Posted by rob on June 18, 2010 under Uncategorized | 
Imatinib-resistant lymphoid clone of chronic myelogenous leukemia in blast phase arising from B cell-committed progenitor leukemic stem cells.
Ann Hematol. 2010 Jun 17;
Authors: Kobayashi S, Sato K, Kobayashi A, Osawa Y, Nakamura Y, Kimura F
PMID: 20556391 [PubMed - as supplied by publisher]
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The myeloproliferative neoplasm-associated JAK2 46/1 haplotype is not overrepresented in chronic myelogenous leukemia.
Ann Hematol. 2010 Jun 16;
Authors: Spolverini A, Jones AV, Hochhaus A, Pieri L, Cross NC, Vannucchi AM
PMID: 20556390 [PubMed - as supplied by publisher]
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A case of acute colitis with severe rectal bleeding in a patient with chronic myeloid leukemia after dasatinib use.
Acta Haematol. 2010;123(4):205-6
Authors: Erkut M, Erkut N, Ersoz S, Arslan M, Sonmez M
PMID: 20375493 [PubMed - indexed for MEDLINE]
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Combination of fludarabine and imatinib induces apoptosis synergistically through loss of mitochondrial membrane potential and increases in caspase-3 enzyme activity in human K562 chronic myleloid leukemia cells.
Cancer Invest. 2010 Jul;28(6):623-8
Authors: Baran Y, Oztekin C, Bassoy EY
In this study, we aimed to show the synergistic apoptotic effects of imatinib/fludarabine combination in human K562 chronic myleloid leukemia (CML) cells. There was a significant increase in cytotoxicity of combination of imatinib and fludarabine as compared to any agent alone. On the other hand, combination of both agents induced apoptosis significantly as confirmed by increases in caspase-3 enzyme activity and decreases in mitochondrial membrane potential. As a summary, the results of this study strongly suggest that combination of imatinib and fludarabine induced cell death synergistically comparing to only imatinib or fludarabine in human K562 CML cells.
PMID: 20307198 [PubMed - indexed for MEDLINE]
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[Different sensitivity of two chronic myeloid leukemia cell lines to interferon-alpha]
Ai Zheng. 2003 Oct;22(10):1047-52
Authors: Li XM, Chen HC, Liu XF, Wu YH, Cao YF
BACKGROUND & OBJECTIVE: The clinical observation has shown that interferon-alpha(IFN-alpha) is one of the most effective therapeutic agents for the malignancies of hemopoietic system and lymphoma. However, IFN-alpha can only induce about 70-80% of the patients with chronic myeloid leukemia (CML) to get hematological remission. The mechanism by which various CML cases respond differently to IFN-alpha is still unclear. METHODS: (1)The effects of IFN-alpha in different concentrations (100, 500, 1,000, 5,000, and 10,000 U/ml) on growth of the two CML cell lines were detected by MTT assay,semisolid colony formation and trypan-blue staining for the cells in liquid culture. (2)The cell apoptosis was examined by flow cytometry(FCM),fluorescence microscopy and gel electrophoresis analysis for DNA fragmentation in 48 hours after IFN-alpha (1,000 U/ml) induction of both KT-1/A3 and K562 cells. (3)The expression levels of bcr/abl chimeric genes were analyzed by relative quantitative RT-PCR at 48 hours after cultivation of both KT-1/A3 and K562 cells with IFN-alpha in 1,000 U/ml. RESULTS: (1)The growth inhibition of KT-1/A3 cells was dose-dependent in IFN-alpha from the concentration of 100 U/ml to 10,000 U/ml. (2)Having been induced with IFN-alpha in 1000 U/ml for 48 hours, the apoptosis rate of KT-1/A3 cells raised from 3.29% to 11.8% and the expression level of bcr/abl chimeric gene in this cell line declined to 66.7% as compared with those of the control. (3)The growth and apoptosis rate as well as bcr/abl gene expression level of K562 cells were not significantly affected by IFN-alpha. CONCLUSION: Different populations of CML cells shows different sensitivity to IFN-alpha.
PMID: 14558948 [PubMed - indexed for MEDLINE]
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To the Editor: A 63-year-old white woman with a history of chronic myelogenous leukemia (CML) was referred to our clinic for evaluation of a 19-month history of worsening blistering and skin fragility of her extremities (). A previous biopsy specimen revealed a pauciinflammatory subepidermal split consistent with porphyria cutanea tarda (PCT) and negative direct immunofluorescence (DIF) with normal serum and urine porphyrin studies. Our biopsy of a characteristic lesion was consistent with PCT, with a negative DIF and repeat porphyrin studies that again were normal. Discontinuation of her thrice weekly naproxen and daily estrogen supplement for 12 weeks did not prevent skin blistering. Imatinib mesylate (IM; Gleevec; Novartis Pharmaceuticals, Cambridge, MA) had been used to treat her CML…
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We report the design and validation of such quantitative assays, using pyrosequencing and mutation-specific RT-PCR techniques, to allow sequential monitoring and illustrate their use in tracking specific KD mutations (e.g. G250E, T315I, and M351T) following changes in therapy. Pyrosequencing and mutation-specific RT-PCR allows sequential monitoring of specific mutations and identification of rapid clonal shifts in response to kinase inhibitor therapy in CML. Rapid reselection of TKI-resistant clones occurs following therapy switch in CML. (Cancer Sci 2010) (Source: Cancer Science)
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