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Robert P. Hasserjian

Researcher at Harvard University

Publications -  343
Citations -  21234

Robert P. Hasserjian is an academic researcher from Harvard University. The author has contributed to research in topics: Medicine & Myeloid leukemia. The author has an hindex of 53, co-authored 284 publications receiving 16118 citations. Previous affiliations of Robert P. Hasserjian include Hammersmith Hospital & Partners HealthCare.

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Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis.

TL;DR: Patients with Ph+ AML were less likely to have splenomegaly or peripheral basophilia and had lower bone marrow cellularity and myeloid/erythroid ratios than patients with CML-MBC and additional specific cytogenetic abnormalities that typically occur in CML -MBC were less common in Ph+AML.
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Modulated expression of notch1 during thymocyte development

TL;DR: Analysis of patterns of expression of NOTCH1 protein in thymocytes of the developing and mature thymus and flow cytometric analysis and immunohistochemical staining of flow-sorted cells indicate a dynamic pattern of Notch1 expression during T-cell differentiation and suggest that downregulation of NOTch1 may be required for maturation of cortical thymocyte.
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Clinicopathologic analysis of follicular lymphoma occurring in children.

TL;DR: Findings indicate that, in contrast to adult follicular lymphomas, dysregulated bcl-2 expression does not play a significant pathogenetic role in most pediatric follicularymphoma, however, bcl -2 expression in pediatric follicle lymphoma identifies a subset of patients in whom disease is often disseminated at clinical presentation and is more refractory to combination chemotherapy.
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α-CTLA-4 mAb-associated Panenteritis: A Histologic and Immunohistochemical Analysis

TL;DR: It is concluded that the panenteritis associated with injection of α-CTLA-4 mAbs demonstrates histology resembling autoimmune enteropathy, and it is suspected that the increased number of regulatory T cells in the gastrointestinal mucosa may play a role in the pathogenicity.