Posted by rob on May 23, 2011 under Uncategorized | 
Erratum to: Discovery of LY2457546: a multi-targeted anti-angiogenic kinase inhibitor with a novel spectrum of activity and exquisite potency in the acute myelogenous leukemia-Flt-3-internal tandem duplication mutant human tumor xenograft model.
Invest New Drugs. 2011 May 20;
Authors: Burkholder TP, Clayton JR, Rempala ME, Henry JR, Knobeloch JM, Mendel D, McLean JA, Hao Y, Barda DA, Considine EL, Uhlik MT, Chen Y, Ma L, Bloem LJ, Akunda JK, McCann DJ, Sanchez-Felix M, Clawson DK, Lahn MM, Starling JJ
PMID: 21597891 [PubMed - as supplied by publisher]
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Retrospective multicenter study on the development of peripheral lymphocytosis following second-line dasatinib therapy for chronic myeloid leukemia.
Am J Hematol. 2011 Apr;86(4):346-50
Authors: Lee SJ, Jung CW, Kim DY, Lee KH, Sohn SK, Kwak JY, Kim HJ, Kim IH, Park S, Kim DH
The current retrospective study investigated the incidence of lymphocytosis following second-line dasatinib therapy in chronic myeloid leukemia (CML) and analyzed the clinical factors predictive of the development of lymphocytosis, as well as association with treatment outcomes. Fifty CML patients who failed imatinib treatment and received dasatinib were included from nine centers in the Republic of Korea. The cumulative incidence of lymphocytosis was assessed, and cytogenetic and molecular response, treatment failure, loss of response, progression to advanced disease, and survival were evaluated and analyzed according to the development of lymphocytosis. After a median of 17 months of dasatinib therapy, 23 patients (46%) developed lymphocytosis (median onset 4 months). No clinical predictive factor for the development of lymphocytosis was found. The group presenting lymphocytosis showed a higher complete cytogenetic response (CCyR; 78.3 vs. 29.6%, P = 0.001) and major molecular response (MMR; 52.2 vs. 14.8%, P = 0.005), in comparison to the group without presenting lymphocytosis. The development of lymphocytosis after dasatinib was identified as a favorable independent marker for predicting a CCyR (P = 0.002) or MMR (P = 0.003). Further study is necessary to identify which subset of lymphocytes was expanded and to reveal the exact mechanism by which dasatinib induces lymphocyte expansion.
PMID: 21442637 [PubMed - indexed for MEDLINE]
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(Source: Journal of Clinical Oncology)
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In this study, we show that dasatinib causes mild thrombocytopenia in mice without altering platelet half-life, suggesting that it inhibits platelet formation. Conversely, the number of megakaryocytes (MKs) in the bone marrow of dasatinib-treated mice was increased and the ploidy of MKs derived from bone marrow progenitor cells in vitro was elevated in the presence of dasatinib. Furthermore, a significant delay in platelet recovery after immune-induced thrombocytopenia was observed in dasatinib-treated mice even though the number of MKs in the bone marrow was increased relative to controls at all time points. Interestingly, the migration of MKs toward a gradient of stromal cell–derived factor 1α (SDF1α) and the formation of proplatelets in vitro were abolished by dasatini…
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CONCLUSIONS:Deletions of derivative chromosome 9 do not appear to be an independent risk factor for survival among patients with CML in chronic phase receiving second generation TKIs. Cancer 2011;. © 2011 American Cancer Society. (Source: Cancer)
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