A Worldwide Support Network For Chronic Myelogenous Leukemia
Posted by rob on October 20, 2005 under Uncategorized | 
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Cayuela JM, Rousselot P, Nicolini F, Espinouse D, Ollagnier C, Bui-Thi MH, Chabane K, Raffoux E, Callet-Bauchu E, Tigaud I, Magaud JP, Hayette S
Leukemia. 2005 Oct 13;
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Gruber FX, Lamark T, Anonli A, Sovershaev MA, Olsen M, Gedde-Dahl T, Hjort-Hansen H, Skogen B
Leukemia. 2005 Oct 13;
Resistance to imatinib during the treatment of chronic myeloid leukaemia (CML) is frequently associated with point mutations in the ABL gene encoding the ATP binding region likely to cause disease relapse. Early diagnosis and monitoring of these mutations may be important in order to prevent rapid expansion of resistant clones. We describe a quantitative mutation-specific PCR assay based on the readily available Taqman platform. Selectivity for the mutated target is conferred by mutation-specific primers destabilised by additional mismatches. The assay can be carried out in parallel to standard BCR-ABL quantification and is therefore more quickly compared to standard sequencing procedures. The sensitivity of the assay reaches 0.1%. It also allows for quantitative assessment of mutated clones. By analysing sequential samples of resistant subjects, we show how mutated clones were selected, maintained or deselected depending on the individual treatment setting. The high sensitivity and practical merits of this method makes it a good candidate for prospective molecular surveillance of patients at high risk for imatinib resistance.Leukemia advance online publication, 13 October 2005; doi:10.1038/sj.leu.2403983.
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Brazzelli V, Prestinari F, Roveda E, Barbagallo T, Bellani E, Vassallo C, Orlandi E, Passamonti F, Borroni G
J Am Acad Dermatol. 2005 Nov ; 53(5 Suppl 1): S240-3
Imatinib mesylate (IM) represents the first-line treatment for chronic myeloid leukemia (CML). We hereby relate 3 cases of an IM-induced pityriasis rosea (PR)-like cutaneous eruption. Patients developed an erythematous, slightly pruritic, macular skin eruption, with many lesions having a peripheral collarette of desquamation, confined to the trunk, limbs, and arms with a vaguely dermatomal diffusion. The histologic findings suggested a reactive process to the drug. Full dermatological recovery was obtained after IM discontinuation, but lesions reappeared upon restoring therapy, suggesting the drug-related nature of the rash. To our knowledge this is the first reported PR-like cutaneous eruption to IM.
Pityriasis rosea-like eruption during treatment with imatinib mesylate: description of 3 cases.
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Brusa G, Mancini M, Campanini F, Calabrò A, Zuffa E, Barbieri E, Santucci MA
Acta Haematol. 2005; 114(3): 150-154
In order to ascertain whether p53 has a role in chronic myeloid leukemia hematopoietic progenitor response to the innovative tyrosine kinase inhibitor STI571 (Imatinib), we overexpressed a wild type (wt) p53 construct in the K562 cell line, generated from a human blast crisis and lacking endogenous p53. Wt p53 overexpression was associated with a significant reduction of bcr-abl expression levels resulting, at least in part, from post-transcriptional events affecting the stability of p210 bcr-abl fusion protein. Moreover, we demonstrated that p53 overexpression enhances the commitment to the apoptotic death fate of K562 following its in vitro exposure to 1 muM STI571. Multiple mechanisms are involved in p53 impact on K562 survival: Most importantly, we found that a greater reduction of bcr-abl transcription by STI571 was associated with the overexpression of wt p53. Further studies are required to elucidate the mechanisms involved in the transcriptional repression of bcr-abl by STI571 and p53 and in their synergic effects on the clonal hematopoiesis of chronic myeloid leukemia. Copyright (c) 2005 S. Karger AG, Basel.
Tyrosine Kinase Inhibitor STI571 (Imatinib) Cooperates with Wild-Type p53 on K562 Cell Line to Enhance Its Proapoptotic Effects.
