Posted by rob on June 21, 2010 under Uncategorized | 
Acute Kidney Injury Presenting a Feature of Leukemic Infiltration during Therapy for Chronic Myelogenous Leukemia.
Intern Med. 2010;49(12):1139-42
Authors: Yuzawa Y, Sato W, Masuda T, Hamada Y, Tatematsu M, Yasuda Y, Ozaki T, Ito I, Mizuno M, Maruyama S, Ito Y, Matsuo S
Chronic myelogenous leukemia (CML) is a myeloproliferative disease that originates in abnormal pluripotent bone marrow stem cells and it is consistently associated with the Philadelphia chromosome and/or BCR/ ABL fusion gene. Renal infiltration of leukemic cells is relatively rare in CML and is associated with renal impairment. We describe a patient who developed acute renal failure by tubulointerstitial nephropathy during treatment with imatinib mesylate for CML. The acute kidney injury was subsequently found to be due to direct leukemic infiltration. Treatment with hydroxycarbamide and prednisolone resulted in stabilization of the renal function for approximately 4 months. Leukemic infiltration into the kidney should always be considered when a patient with CML presents with renal impairment, regardless of the clinical stage, as the renal failure often responds well to chemotherapy.
PMID: 20558931 [PubMed - in process]
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A single dose pegfilgrastim for supporting neutrophil recovery in patients treated for high-risk acute myeloid leukemia by the EMA 2000 schedule.
Hematology. 2010 Jun;15(3):125-31
Authors: Derbel O, Cannas G, Le QH, Elhamri M, Chelghoum Y, Nicolas-Virelizier E, Nicolini F, Troncy J, Barraco F, Michallet M, Thomas X
Dose intensity has been demonstrated to be one determinant for treatment efficacy in younger adults with high-risk (relapsed and refractory) acute myelogenous leukemia. Between 2000 and 2006, 56 patients entered the EMA 2000 study and received timed sequential reinduction chemotherapy. From 2004, chemotherapy was also followed by one subcutaneous dose of pegfilgrastim. Thirty-six patients reached a complete remission, while nine obtained a partial remission. Median time to granulocyte and platelet recovery was 34 and 38 days respectively. The major non-hematologic toxicities were severe infections but despite this 23 remitters could proceed to their post-remission treatment, although 13 did not because of severe toxicity or early relapse. The median overall survival was 9.3 months. The EMA 2000 regimen is a highly effective treatment with a response rate of 64% and a low early death rate. The period of critical neutropenia was relatively short in both phases and the supportive use of pegfilgrastim, although showing a trend toward reduced neutropenic period, did not appear to reduce the risk of infection in this group and may not be a critical requirement for reducing the risk of treatment-related toxicity.
PMID: 20557669 [PubMed - in process]
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Rapid clonal shifts in response to kinase inhibitor therapy in chronic myelogenous leukemia are identified by quantitation mutation assays.
Cancer Sci. 2010 May 22;
Authors: Yin CC, Cortes J, Galbincea J, Reddy N, Breeden M, Jabbour E, Luthra R, Jones D
Treatment of CML with the tyrosine kinase inhibitor (TKI) imatinib mesylate results in the emergence of point mutations within the kinase domain (KD) of the BCR-ABL1 fusion transcript. The introduction of next-generation TKIs that can overcome the effects of some BCR-ABL1 KD mutations requires quantitative mutation profiling methods to assess responses. 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).
PMID: 20557306 [PubMed - as supplied by publisher]
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ABL alternative splicing is quite frequent in normal population – letter.
Mol Cancer Ther. 2010 Mar;9(3):772; author reply 772
Authors: Santamaria I, Pitiot AS, Balbin M
PMID: 20197392 [PubMed - indexed for MEDLINE]
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Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-010-1009-yAuthors
Ambra Spolverini, Università di Firenze, Istituto Toscano Tumori UF di Ematologia, Dipartimento di Area Critica Medico-Chirurgica Florence ItalyAmy V. Jones, University of Southampton Wessex Regional Genetics Laboratory, Salisbury, UK and Human Genetics Division, School of Medicine Southampton UKAndreas Hochhaus, Universitätsklinikum Jena Klinik für Innere Medizin II Jena GermanyLisa Pieri, Università di Firenze, Istituto Toscano Tumori UF di Ematologia, Dipartimento di Area Critica Medico-Chirurgica Florence ItalyNicholas C. P. Cross, University of Southampton Wessex Regional Genetics Laboratory, Salisbury, UK and Human Genetics Division, School of Medicine Southampton UKAlessandro M. Van…
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Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-010-1008-zAuthors
Shinichi Kobayashi, National Defense Medical College Division of Hematology, Department of Internal Medicine 3-2 Namiki Tokorozawa Saitama 359-8513 JapanKen Sato, National Defense Medical College Division of Hematology, Department of Internal Medicine 3-2 Namiki Tokorozawa Saitama 359-8513 JapanAyako Kobayashi, National Defense Medical College Division of Hematology, Department of Internal Medicine 3-2 Namiki Tokorozawa Saitama 359-8513 JapanYukiko Osawa, National Defense Medical College Division of Hematology, Department of Internal Medicine 3-2 Namiki Tokorozawa Saitama 359-8513 JapanYukitsugu Nakamura, National Defense Medical College Division of Hematology, Department of Internal Medicine …
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