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10.1186/s13045-015-0157-x

http://scihub22266oqcxt.onion/10.1186/s13045-015-0157-x
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C4459446!4459446!26022368
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suck abstract from ncbi


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pmid26022368      J+Hematol+Oncol 2015 ; 8 (ä): ä
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  • Targeting neoplastic B cells and harnessing microenvironment: the ?double face? of ibrutinib and idelalisib #MMPMID26022368
  • Maffei R; Fiorcari S; Martinelli S; Potenza L; Luppi M; Marasca R
  • J Hematol Oncol 2015[]; 8 (ä): ä PMID26022368show ga
  • Tyrosine kinase inhibitors (TKIs) targeting signaling molecules downstream B cell receptor (BCR) are powerfully spreading in the therapeutic landscape of B cell lymphoproliferative disease, due to a manageable toxicity profile and encouraging clinical effectiveness. In particular, ibrutinib, previously called PCI-32765, is a potent inhibitor of Bruton tyrosine kinase (Btk), recently approved for the treatment of relapsed mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL). Moreover, idelalisib (formerly GS-1101 and CAL-101) is a selective reversible inhibitor of the p110? isoform of phosphoinositol 3 kinase (PI3K) approved for the treatment of patients with relapsed follicular lymphoma (FL) and CLL. These agents directly affect the neoplastic clone, disrupting the supportive platform provided by BCR signaling cascade and by other microenvironmental mutualistic interactions, and also interfering with chemokine gradients and adhesive properties of neoplastic B cells. In the present review, we describe the clinical efficacy of ibrutinib and idelalisib in CLL and B cell non-Hodgkin lymphoma (B-NHL), then focusing on the mode of action (MOA) of these TKIs towards the neoplastic B cell compartment. At last, the review would further expand the view on potential additional targets of ibrutinib and idelalisib belonging to other microenvironmental cellular elements.
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