ArticleNature communications2024
Whole-exome sequencing reveals genomic landscape of intrahepatic cholangiocarcinoma and identifies SAV1 as a potential driver.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Global patterns of mutational profiles in biliary tract cancer.Journal of hepatology · 2026Article
- Inactivating LATS2 variation drives tumor progression and resistance to anti-PD-1 therapy in intrahepatic cholangiocarcinoma.Clinical and molecular hepatology · 2026Article
- Research on the Hippo Pathway in Cancer.Cells · 2026Review
- Hongwu mixture exerts inhibition on triple-negative breast cancer by regulating SAV1/Hippo signaling through ZNF143.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Pharmaco-genomic characterization of pancreatic and biliary tract cancer tumoroids for drug response.iScience · 2026Article
- Aflatoxins and Human Health: Global Exposure, Disease Burden, and One Health Strategies.Toxins · 2026Review
- Whole-Exome Profiling of Epstein-Barr Virus-Positive Neuroendocrine Carcinoma of the Nasopharynx.Endocrine pathology · 2026Article
- Frequent EPHA2 receptor mutations in cholangiocarcinoma disrupt receptor forward signaling supporting a tumor suppressor role.Biochimica et biophysica acta. Molecular cell research · 2026Article
- Genetic Aberrations in Normal Tissues Adjacent to Biliary Tract Cancers.Biomedicines · 2025Article
- Review: Progress of the NLRP3 inflammasome in tumours and perspectives for cholangiocarcinoma.Cell communication and signaling : CCS · 2025Review
- Advancing Precision Medicine: The Role of Genetic Testing and Sequencing Technologies in Identifying Biological Markers for Rare Cancers.Cancer medicine · 2025Review
- Immunotherapy in biliary tract cancer: reshaping the tumour microenvironment and advancing precision combination strategies.Frontiers in immunology · 2025Review
- Impact of Antiviral Treatment on Survival in HBV-Related Intrahepatic Cholangiocarcinoma Patients After Hepatectomy: A 14-Year Retrospective Follow-Up Study Based on the Propensity Score Matching Method.Therapeutics and clinical risk management · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrahepatic cholangiocarcinoma (ICC) is the second most common primary hepatic malignancy after hepatocellular carcinoma, with poor prognosis and limited treatment options. The genomic features of ICC in Chinese patients remain largely unknown. In this study, we perform deep whole-exome sequencing of 204 Chinese primary ICCs and characterize genomic alterations and clonal evolution, and reveal their associations with patient outcomes. We identify six mutational signatures, including Signatures A and F, which are highly similar to previously described signatures linked to aristolochic acid and aflatoxin exposures, respectively. We also identify 13 significantly mutated genes in the ICC samples, including SAV1. We find that SAV1 was mutated in 2.9% (20/672) of 672 ICC samples. SAV1 mutation is associated with lower SAV1 protein levels, higher rates of tumor recurrence, and shorter overall patient survival. Biofunctional investigations reveal a tumor-suppressor role of SAV1: its inactivation suppresses Hippo signaling, leading to YAP activation, thereby promoting tumor growth and metastasis. Collectively, our results delineate the genomic landscape of Chinese ICCs and identify SAV1 as a potential driver of ICC.
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.