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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Induction of aneuploidy by increasing chromosomal instability during dedifferentiation of hepatocellular carcinoma
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Induction of aneuploidy by increasing chromosomal instability during dedifferentiation of hepatocellular carcinoma

机译：通过增加肝细胞癌去分化过程中的染色体不稳定性来诱导非整倍性

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To gain more insight into the role of chromosomal instability (CIN), the cytogenetic hallmark of most solid tumors, we performed fluorescence in situ hybridization (FISH) on interphase nuclei of cytological specimens enabling the correct detection of chromosome copies in intact tumor cells of 18 well (G1), moderately (G2), or poorly (G3) differentiated hepatocellular carcinomas (HCCs). A close correlation between the morphological dedifferentiation and increasing copy numbers and variation of FISH signals was seen for chromosomes 1 and 8, respectively (P ≤ 0.0002). Four HCC G1 had constant chromosome patterns for chromosomes 1 and/or 8 with a mean of signals per nucleus ≤5.08 and ≤3 different signal combinations, indicating a low level of CIN, as confirmed by FISH using probes for centromeres of chromosomes 3, 7, and 17. In contrast to this, five HCC G2-3 revealed ≥8.46 signals per nucleus and 23-41 different signal combinations, indicating high levels of CIN. In the remaining cases, signal counts from 5.96-8.46 and 7-15 combinations were seen. Here, nuclei with constant aberration patterns and low copy numbers occurred alongside nuclei with inconstant patterns and high copy numbers. It is evident that in these cases a transition from well to moderately differentiated HCC developed in parallel to an increase in CIN, possibly induced by a major dysregulation of mitotic control mechanisms. In conclusion, CIN may induce a stepwise increase of aneuploidy in HCC that is mirrored by the morphological dedifferentiation of tumor cells.
机译：为了深入了解大多数实体瘤的细胞遗传学特征染色体不稳定（CIN）的作用，我们在细胞学标本的相间核上进行了荧光原位杂交（FISH），从而能够正确检测18个完整肿瘤细胞中的染色体拷贝（G1），中度（G2）或差度（G3）分化的肝细胞癌（HCC）。分别在1号和8号染色体上观察到形态学去分化与增加的拷贝数和FISH信号的变化之间密切相关（P≤0.0002）。四个HCC G1在1号和/或8号染色体上具有恒定的染色体模式，每个核的平均信号≤5.08和≤3个不同信号组合，表明CIN水平低，如FISH使用3、7号染色体着丝粒探针所证实的那样，和17。与此相反，五个HCC G2-3显示每个核≥8.46信号以及23-41个不同的信号组合，表明CIN水平很高。在其余情况下，可以看到5.96-8.46和7-15组合的信号计数。在此，具有恒定像差模式和低拷贝数的原子核与具有恒定模式和高拷贝数的原子核同时出现。显然，在这些情况下，从良好分化为中等分化的肝癌的转变与CIN的增加同时发生，这可能是由有丝分裂控制机制的严重失调引起的。总之，CIN可能诱导HCC中非整倍性逐步增加，这可通过肿瘤细胞的形态学去分化来反映。

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