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Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias

机译:蛋白激酶CK2:费城阳性白血病的靶向BCR-ABL伙伴。

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摘要

BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL specific tyrosine kinase inhibitors (TKIs). However, BCR-ABL TKIs do not allow completely eradicating both CML and ALL. Furthermore, ALL therapy is associated with much worse responses to TKIs than those observed in CML. The identification of additional pathways that mediate BCR-ABL leukemogenesis is indeed mandatory to achieve synthetic lethality together with TKI. Here, we review the role of BCR-ABL/protein kinase CK2 interaction in BCR-ABL leukemias, with potentially relevant implications for therapy.
机译:BCR-ABL介导的白血病,无论是慢性粒细胞白血病(CML)还是费城阳性的急性淋巴细胞白血病(ALL),都是靶向性癌症分子疗法的典范,因为BCR-ABL特异性酪氨酸激酶抑制剂(TKIs)获得了令人印象深刻的临床反应)。但是,BCR-ABL TKI不允许完全消除CML和ALL。此外,与CML相比,ALL疗法对TKI的反应差得多。确实必须鉴定介导BCR-ABL白血病发生的其他途径,以与TKI一起实现合成杀伤力。在这里,我们回顾了BCR-ABL /蛋白激酶CK2相互作用在BCR-ABL白血病中的作用,可能与治疗有关。

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