Meta-dimensional data integration identifies critical pathways for susceptibility, tumorigenesis and progression of endometrial cancer

7Citations
Citations of this article
36Readers
Mendeley users who have this article in their library.

Abstract

Endometrial Cancer (EC) is one of the most common female cancers. Genomewide association studies (GWAS) have been investigated to identify genetic polymorphisms that are predictive of EC risks. Here we utilized a meta-dimensional integrative approach to seek genetically susceptible pathways that may be associated with tumorigenesis and progression of EC. We analyzed GWAS data obtained from Connecticut Endometrial Cancer Study (CECS) and identified the top 20 EC susceptible pathways. To further verify the significance of top 20 EC susceptible pathways, we conducted pathway-level multi-omics analyses using EC exome-Seq, RNA-Seq and survival data, all based on The Cancer Genome Atlas (TCGA) samples. We measured the overall consistent rankings of these pathways in all four data types. Some well-studied pathways, such as p53 signaling and cell cycle pathways, show consistently high rankings across different analyses. Additionally, other cell signaling pathways (e.g. IGF-1/mTOR, rac-1 and IL-5 pathway), genetic information processing pathway (e.g. homologous recombination) and metabolism pathway (e.g. sphingolipid metabolism) are also highly associated with EC risks, diagnosis and prognosis. In conclusion, the meta-dimensional integration of EC cohorts has suggested some common pathways that may be associated from predisposition, tumorigenesis to progression.

Cite

CITATION STYLE

APA

Wei, R., De Vivo, I., Huang, S., Zhu, X., Risch, H., Moore, J. H., … Garmire, L. X. (2016). Meta-dimensional data integration identifies critical pathways for susceptibility, tumorigenesis and progression of endometrial cancer. Oncotarget, 7(34), 55249–55263. https://doi.org/10.18632/oncotarget.10509

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free