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The DOI matches its Crossref record; 135 of the 135 references it cites were found in a registry or an index.

Molecular biology of bcr-abl1–positive chronic myeloid leukemia

Open access
Quintás-Cardama, Alfonso, Cortes, Jorge·2009·Blood

Abstract

Chronic myeloid leukemia (CML) has been regarded as the paradigmatic example of a malignancy defined by a unique molecular event, the BCR-ABL1 oncogene. Decades of research zeroing in on the role of BCR-ABL1 kinase in the pathogenesis of CML have culminated in the development of highly efficacious therapeutics that, like imatinib mesylate, target the oncogenic kinase activity of BCR-ABL1. In recent years, most research efforts in CML have been devoted to developing novel tyrosine kinase inhibitors (TKIs) as well as to elucidating the mechanisms of resistance to imatinib and other TKIs. Nonetheless, primordial aspects of the pathogenesis of CML, such as the mechanisms responsible for the transition from chronic phase to blast crisis, the causes of genomic instability and faulty DNA repair, the phenomenon of stem cell quiescence, the role of tumor suppressors in TKI resistance and CML progression, or the cross-talk between BCR-ABL1 and other oncogenic signaling pathways, still remain poorly understood. Herein, we synthesize the most relevant and current knowledge on such areas of the pathogenesis of CML.

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Metadata

Authors
Quintás-Cardama, A., & Cortes, J.
Venue
Blood
Published
2009-02-19
Volume
113
Issue
8
Pages
1619-1630
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
OpenAlex
W2074198797
Cited by
745
References
135
FWCI
22.13
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Molecular biology of bcr-abl1–positive chronic myeloid leukemia. https://app.cochat.ai/papers/10.1182/blood-2008-03-144790
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Quintás-Cardama, A., & Cortes, J. (2009). Molecular biology of bcr-abl1–positive chronic myeloid leukemia. Blood. https://doi.org/10.1182/blood-2008-03-144790

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