Genomic Instability in Chronic Myeloid Leukemia: Targets for Therapy?
Genomic Instability in Chronic Myeloid Leukemia: Targets for Therapy?
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DOI：
10.1007/s11899-012-0119-0
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发表时间：
2012-06-01
影响因子：
2.9
通讯作者：
Rassool, F. V.
中科院分区：
文献类型：
--
作者：
Muvarak, N.;Nagaria, P.;Rassool, F. V.
费城阳性（Ph+）慢性髓细胞白血病（CML）的特征是在疾病进展过程中发生非随机遗传学和细胞遗传学异常。许多这些异常是基因的标记，当改变时，可以驱动母细胞转化过程。因此，这种遗传改变可能是由受损的DNA损伤和修复反应引起的潜在基因组不稳定性的表现，导致CML的晚期和对治疗的抗性。本文探讨了可能导致CML基因组不稳定的分子途径，以及这些途径成分成为治疗靶点的潜力。
Philadelphia positive (Ph+) chronic myeloid leukemia (CML) is characterized by the occurrence of nonrandom genetic and cytogenetic abnormalities during disease progression. Many of these abnormalities are markers for genes which, when altered, can drive the blastic transformation process. Thus, such genetic alterations may be manifestations of an underlying genomic instability resulting from a compromised DNA damage and repair response, leading to advanced stages of CML and resistance to therapy. This article examines the molecular pathways that may lead to genomic instability in CML and the potential of these pathway constituents to be therapeutic targets.