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Gian Maria Borleri

Researcher at Mario Negri Institute for Pharmacological Research

Publications -  12
Citations -  899

Gian Maria Borleri is an academic researcher from Mario Negri Institute for Pharmacological Research. The author has contributed to research in topics: Idarubicin & Transplantation. The author has an hindex of 8, co-authored 12 publications receiving 880 citations. Previous affiliations of Gian Maria Borleri include University of Trieste.

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Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis

TL;DR: It is concluded that CDC and ADCC are major mechanisms of action of rituximab on B-cell lymphomas and that a heterogeneous susceptibility of different lymphoma cells to complement may be at least in part responsible for the heterogeneity of the response of different patients to ritUXimab in vivo.
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Primary effusion lymphoma after heart transplantation : a new entity associated with human herpesvirus-8

TL;DR: Despite the characteristic local growth of this peculiar type of lymphoma, it is demonstrated at the molecular level, an early neoplastic spread to the bone marrow suggesting the need to investigate in more detail the origin of the disease, as well as the molecular mechanisms controlling its systemic dissemination.
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Granulocyte colony-stimulating factor following peripheral-blood progenitor-cell transplant in non-Hodgkin's lymphoma.

TL;DR: Provided an optimal dose of circulating progenitors is infused, NHL patients transplanted with PBPC do not benefit by the administration of hematopoietic growth factors.
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The Role of Idarubicin in Adult Acute Lymphoblastic Leukaemia: From Drug Resistance Studies to Clinical Application

TL;DR: Idarubicin is a very effective drug for the early management of adult acute lymphoblastic leukaemia and may be presently considered (along with cyclosporin-A or other modulator) as the reference anthracycline for cases overexpressing the P-glycoprotein drug resistance mechanism.
Journal Article

Redundant functions of B-Myb and c-Myb in differentiating myeloid cells

TL;DR: It is demonstrated that although the DNA-binding domain of c-myb is required for both the differentiation block and the shift in cell cycle after PMA treatment, phosphorylation by casein kinase II and mitogen-activated protein kinase at positions 11 and 12 or 532 of c -myb, respectively, are not.