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染色体 7 增益补偿胶质母细胞瘤中染色体 10 的缺失。

Chromosome 7 Gain Compensates for Chromosome 10 Loss in Glioma.

机构信息

Cancer Data Science Laboratory, Computational Precision Oncology Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

MSD, Beijing, China.

出版信息

Cancer Res. 2024 Oct 15;84(20):3464-3477. doi: 10.1158/0008-5472.CAN-24-1366.

Abstract

The co-occurrence of chromosome 10 loss and chromosome 7 gain in gliomas is the most frequent loss-gain co-aneuploidy pair in human cancers. This phenomenon has been investigated since the late 1980s without resolution. Expanding beyond previous gene-centric studies, we investigated the co-occurrence in a genome-wide manner, taking an evolutionary perspective. Mining of large-scale tumor aneuploidy data confirmed the previous finding of a small-scale longitudinal study that the most likely order is chromosome 10 loss, followed by chromosome 7 gain. Extensive analysis of genomic and transcriptomic data from both patients and cell lines revealed that this co-occurrence can be explained by functional rescue interactions that are highly enriched on chromosome 7, which could potentially compensate for any detrimental consequences arising from the loss of chromosome 10. Transcriptomic data from various normal, noncancerous human brain tissues were analyzed to assess which tissues may be most predisposed to tolerate compensation of chromosome 10 loss by chromosome 7 gain. The analysis indicated that the preexisting transcriptomic states in the cortex and frontal cortex, where gliomas arise, are more favorable than other brain regions for compensation by rescuer genes that are active on chromosome 7. Collectively, these findings suggest that the phenomenon of chromosome 10 loss and chromosome 7 gain in gliomas is orchestrated by a complex interaction of many genes residing within these two chromosomes and provide a plausible reason why this co-occurrence happens preferentially in cancers originating in certain regions of the brain.  Significance: Increased expression of multiple rescuer genes on the gained chromosome 7 could compensate for the downregulation of several vulnerable genes on the lost chromosome 10, resolving the long-standing mystery of this frequent co-occurrence in gliomas.

摘要

10 号染色体缺失和 7 号染色体获得在神经胶质瘤中共同发生,这是人类癌症中最常见的染色体丢失-增益非整倍性对。自 20 世纪 80 年代末以来,人们一直在研究这一现象,但尚未得出明确结论。我们超越了以前以基因为中心的研究,从进化的角度进行了全基因组范围内的共同发生研究。对大规模肿瘤非整倍体数据的挖掘证实了以前的一项小规模纵向研究的发现,即最有可能的顺序是 10 号染色体缺失,其次是 7 号染色体获得。对来自患者和细胞系的基因组和转录组数据的广泛分析表明,这种共同发生可以通过功能挽救相互作用来解释,这些相互作用在 7 号染色体上高度富集,这可能潜在地补偿 10 号染色体缺失带来的任何不利后果。对来自各种正常、非癌性人脑组织的转录组数据进行了分析,以评估哪些组织可能最容易耐受 7 号染色体获得对 10 号染色体缺失的补偿。分析表明,在皮质和额皮质(神经胶质瘤发生的部位)中,预先存在的转录组状态比其他脑区更有利于 7 号染色体上活跃的挽救基因的补偿。总之,这些发现表明,神经胶质瘤中 10 号染色体缺失和 7 号染色体获得的现象是由这两条染色体上许多基因的复杂相互作用所协调的,并为为什么这种共同发生优先发生在某些脑区起源的癌症中提供了一个合理的解释。  意义:获得的 7 号染色体上多个挽救基因的表达增加可能补偿丢失的 10 号染色体上几个脆弱基因的下调,解决了这种在神经胶质瘤中频繁共同发生的长期谜团。

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