ArticleProceedings of the National Academy of Sciences of the United States of America2026
MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Bioinformatics Screening and Preliminary Experimental Verification of Integrated Stress Response-Associated MYC and BAG3 in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2026Article
Corrections and comments
- Update of
Authors and funding
8 authors.
Funding
Abstract
MYC amplification contributes to poor survival and outcome in pancreatic ductal adenocarcinoma (PDAC). Here we show that in PDAC cell lines with amplified MYC, MondoA is required for viability, facilitating proliferation while suppressing apoptosis in vitro and in vivo. Transcriptional and genomic profiling demonstrates that loss of MondoA leads to altered expression of direct MondoA targets as well as MYC target genes and is accompanied by shifts in genomic occupancy of MYC, MNT, and the MondoA paralog ChREBP. This altered genomic binding by MYC network members is associated with transcriptional perturbation of multiple metabolic and stress pathways, as well as global changes in N6-methyladenosine modification (m
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