癌症中 FHIT 基因改变的综合分析。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-01-01 Epub Date: 2024-01-18 DOI:10.1080/15384101.2024.2304509
Lucía Simón-Carrasco, Elena Pietrini, Andrés J López-Contreras
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引用次数: 0

摘要

脆性组氨酸三聚体二腺苷三磷酸酶(FHIT)基因位于常见脆性位点 FRA3B,编码一种水解二核苷酸 Ap3A 的酶。虽然 FHIT 缺失是癌症中最常见的拷贝数改变之一,但其与癌症的发生和发展的相关性仍不清楚。在消化道癌症中,FHIT经常丢失,这与这些组织中的癌症驱动因素相吻合。然而,由于 FRA3B 基因座固有的脆弱性,FHIT 缺失也可能是一种客体事件。此外,FHIT 酶活性和 Ap3A 水平的生理相关性在很大程度上还不清楚。在此,我们对 FHIT 状态与其他突变和表型改变的关系进行了系统的泛癌症分析,并结合文献对我们的发现进行了批判性讨论,从而提供了一个关于 FHIT 在癌症中的影响的整体观点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Integrated analysis of FHIT gene alterations in cancer.

The Fragile Histidine Triad Diadenosine Triphosphatase (FHIT) gene is located in the Common Fragile Site FRA3B and encodes an enzyme that hydrolyzes the dinucleotide Ap3A. Although FHIT loss is one of the most frequent copy number alterations in cancer, its relevance for cancer initiation and progression remains unclear. FHIT is frequently lost in cancers from the digestive tract, which is compatible with being a cancer driver event in these tissues. However, FHIT loss could also be a passenger event due to the inherent fragility of the FRA3B locus. Moreover, the physiological relevance of FHIT enzymatic activity and the levels of Ap3A is largely unclear. We have conducted here a systematic pan-cancer analysis of FHIT status in connection with other mutations and phenotypic alterations, and we have critically discussed our findings in connection with the literature to provide an overall view of FHIT implications in cancer.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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