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首页> 外文期刊>Cancer genetics and cytogenetics >Jumping translocations in bone marrow cells of pediatric patients with hematologic malignancies: a rare cytogenetic phenomenon.
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Jumping translocations in bone marrow cells of pediatric patients with hematologic malignancies: a rare cytogenetic phenomenon.

机译:患有血液系统恶性肿瘤的小儿骨髓细胞的跳跃易位:一种罕见的细胞遗传学现象。

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摘要

Jumping translocations (JTs) are uncommon constitutional or acquired chromosomal aberrations. JTs are caused by the translocation of a section of one chromosome into two or more different recipient chromosomes. Several mechanisms, such as pericentromeric heterochromatin decondensation, shortened telomeres, illegitimate recombination, virus infection, and chromosome instability, are proposed to induce JTs. However, the pathogenesis of JTs remains elusive (1-3).JTs have been observed in many types of neoplasia, including hematopoietic cancers. In these cases, JTs usually represent secondary changes and are associated with poor prognosis. The donor breakpoint occurs most frequently on chromosome 1q, contrary to the recipient sites, which are present on all chromosomes (4). Interestingly, most JTs are described in adult patients; the data for pediatric patients are rather scarce (4,5).
机译:跳跃易位(JT)是不常见的体质性或后天性染色体畸变。 JT是由一条染色体的一部分易位成两个或多个不同的受体染色体引起的。提出了多种机制来诱导JT,例如着丝粒着丝粒异染色质解聚,端粒缩短,非法重组,病毒感染和染色体不稳定性。然而,JTs的发病机制仍然难以捉摸(1-3).JTs已在许多类型的肿瘤形成中被观察到,包括造血系统癌症。在这些情况下,JT通常代表继发性变化,并与不良预后相关。供体断点最常出现在1q号染色体上,这与所有染色体上都存在的受体位点相反(4)。有趣的是,大多数JT都是在成年患者中描述的。儿科患者的数据很少(4,5)。

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