ReviewCancer control : journal of the Moffitt Cancer Center
Integrative Molecular Insights Into Epidemiological, Genetic, and Metabolic Risk Factors of Gallbladder Cancer: Implications for Biomarkers, Therapeutic Targeting, and Future Perspectives.
Review in Cancer control : journal of the Moffitt Cancer Center. 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
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
2 citing papers in PubMed.
- Molecular convergence in gallbladder cancer: MEK-ERK signalling at the crossroads of oncogenic hubs and pathway cross-talks.Cancer cell international · 2026Review
- Response of HER2 positive gallbladder adenocarcinoma to trastuzumab emtansine (T-DM1): a case report and literature review.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gallbladder cancer (GBC) is a rare yet highly aggressive malignancy of the biliary tract, characterized by a five-year survival rate of less than 5%. Its asymptomatic onset and the lack of reliable early diagnostic tools contribute to delayed detection and poor clinical outcomes. Although epidemiological and genetic studies have identified numerous risk factors, the molecular mechanisms linking these factors to tumor initiation and progression remain incompletely understood. This review integrates current evidence on the multifactorial etiology of GBC-including geographic variation, genetic predisposition, environmental exposures, chronic inflammation, and infections-with emerging insights into metabolic and molecular dysregulation. Particular focus is placed on metabolic reprogramming as a central driver of carcinogenesis. Altered lipid metabolism, bile acid signaling, and redox imbalance interact with inflammatory and oncogenic pathways, fostering a permissive microenvironment for malignant transformation. Key molecular cascades include inflammation-driven NF-κB activation, bile acid-induced oxidative stress, PI3K/AKT-mediated metabolic remodeling, and DNA damage and repair defects. By consolidating diverse epidemiological and mechanistic data into a unified molecular-metabolic framework, this narrative review identifies new opportunities for biomarker discovery, metabolic imaging, early detection, and targeted therapeutic development, advancing translational research to improve outcomes in this devastating disease.
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.