Evidence map›Paper›PMID 33481017›Full record

ArticleHuman molecular genetics2021

Multi-omics analysis to identify susceptibility genes for colorectal cancer.

Yuan Yuan, Jiandong Bao, Zhishan Chen, Anna Díez Villanueva, Wanqing Wen, Fangqin Wang, Dejian Zhao, Xianghui Fu, Qiuyin Cai, Jirong Long and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 3 countries.

Yuan YuanThe Fourth Affiliated Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 322000, China.
Jiandong BaoDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Zhishan ChenDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Anna Díez VillanuevaUnit of Biomarkers and Susceptibility, Oncology Data Analytics Program, Catalan Institute of Oncology (ICO); Colorectal Cancer Group, ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL); Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP); Faculty of Medicine, Department of Clinical Sciences, University of Barcelona, Barcelona 08908, Spain.
Wanqing WenDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Fangqin WangThe Fourth Affiliated Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 322000, China.
Dejian ZhaoDepartments of Genetics, Neurology and Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Xianghui FuDivision of Endocrinology and Metabolism, State Key Laboratory of Biotherapy, West China Hospital, Chengdu, Sichuan 610041, China.
Qiuyin CaiDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Jirong LongDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Xiao-Ou ShuDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Deyou ZhengDepartments of Genetics, Neurology and Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Victor MorenoUnit of Biomarkers and Susceptibility, Oncology Data Analytics Program, Catalan Institute of Oncology (ICO); Colorectal Cancer Group, ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL); Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP); Faculty of Medicine, Department of Clinical Sciences, University of Barcelona, Barcelona 08908, Spain.
Wei ZhengDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Weiqiang LinThe Fourth Affiliated Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 322000, China.
Xingyi GuoDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203, USA.
Vanderbilt University · USZhejiang University · CNAlbert Einstein College of Medicine · USInstitut Català d'Oncologia · ESInstitut d'Investigació Biomédica de Bellvitge · ESState Key Laboratory of Biotherapy

Funding

Transcriptome-wide association study to identify susceptibility genes for colorectal cancerR37CA227130 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GUO, XINGYI · 2018 to 2023
$3.7M
Colorectal cancer risk loci: GWAS, fine-mapping, and functional analysisR01CA188214 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LONG, JIRONG, ZHENG, WEI · 2014 to 2018
$3.1M
NCI NIH HHS R01 CA188214NCI NIH HHS R37 CA227130
6 · The paper itself

Abstract

Most genetic variants for colorectal cancer (CRC) identified in genome-wide association studies (GWAS) are located in intergenic regions, implying pathogenic dysregulations of gene expression. However, comprehensive assessments of target genes in CRC remain to be explored. We conducted a multi-omics analysis using transcriptome and/or DNA methylation data from the Genotype-Tissue Expression, The Cancer Genome Atlas and the Colonomics projects. We identified 116 putative target genes for 45 GWAS-identified variants. Using summary-data-based Mendelian randomization approach (SMR), we demonstrated that the CRC susceptibility for 29 out of the 45 CRC variants may be mediated by cis-effects on gene regulation. At a cutoff of the Bonferroni-corrected PSMR < 0.05, we determined 66 putative susceptibility genes, including 39 genes that have not been previously reported. We further performed in vitro assays for two selected genes, DIP2B and SFMBT1, and provide functional evidence that they play a vital role in colorectal carcinogenesis via disrupting cell behavior, including migration, invasion and epithelial-mesenchymal transition. Our study reveals a large number of putative novel susceptibility genes and provides additional insight into the underlying mechanisms for CRC genetic risk loci.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseTranscriptomeCarcinogenesisCell Line, TumorCell ProliferationColorectal NeoplasmsDNA MethylationGene Expression Regulation, NeoplasticGenomeGenome-Wide Association StudyHumansNerve Tissue ProteinsPolymorphism, Single NucleotideRepressor ProteinsRisk FactorsDIP2B protein, humanNerve Tissue ProteinsRepressor ProteinsSFMBT1 protein, human

Identifiers

PMID33481017
PMCPMC8485221
OpenAlexW3122126519

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.