Evidence map›Paper›PMID 26980625›Full record

ReviewBiochimica et biophysica acta2016

The inflammatory inception of gallbladder cancer.

Jaime A Espinoza, Carolina Bizama, Patricia García, Catterina Ferreccio, Milind Javle, Juan F Miquel, Jill Koshiol, Juan C Roa

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
10.0field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

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  16. Frontiers in cellular and infection microbiology · 2025
    Article
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  20. Risk Factors and Prognostic Factors in GBC.Journal of clinical medicine · 2024
    Review

20 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 3 countries.

Jaime A EspinozaSciLifeLab, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, Stockholm SE171 76, Sweden.
Carolina BizamaDepartment of Pathology, Advanced Center for Chronic Diseases (ACCDiS), UC-Center for Investigational Oncology (CITO), School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile.
Patricia GarcíaDepartment of Pathology, Advanced Center for Chronic Diseases (ACCDiS), UC-Center for Investigational Oncology (CITO), School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile.
Catterina FerreccioDepartment of Public Health, Advanced Center for Chronic Diseases (ACCDiS), School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile.
Milind JavleDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Juan F MiquelDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile.
Jill KoshiolDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda 20850, MD, USA.
Juan C RoaDepartment of Pathology, Advanced Center for Chronic Diseases (ACCDiS), UC-Center for Investigational Oncology (CITO), School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile. Electronic address: jcroa@med.puc.cl.
Pontificia Universidad Católica de Chile · CLAdvanced Center for Chronic Diseases · CLDivision of Cancer Epidemiology and GeneticsKarolinska Institutet · SEThe University of Texas MD Anderson Cancer Center · US

Funding

Etiology of Biliary Tract CancerZIACP010218 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI KOSHIOL, JILL · 2011 to 2025
$30.4M
Intramural NIH HHS ZIA CP010218
6 · The paper itself

Abstract

Gallbladder cancer is a lethal disease with notable geographical variations worldwide and a predilection towards women. Its main risk factor is prolonged exposure to gallstones, although bacterial infections and other inflammatory conditions are also associated. The recurrent cycles of gallbladder epithelium damage and repair enable a chronic inflammatory environment that promotes progressive morphological impairment through a metaplasia-dysplasia-carcinoma, along with cumulative genome instability. Inactivation of TP53, which is mutated in over 50% of GBC cases, seems to be the earliest and one of the most important carcinogenic pathways involved. Increased cell turnover and oxidative stress promote early alteration of TP53, cell cycle deregulation, apoptosis and replicative senescence. In this review, we will discuss evidence for the role of inflammation in gallbladder carcinogenesis obtained through epidemiological studies, genome-wide association studies, experimental carcinogenesis, morphogenetic studies and comparative studies with other inflammation-driven malignancies. The evidence strongly supports chronic, unresolved inflammation as the main carcinogenic mechanism of gallbladder cancer, regardless of the initial etiologic trigger. Given this central role of inflammation, evaluation of the potential for GBC prevention removing causes of inflammation or using anti-inflammatory drugs in high-risk populations may be warranted.

Indexed as

Autoimmune DiseasesBacterial InfectionsGallbladder NeoplasmsGallstonesHumansInflammationChronic inflammationGallbladder cancerGallstonesMetaplasiaSalmonella TyphiTP53

Identifiers

PMID26980625
PMCPMC6287912
OpenAlexW2299988691

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.