SMC3 protein levels impact on karyotype and outcome in acute myeloid leukemia
SMC3 protein levels impact on karyotype and outcome in acute myeloid leukemia
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DOI：
10.1038/s41375-018-0287-6
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发表时间：
2019-03-01
期刊：
影响因子：
11.4
通讯作者：
Kraemer, Alwin
中科院分区：
文献类型：
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作者：
Kraft, Bianca;Lombard, Jan;Kraemer, Alwin
染色体不稳定性（CIN）是人类实体瘤和血液系统恶性肿瘤遗传异质性和克隆多样化的主要因素。它的水平随着年龄的增长而增加，无论是在正常细胞还是恶性细胞中[1-3]。在老年健康个体中，血细胞中染色体畸变的克隆嵌合现象与随后发生骨髓恶性肿瘤的风险增加相关[3]。染色体畸变是有丝分裂错误的结果。为了准确的染色体分离，姐妹染色单体紧密相连，直到纺锤体组装检查点得到满足，允许后期促进复合物（APC/C）介导的后期开始。直到分裂后期，姐妹染色单体凝聚力由四个亚基（SMC 1A、SMC 3、Rad 21以及SA-1或SA-2）组成的环形凝聚素复合体建立。
Chromosomal instability (CIN) is a major contributor to genetic heterogeneity and clonal diversification in both human solid tumors and hematological malignancies. Its levels increase with advancing age both in normal and malignant cells [1–3]. In elderly healthy individuals clonal mosaicism for chromosomal aberrations in blood cells is associated with an increased risk for the development of a subsequent myeloid malignancy [3]. Chromosomal aberrations arise as a consequence of errors during mitosis. For accurate chromosome segregation, sister chromatids are tightly associated until the spindle assembly checkpoint is satisfied, allowing for anaphasepromoting complex (APC/C)-mediated anaphase onset. Until anaphase, sister chromatid cohesion is established by the ring-shaped cohesin complex consisting of four subunits (SMC1A, SMC3, Rad21, and either SA-1 or SA-2).