Abstract
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.
Original language | English (US) |
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Pages (from-to) | 643-649 |
Number of pages | 7 |
Journal | Leukemia Research |
Volume | 32 |
Issue number | 4 |
DOIs | |
State | Published - Apr 2008 |
Keywords
- AKT
- BCR-ABL
- Chronic myeloid leukemia
- CrkL
- Imatinib
- Resistance
- STAT5
- Survival pathways
- Tyrosine kinase
ASJC Scopus subject areas
- Cancer Research
- Hematology
- Oncology