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PKC412 inhibits in vitro growth of neoplastic human mast cells expressing the D816V-mutated variant of KIT: comparison with AMN107, imatinib, and cladribine (2CdA) and evaluation of cooperative drug
It is shown that the novel TK-targeting drugs PKC412 and AMN107 counteract TK activity of D8 16V KIT and inhibit the growth of Ba/F3 cells with doxycycline-inducible expression of KIT D816V as well as the growthof primary neoplastic mast cells and HMC-1 cells harboring this KIT mutation.
Long‐term effects of compost amendment of soil on functional and structural diversity and microbial activity
We studied the effects of applying different composts (urban organic waste, green waste, manure and sewage sludge), mineral fertilizer and compost plus mineral fertilizer on chemical, biological and
Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML
Treatment with nilotinib may be associated with an increased risk of vascular adverse events, including PAOD development, and although the exact mechanisms remain unknown, it is recommended to screening for pre‐existing PAOD and for vascular risk factors such as diabetes mellitus in all patients before starting nilotin ib and in the follow up duringnilotinib‐therapy.
Identification of mcl-1 as a BCR/ABL-dependent target in chronic myeloid leukemia (CML): evidence for cooperative antileukemic effects of imatinib and mcl-1 antisense oligonucleotides.
MCL-1 is identified as a BCR/ABL-dependent survival factor and interesting target in CML, and the mcl-1 ASO was found to synergize with imatinib in producing growth inhibition in these cells.
Identification of heme oxygenase-1 as a novel BCR/ABL-dependent survival factor in chronic myeloid leukemia.
Overexpression of HO-1 in the CML-derived cell line K562 was found to counteract STI571-induced apoptosis and identifyHO-1 as a novel BCR/ABL-driven survival molecule and potential target in leukemic cells in patients with CML.
CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasms.
An aminopyrimidine derivative (CYT387), which inhibits JAK1, JAK2, and tyrosine kinase 2 (TYK2) at low nanomolar concentrations, with few additional targets is identified, adding to increasing evidence that kinase inhibitor monotherapy of malignant disease is not curative, suggesting a need for drug combinations to optimally target the malignant cells.
TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms.
The data are consistent with a model where JAK2(V617F) promotes clonal selection by conferring TNFα resistance to a preneoplastic T NFα sensitive cell, while simultaneously generating a TNF α-rich environment.
Evaluation of antileukaemic effects of rapamycin in patients with imatinib‐resistant chronic myeloid leukaemia
This data indicates that the mammalian target of rapamycin (mTOR) is involved in the regulation of growth of neoplastic cells in chronic myeloid leukaemia (CML).
Low-level expression of proapoptotic Bcl-2-interacting mediator in leukemic cells in patients with chronic myeloid leukemia: role of BCR/ABL, characterization of underlying signaling pathways, and
The data identify BCR/ABL as a Bim suppressor in CML cells and suggest that reexpression of Bim by novel tyrosine kinase inhibitors, proteasome inhibition, or by targeting signaling pathways downstream of BCR-ABL may be an attractive therapeutic approach in imatinib-resistant CML.
Identification of MCL1 as a novel target in neoplastic mast cells in systemic mastocytosis: inhibition of mast cell survival by MCL1 antisense oligonucleotides and synergism with PKC412.
Examination of expression and functional role of MCL-1 in neoplastic MCs and synergistic effects observed with PKC412, AMN107, and imatinib show that MCL, a Bcl-2 family member, is a novel survival factor and an attractive target in ne plastic MCs.