Evidence map›Paper›PMID 40964363›Full record

ArticlebioRxiv : the preprint server for biology2025

Interactions Between Dietary Metabolites and Regulatory Risk Variants for Human Colon Cancer.

Tania N Fabo, Robin M Meyers, Evin Padhi, Laura N Kellman, Yang Zhao, Soumya Kundu, David L Reynolds, Ziwei Chen, Xue Yang, Lisa Ko and 3 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Tania N FaboProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-8987-0672
Robin M MeyersProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-1802-7231
Evin PadhiDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-2578-2435
Laura N KellmanProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-1073-8936
Yang ZhaoProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.
Soumya KunduDepartment of Computer Science, Stanford University School of Medicine, Stanford, CA, USA.
David L ReynoldsProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.
Ziwei ChenDepartment of Computer Science, Stanford University School of Medicine, Stanford, CA, USA.
Xue YangProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.
Lisa KoProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-3732-0580
Ibtihal ElfakiProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-9951-9974
Stephen B MontgomeryDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-5200-3903
Paul A KhavariProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.

Funding

Mechanisms of Epidermal Homeostasis and Early NeoplasiaR01AR043799 · NIAMS · STANFORD UNIVERSITY · PI PAUL KHAVARI · 1998 to 2026
$9.1M
Regulatory Variants in HUMAN SKIN DISEASESR01AR076965 · NIAMS · STANFORD UNIVERSITY · PI PAUL KHAVARI · 2020 to 2026
$3.6M
Regulators of TumorigenesisR01CA142635 · NCI · STANFORD UNIVERSITY · PI KHAVARI, PAUL · 2011 to 2020
$3.5M
Atlas of Regulatory Variants in Diseases (ARVID)U24HG010856 · NHGRI · STANFORD UNIVERSITY · PI KHAVARI, PAUL · 2020 to 2024
$3.3M
NCI NIH HHS R01 CA142635NHGRI NIH HHS U24 HG010856NIAMS NIH HHS R01 AR043799NIAMS NIH HHS R01 AR076965
6 · The paper itself

Abstract

Interactions between genetic variants and environmental factors influence malignancy risk, including for colorectal cancer (CRC). Prevalent CRC susceptibility loci reside predominantly in noncoding regulatory DNA where they may interact with dietary influences to dysregulate expression of specific genes predisposing to neoplasia. The impacts of CRC protective and risk dietary metabolites, butyrate and deoxycholic acid, were thus studied on the transcription-directing activity of 3703 regulatory CRC-associated variants via massively parallel reporter assays (MPRA) in human colonic cells. 1595 variant-dietary metabolite interactions were identified, pointing to dysregulation of MED13L, NKD2, and several modulators of Wnt/β-catenin signaling in potential CRC gene-environment interactions (GxE). Opposing impacts of butyrate and deoxycholic acid were also uncovered, indicating dietary influences may converge on common CRC risk loci and nominating FOSL1 and SP1 as mediators of these opposing responses. Coupling MPRA to relevant environmental factors offers an approach to extend insight into GxE in common human cancers.

Indexed as

Cancerdietenvironmentgene regulation

Identifiers

PMID40964363
PMCPMC12439979

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.