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Phosphorylation levels of BCR-ABL, CrkL, AKT and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative pathway usage as a survival strategy.

Authors: Jilani, Iman  Kantarjian, Hagop  Gorre, Mercedes  Cortes, Jorge  Ottmann, Oliver  Bhalla, Kapil  Giles, Francis J  Albitar, Maher 
Citation: Jilani I, etal., Leuk Res. 2008 Apr;32(4):643-9. doi: 10.1016/j.leukres.2007.08.009. Epub 2007 Sep 27.
Pubmed: (View Article at PubMed) PMID:17900686
DOI: Full-text: DOI:10.1016/j.leukres.2007.08.009

Ex-vivo studies have suggested that imatinib-resistance in chronic myeloid leukemia (CML) patients occurs despite adequate suppression of BCR-ABL activity. Whether BCR-ABL phosphorylation levels differ between imatinib-sensitive and -resistant patients is not known. We compared the phosphorylation of BCR-ABL in 54 previously untreated CML patients and 62 imatinib-resistant CML patients with progressive disease. Resistant patients had significantly lower levels of BCR-ABL, CrkL and AKT phosphorylation than previously untreated patients, but STAT5 phosphorylation showed no difference. These observations suggest that imatinib- resistance is not necessarily dependent on higher activity in BCR-ABL-dependent pathways, but is likely due to the activation of other pathways.


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CRRD Object Information
CRRD ID: 13674160
Created: 2018-07-10
Species: All species
Last Modified: 2018-07-10
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.