Evidence map›Paper›PMID 41395591›Full record

ArticleBreast cancer (Dove Medical Press)2025

Common Biomarkers and Pathogenesis of Inflammatory Bowel Disease and Breast Cancer: Mendelian Randomization and Multi-Omics Studies.

Daqing Zhang, Yongjun Guan, Haitao Tang, Qingze Xue, Xiaoqiang Li, Xu Bin, Faping You

Abstract read
In one paragraph

Article in Breast cancer (Dove Medical Press), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

7 authors.

Daqing ZhangDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University,State Key Lab of Digestive Health,National Clinical Research Center for Digestive Diseases, Beijing, People's Republic of China.
Yongjun GuanDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University,State Key Lab of Digestive Health,National Clinical Research Center for Digestive Diseases, Beijing, People's Republic of China.
Haitao TangDepartment of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.
Qingze XueDepartment of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.
Xiaoqiang LiDepartment of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.
Xu BinDepartment of Pathology, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.
Faping YouDepartment of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Inflammatory bowel disease (IBD) and breast cancer represent significant global health burdens. Although epidemiological studies have suggested a potential link between them, the causal relationship and underlying molecular mechanisms remain unclear. This study employed Mendelian randomization (MR) and multi-omics approaches to investigate the causal association between IBD and breast cancer and to explore shared genetic biomarkers and pathological pathways. Methods: A two-sample MR analysis was performed using genome-wide association study (GWAS) data. Shared genes were identified and validated using the GEO and TCGA databases. THBS3 expression was further verified in human breast cancer tissues via immunohistochemistry and RT-PCR. Immune infiltration analysis, drug sensitivity assessment, molecular docking, ceRNA network construction, and pathway enrichment analyses (GSEA and GSVA) were conducted to explore the functional role of THBS3. Results: MR analysis indicated that IBD significantly increases the risk of breast cancer. THBS3 was identified as a commonly overexpressed gene in both diseases and was associated with poor prognosis. THBS3-high breast cancer patients exhibited resistance to Dinaciclib, Daporinad, and Rapamycin. Molecular docking and dynamics simulations confirmed a strong binding affinity between THBS3 and Rapamycin. A ceRNA network linked THBS3 to miR-423-5p and chemotherapy resistance-related lncRNAs. Pathway analyses revealed THBS3 involvement in extracellular matrix receptor interaction and proteasome pathways. Conclusion: This study provides genetic evidence supporting IBD as a risk factor for breast cancer and highlights THBS3 as a key shared biomarker. THBS3 may promote breast cancer progression through immune regulation, ECM remodeling, and drug resistance mechanisms, suggesting its potential as a therapeutic target. These findings support enhanced breast cancer screening in IBD patients.

Indexed as

breast cancerCrohn’s diseaseIBDMendelian randomizationulcerative colitis

Identifiers

PMID41395591
PMCPMC12700015

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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.