adult mouse bone marrow that harbor T lymphoid developmental potential.
• Genome-wide analysis reveals conserved and divergent features of Notch1/RBPJ binding in human and murine T-lymphoblastic leukemia cells.
• RBP-J promotes the maturation of neuronal progenitors.
• Notch signaling is a critical regulator of allogeneic CD4+ T-cell responses mediating graft-versus-host disease.
• Notch ankyrin repeat domain variation influences leukemogenesis and Myc transactivation.
• Deletion-based mechanisms of Notch1 activation in T-ALL: key roles for RAG recombinase and a conserved internal translational start site in Notch1.
• Transformation by Tribbles homolog 2 (Trib2) requires both the Trib2 kinase domain and COP1 binding.
• NOTCH1 and NOTCH3 coordinate esophageal squamous differentiation through a CSL-dependent transcriptional network.
• Hooked on Hes: a T-ALL of addiction.
• Notch dimerization is required for leukemogenesis and T-cell development.
• Differential ability of Tribbles family members to promote degradation of C/EBPalpha and induce acute myelogenous leukemia.
• HIV-1 Rev-binding protein accelerates cellular uptake of iron to drive Notch-induced T cell leukemogenesis in mice.
• Distinct roles for PTEN in prevention of T cell lymphoma and autoimmunity in mice.
• New roles for Notch in tuberous sclerosis.
• Pre-TCR signaling inactivates Notch1 transcription by antagonizing E2A.
• Murine Jagged1/Notch signaling in the second heart field orchestrates Fgf8 expression and tissue-tissue interactions during outflow tract development.
• Active Notch1 confers a transformed phenotype to primary human melanocytes.
• Menin regulates the function of hematopoietic stem cells and lymphoid progenitors.
• Notch signaling specifies megakaryocyte development from hematopoietic stem cells.
• Leukemia-associated NOTCH1 alleles are weak tumor initiators but accelerate K-ras-initiated leukemia.
• Notch2 paves the way to mast cells by Hes1 and Gata3.
• Canonical notch signaling is dispensable for the maintenance of adult hematopoietic stem cells.
• Endothelial expression of the Notch ligand Jagged1 is required for vascular smooth muscle development.
• Tribbles homolog 2 (Trib2) and HoxA9 cooperate to accelerate acute myelogenous leukemia.
• Notch signaling in leukemia.
• Distinct gene expression profiles of acute myeloid/T-lymphoid leukemia with silenced CEBPA and mutations in NOTCH1.
• The transcriptional coactivator Maml1 is required for Notch2-mediated marginal zone B-cell development.
• Notch signaling in vascular smooth muscle cells is required to pattern the cerebral vasculature.
• Notch1 co-opts lymphoid enhancer factor 1 for survival of murine T-cell lymphomas.
• Notch1 engagement by Delta-like-1 promotes differentiation of B lymphocytes to antibody-secreting cells.
• Notch directly regulates Gata3 expression during T helper 2 cell differentiation.
• Immunology. Keeping a tight leash on Notch.
• Notch activity synergizes with B-cell-receptor and CD40 signaling to enhance B-cell activation.
• Cooperative assembly of higher-order Notch complexes functions as a switch to induce transcription.
• An essential role for Notch in neural crest during cardiovascular development and smooth muscle differentiation.
• T-lymphoid, megakaryocyte, and granulocyte development are sensitive to decreases in CBFbeta dosage.
• Tribbles homolog 2 inactivates C/EBPalpha and causes acute myelogenous leukemia.
• The requirement for Notch signaling at the beta-selection checkpoint in vivo is absolute and independent of the pre-T cell receptor.
• c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma.
• Identification of a conserved negative regulatory sequence that influences the leukemogenic activity of NOTCH1.
• Impaired notch signaling promotes de novo squamous cell carcinoma formation.
• Notch1 promotes survival of E2A-deficient T cell lymphomas through pre-T cell receptor-dependent and -independent mechanisms.
• Notch-dependent T-lineage commitment occurs at extrathymic sites following bone marrow transplantation.
• The tumor suppressor menin regulates hematopoiesis and myeloid transformation by influencing Hox gene expression.
• Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies.
• Lasting longer without oxygen: The influence of hypoxia on Notch signaling.
• Notch signaling is an important regulator of type 2 immunity.
• Notch signaling controls the generation and differentiation of early T lineage progenitors.
• Notch signaling represses myocardin-induced smooth muscle cell differentiation.
• Regulation of lymphoid development, differentiation, and function by the Notch pathway.
• Notch subunit heterodimerization and prevention of ligand-independent proteolytic activation depend, respectively, on a novel domain and the LNR repeats.
• T cell acute lymphoblastic leukemia/lymphoma: a human cancer commonly associated with aberrant NOTCH1 signaling.
• Notch and T cell malignancy.
• Mastermind critically regulates Notch-mediated lymphoid cell fate decisions.
• Tie2-Cre-induced inactivation of a conditional mutant Nf1 allele in mouse results in a myeloproliferative disorder that models juvenile myelomonocytic leukemia.
• Notch 1 signaling regulates peripheral T cell activation.
• NF-kB inhibitor blocks B cell development at two checkpoints.
• Notch and the immune system.
• Localization of BCR-ABL to F-actin regulates cell adhesion but does not attenuate CML development.
• Notch signaling augments T cell responsiveness by enhancing CD25 expression.
• From the yolk sac to the spleen: New roles for Notch in regulating hematopoiesis.
• Notch signaling in lymphopoiesis.
• Notch and cancer: best to avoid the ups and downs.
• Growth suppression of pre-T acute lymphoblastic leukemia cells by inhibition of notch signaling.
• Notch signaling in cancer.
• BCR-ABL-induced adhesion defects are tyrosine kinase-independent.
• The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl.
• An invitation to T and more: notch signaling in lymphopoiesis.
• Differential requirement for LAT and SLP-76 in GPVI versus T cell receptor signaling.
• Deltex1 redirects lymphoid progenitors to the B cell lineage by antagonizing Notch1.

Schools

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• University Of Rochester

• Brigham and Women39s Hospital

Doctors Specialties

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• Clinical Pathology
• Pathology

Accepted Insurances

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Awards

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• Elected Member

Education

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• Brigham and Women's Hospital
• University of Rochester School of Medicine and Dentistry

Hospital

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• Hospital of the University of Pennsylvania
• Penn Presbyterian Medical Center

Helpful Reviews

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Medicare Facts

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National Provider Identifier [NPI]	1740225291
Last Name Of The Provider	PEAR
First Name Of The Provider	WARREN
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