ArticleScientific reports2026
Comparative analysis of genomic profiles and clinical outcomes in cholangiocarcinoma and gallbladder cancer.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Cholangiocarcinoma (CCA) and gallbladder cancer (GBC) exhibit distinct biological behaviors and treatment responses, potentially driven by differences in their genomic landscapes. However, genomic investigations of biliary tract carcinoma (BTC) remain limited. A retrospective analysis was performed on next-generation sequencing data from 258 patients with BTC (188 with CCA, 70 with GBC), with an external cohort from Memorial Sloan-Kettering Cancer Center (MSKCC cohort) included for comparison. The most frequently altered genes in BTC included TP53 (56.6%), KRAS (27.9%), CDKN2A (21.3%), TERT (17.8%), and MCL1 (14.3%). CCA was predominantly characterized by mutations in ARID1A (15.4% vs. 5.7%, P = 0.04) and PBRM1 (10.1% vs. 0%, P = 0.003), as well as MCL1 amplifications (17.0% vs. 5.7%, P = 0.03), while GBC showed higher frequencies of TP53 alterations (78.6% vs. 47.9%, P < 0.001), ARID2 (15.7% vs. 3.7%, P = 0.002), TERT (24.3% vs. 11.2%, P = 0.02), CCNE1 amplifications (21.4% vs. 2.7%, P < 0.001), and SOX2 amplifications (4.3% vs. 0%, P = 0.02). GBC also exhibited an enrichment of alterations in the DNA damage response (DDR) (84.3% vs. 71.3%, P = 0.04) and p53 signaling (88.6% vs. 59.6%, P < 0.001) pathways. Additionally, 39.9% of patients with BTC harbored at least one actionable genomic alteration. Germline variants were detected in 7.0% (18/258) of patients, with the majority occurring in DDR (61.1%) and p53 (22.2%) pathways. Comparisons with the MSKCC cohort revealed similar genomic features and alterations. Patients with CCA exhibited significantly longer overall survival (OS) than patients with GBC (median OS, 41.2 vs. 24.3 months, P = 0.003). In the MSKCC cohort, high tumor mutational burden (TMB-H
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.