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, non-cancerous 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 pre-existing 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.

中文翻译：

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7 号染色体的增加补偿了神经胶质瘤中 10 号染色体的缺失


神经胶质瘤中 10 号染色体丢失和 7 号染色体增加的共发生是人类癌症中最常见的丢失-增益共非整倍体对。自 1980 年代后期以来，人们一直在研究这种现象，但没有得到解决。超越了以前的以基因为中心的研究，我们从进化的角度以全基因组的方式研究了共现。对大规模肿瘤非整倍体数据的挖掘证实了先前一项小规模纵向研究的发现，即最可能的顺序是 10 号染色体丢失，然后是 7 号染色体增加。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，这种共现可以用 7 号染色体上高度富集的功能拯救相互作用来解释，这可能会补偿 10 号染色体丢失引起的任何有害后果。分析来自各种正常、非癌性人脑组织的转录组数据，以评估哪些组织可能最容易耐受 7 号染色体增益对 10 号染色体丢失的补偿。分析表明，神经胶质瘤出现的皮层和额叶皮层中预先存在的转录组状态比其他大脑区域更有利于 7 号染色体上活跃的拯救基因的补偿。总的来说，这些发现表明，神经胶质瘤中 10 号染色体丢失和 7 号染色体增加的现象是由位于这两条染色体内的许多基因的复杂相互作用精心策划的，并提供了一个合理的理由，为什么这种共存优先发生在起源于大脑某些区域的癌症中。