ArticlePeerJ2026
Multi-omics evidence reveals a causal role of endoplasmic reticulum stress in cancer development.
Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum stress (ERS) plays a crucial role in the pathogenesis of various diseases, but its causal involvement and therapeutic potential in cancer remain unclear. In this study, we integrated genome-wide association study (GWAS) data from 18 common cancers with quantitative trait loci (cis-eQTL, cis-mQTL, and cis-pQTL) to explore the causal effects of ERS-related genes on cancer. A total of 1,350 ERS-related genes were retrieved from the GeneCards database. Mendelian randomization (MR) and Bayesian colocalization analyses were conducted to assess causality and shared genetic variants across mRNA expression, DNA methylation, and protein expression levels. External datasets were used for expression validation and diagnostic efficacy assessment. To provide experimental evidence, immunohistochemical (IHC) staining was performed to verify the expression and localization of key ERS-related genes in tumor and adjacent normal tissues. Functional enrichment, cellular localization, and drug sensitivity analyses were further applied to reveal potential biological mechanisms. We identified nine ERS-related genes and 15 methylation sites with potential causal relationships to specific cancer types. Both external validation and IHC analysis consistently confirmed the associations of
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.