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Maintaining Low BCR-ABL Signaling Output to Restrict CML Progression and Enable Persistence
Deregulated BCR-ABL oncogenic activity leads to transformation, oncogene addiction and drives disease progression in chronic myeloid leukemia (CML). Inhibition of BCR-ABL using Abl-specific kinase inhibitors (TKI) such as imatinib induces remarkable clinical responses. However, approximately only le...
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| Formato: | Online Artículo Texto |
| Lenguaje: | English |
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Springer US
2014
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| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3930845/ https://www.ncbi.nlm.nih.gov/pubmed/24500518 http://dx.doi.org/10.1007/s11899-013-0196-8 |