BCR-ABL1阴性骨髓增殖性肿瘤中驱动突变与细胞凋亡失调之间的联系

Cristina Mambet, L. Matei, L. Necula, C. Diaconu
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引用次数: 7

摘要

目前对BCR-ABL1阴性骨髓增殖性肿瘤发病机制的理解主要集中在JAK2、MPL或CALR基因的表型驱动突变,以及JAK-STAT通路的组成性激活。尽管如此,仍然需要更好地表征由这些遗传改变引发的细胞过程,如细胞凋亡,它可能在髓系的病理扩张中发挥作用,特别是在骨髓巨核细胞的形态异常中。在本文中,我们将探讨MPN驱动突变与异常凋亡之间的联系,这可能会转化为新的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A link between the driver mutations and dysregulated apoptosis in BCR-ABL1 negative myeloproliferative neoplasms
ABSTRACT The current understanding of BCR-ABL1 negative myeloproliferative neoplasms pathogenesis is centred on the phenotypic driver mutations in JAK2, MPL, or CALR genes, and the constitutive activation of JAK-STAT pathway. Nonetheless, there is still a need to better characterize the cellular processes that are triggered by these genetic alterations, such as apoptosis that might play a role in the pathological expansion of the myeloid lineages and, especially, in the morphological anomalies of the bone marrow megakaryocytes. In this article we will explore the connection between the driver mutations in MPN and the abnormal apoptosis that might be translated in new therapeutic strategies.
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