Integration of Mendelian randomization and transcriptome wide association studies for causal gene identification in ovarian cancer genetic architecture

整合孟德尔随机化和全转录组关联研究以鉴定卵巢癌遗传结构中的致病基因

阅读:2

Abstract

BACKGROUND: Ovarian cancer remains one of the most lethal gynecological malignancies with limited understanding of its genetic architecture and causal mechanisms. While genome-wide association studies have identified numerous susceptibility loci, the causal relationships between gene expression and ovarian cancer risk remain poorly understood. METHODS: We conducted a comprehensive genetic analysis integrating two-sample Mendelian randomization (MR) and transcriptome-wide association studies (TWAS) using expression quantitative trait loci (eQTL) data from the GTEx project and ovarian cancer GWAS data from the Ovarian Cancer Association Consortium (OCAC). Summary-data-based Mendelian randomization (SMR) analysis was performed to assess causal relationships between gene expression and ovarian cancer risk. Additionally, we analyzed survival outcomes in 3595 ovarian cancer patients from the SEER database to examine the clinical implications of radiation timing and constructed a prognostic nomogram incorporating genetic and clinical factors. RESULTS: MR analysis identified three genes with significant causal associations with ovarian cancer risk. GSTZ1 variant rs11621440 demonstrated a protective effect (OR = 0.999, 95% CI 0.999-1.000, FDR = 0.001), while PNP variant rs8015430 (OR = 1.006, 95% CI 1.002-1.010, FDR = 0.002) and KIAA1715 variant rs864697 (OR = 0.999, 95% CI 0.999-1.000, FDR = 0.002) showed increased risk associations. TWAS analysis revealed multiple genes with transcriptome-wide significant associations, including SIGLEC family genes (SIGLEC14, SIGLEC12, SIGLEC5) associated with increased risk through decreased expression, and metabolic genes (OCTN2, MSR1) associated with risk through increased expression. Survival analysis demonstrated that radiation timing significantly impacts prognosis, with postoperative radiation showing superior outcomes compared to preoperative radiation (HR = 1.49, 95% CI 1.23-1.82, p = 5.8 × 10(-5)). CONCLUSIONS: This study provides robust genetic evidence for causal relationships between specific gene expression patterns and ovarian cancer risk.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。