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首页> 外文期刊>Cell biology international. >Centrosome aberrations in hematological malignancies.
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Centrosome aberrations in hematological malignancies.

机译：血液系统恶性肿瘤的中心体畸变。

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As the primary microtubule organizing center of most eukaryotic cells, centrosomes play a fundamental role in proper formation of the mitotic spindle and subsequent chromosome separation. Normally, the single centrosome of a G(1) cell duplicates precisely once prior to mitosis in a process that is intimately linked to the cell division cycle via cyclin-dependent kinase (cdk) 2 activity that couples centrosome duplication to the onset of DNA replication at the G(1)/S transition. Accurate control of centrosome duplication is critical for symmetric mitotic spindle formation and thereby contributes to the maintenance of genome integrity. Numerical and structural centrosome abnormalities are hallmarks of almost all solid tumors and have been implicated in the generation of multipolar mitoses and chromosomal instability. In addition to solid neoplasias, centrosome aberrations have recently been described in several different hematological malignancies like acute myeloid leukemias, myelodysplastic syndromes, Hodgkin's as well as non-Hodgkin's lymphomas, chronic lymphocytic leukemias and multiple myelomas. In analogy to many solid tumors a correlation between centrosome abnormalities on the one hand and karyotype aberrations as well as clinical aggressiveness on the other hand seems to exist in myeloid malignancies, chronic lymphocytic leukemias and at least some types of non-Hodgkin's lymphomas. Molecular mechanisms responsible for the development of centrosome aberrations are just beginning to be unraveled. In general, two models with distinct functional consequences can be envisioned. First, centrosome aberrations can arise as a consequence of abortive mitotic events and impaired cytokinesis. Second, evidence has been provided that centrosome amplification can also precede genomic instability and arise in normal, diploid cells. Accordingly, this review will focus on recent advances in the understanding of both, causes and consequences of centrosome aberrations in hematological malignancies.
机译：作为大多数真核细胞的主要微管组织中心，中心体在有丝分裂纺锤体的正确形成和随后的染色体分离中起着基本作用。通常，G（1）细胞的单个中心体在有丝分裂之前精确复制一次，该过程通过细胞周期蛋白依赖性激酶（cdk）2活性将中心体复制与DNA复制的发生联系起来，从而与细胞分裂周期密切相关。在G（1）/ S过渡处。中心体复制的精确控制对于对称有丝分裂纺锤体形成至关重要，因此有助于维持基因组完整性。中心体的数字和结构异常是几乎所有实体瘤的标志，并与多极有丝分裂的产生和染色体的不稳定性有关。除了实体瘤，最近在一些不同的血液系统恶性肿瘤中也发现了中心体畸变，例如急性髓细胞性白血病，骨髓增生异常综合症，霍奇金淋巴瘤和非霍奇金淋巴瘤，慢性淋巴细胞性白血病和多发性骨髓瘤。与许多实体瘤类似，一方面髓样恶性肿瘤，慢性淋巴细胞性白血病和至少某些类型的非霍奇金淋巴瘤与一方面的中心体异常和核型异常以及临床侵袭性之间存在相关性。导致中心体像差发展的分子机制才刚刚被阐明。通常，可以设想具有不同功能后果的两个模型。首先，由于流产的有丝分裂事件和胞质分裂受损，会引起中心体畸变。第二，已经提供了证据，中心体扩增也可以先于基因组不稳定性，并出现在正常的二倍体细胞中。因此，本综述将集中在对血液恶性肿瘤中心体畸变的原因和后果的理解方面的最新进展。

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