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Jerome Tamburini

Researcher at University of Paris

Publications -  151
Citations -  11002

Jerome Tamburini is an academic researcher from University of Paris. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 38, co-authored 135 publications receiving 9567 citations. Previous affiliations of Jerome Tamburini include Paris Descartes University & French Institute of Health and Medical Research.

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Control of Pim2 kinase stability and expression in transformed human haematopoietic cells

TL;DR: It is shown that both Pim2 degradation realized by the proteasome in an ubiquitin-independent manner and Pim1 translation are constitutive and not constitutive, respectively.

Iconography : Indications and outcome of splenectomy in hematologic disease

TL;DR: Splenectomy has its place in hemoglobinopathies and hemolytic diseases, improves thrombocytopenia in refractory immune throm bocytopenic purpura, can reverse sequelae linked to voluminous splenomegaly secondary to myelofibrosis, or can be used for diagnostic purposes or for splenomesgaly in lymphoproliferative syndromes.
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CDC25A governs proliferation and differentiation of FLT3-ITD acute myeloid leukemia.

TL;DR: Analysis of cell cycle regulation in acute myeloid leukemia cells expressing the FLT3-ITD mutated tyrosine kinase receptor identifies CDC25A as an early cell cycle transducer of FLT 3-ITd oncogenic signaling, and as a promising target to inhibit proliferation and re-induce differentiation of FLt3- ITD AML cells.
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Retraction Note: LAMP2 expression dictates azacytidine response and prognosis in MDS/AML.

TL;DR: Low levels of LAMP2 expression in CD34+ blasts from MDS/AML patients correlated with lack of sensitivity to Aza and were predictive of poor overall survival, so patients at diagnosis or who become CD34/LAMP2Low during the course of treatment with Aza might benefit from a lysosome inhibitor already used in the clinic.
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Cytokine pattern in Kaposi's sarcoma associated with immune restoration disease in HIV and tuberculosis co-infected patients.

TL;DR: Analysis of VEGF and pro-inflammatory cytokines led us to hypothesize that Kaposi's sarcoma could be promoted by the tuberculosis immune response.