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Nestal de Moraes G, Souza PS, Costas FC, et al. The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia. Leuk Res Treatment. 2012;2012:671702doi: 10.1155/2012/671702.
Nestal de Moraes, G., Souza, P. S., Costas, F. C., Vasconcelos, F. C., Reis, F. R., & Maia, R. C. (2012). The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia. Leukemia research and treatment, 2012671702. https://doi.org/10.1155/2012/671702
Nestal de Moraes, Gabriela, et al. "The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia." Leukemia research and treatment vol. 2012 (2012): 671702. doi: https://doi.org/10.1155/2012/671702
Nestal de Moraes G, Souza PS, Costas FC, Vasconcelos FC, Reis FR, Maia RC. The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia. Leuk Res Treatment. 2012;2012:671702. doi: 10.1155/2012/671702. Epub 2012 Apr 24. PMID: 23259070; PMCID: PMC3505928.
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Leuk Res Treatment. 2012;2012:671702. doi: 10.1155/2012/671702. Epub 2012 Apr 24.

The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia.

Leukemia research and treatment

Gabriela Nestal de Moraes, Paloma Silva Souza, Fernanda Casal de Faria Costas, Flavia Cunha Vasconcelos, Flaviana Ruade Souza Reis, Raquel Ciuvalschi Maia

Affiliations

  1. Laboratório de Hemato-Oncologia Celular e Molecular, Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer (INCA), Praça da Cruz Vermelha 23, 6° andar, Centro, 20230-130 Rio de Janeiro, RJ, Brazil.

PMID: 23259070 PMCID: PMC3505928 DOI: 10.1155/2012/671702

Abstract

Chronic myeloid leukemia (CML) is a clonal hematopoietic disorder characterized by the presence of the Philadelphia chromosome which resulted from the reciprocal translocation between chromosomes 9 and 22. The pathogenesis of CML involves the constitutive activation of the BCR-ABL tyrosine kinase, which governs malignant disease by activating multiple signal transduction pathways. The BCR-ABL kinase inhibitor, imatinib, is the front-line treatment for CML, but the emergence of imatinib resistance and other tyrosine kinase inhibitors (TKIs) has called attention for additional resistance mechanisms and has led to the search for alternative drug treatments. In this paper, we discuss our current understanding of mechanisms, related or unrelated to BCR-ABL, which have been shown to account for chemoresistance and treatment failure. We focus on the potential role of the influx and efflux transporters, the inhibitor of apoptosis proteins, and transcription factor-mediated signals as feasible molecular targets to overcome the development of TKIs resistance in CML.

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