ArticleJCI insight2022
Inactivation of Hippo pathway characterizes a poor-prognosis subtype of esophageal cancer.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Impaired TGF-β signaling via AHNAK family mutations elicits an esophageal cancer subtype with sensitivities to genotoxic therapy and immunotherapy.Cancer immunology, immunotherapy : CII · 2024Trial
- Early targeting of the YAP/TEAD-PKC-NF-κB axis alleviates post-traumatic osteoarthritis.iScience · 2026Article
- Epigenetic silencing of TBX1 inactivates the Hippo pathway to potentiate chemoresistance in esophageal squamous cell carcinoma.Cell death & disease · 2026Article
- Synergistic photothermal therapy of esophageal cancer using Pt@MOF@PSs nanozymes.Frontiers in bioengineering and biotechnology · 2026Article
- Recent advances in the role of atypical cadherin FAT1 in tumorigenesis (Review).Oncology letters · 2025Review
- The association of FAT1 mutations with therapeutic outcomes in AML, especially in receiving venetoclax combination.Frontiers in oncology · 2025Article
- A novel amino acid metabolism-related gene signature to predict the overall survival of esophageal squamous cell carcinoma patients.Journal of thoracic disease · 2024Article
- De novo variants in FRYL are associated with developmental delay, intellectual disability, and dysmorphic features.American journal of human genetics · 2024Article
- Chaetocin exhibits anticancer effects in esophageal squamous cell carcinoma via activation of Hippo pathway.Aging · 2023Article
- The Molecular Characterization of Genetic Abnormalities in Esophageal Squamous Cell Carcinoma May Foster the Development of Targeted Therapies.Current oncology (Toronto, Ont.) · 2023Review
- Deciphering the Hypoxia-immune interface in esophageal squamous carcinoma: a prognostic network model.Frontiers in oncology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identification of molecular subtypes that reflect different prognoses and treatment responses, especially immune checkpoint inhibitors (ICIs) in esophageal squamous cell carcinoma (ESCC), is essential for treatment decisions. We performed targeted sequencing in 201 patients with ESCC to discover genetic subtypes and validate our findings via multiple data sets. We identified 3 driver genes (FCGBP, GRIN2B, and FRY), and recurrent truncating mutations in FRY impaired its tumor-suppressive function and promoted tumor proliferation. A 3-gene mutation signature (FAT1, FAT3, and FRY) recognized a molecular subtype named "FAT/FRY" with frequent Hippo pathway-related mutations. In multiple ESCC cohorts, the patients with the FAT/FRY subtype had poorer prognosis than did patients in the WT group. Transcriptome analysis indicated that the FAT/FRY subtype was characterized by inactivation of the Hippo pathway, hypoxia, chemoresistance, higher infiltration of CD8+ T cells and activated DCs, and a transcriptome similar to that of cancer responders. Furthermore, the 3-gene signature predicted better survival for patients treated with ICIs, partially explained by its positive correlation with the tumor mutation burden and neoantigen burden. The 3-gene signature is a biomarker to recognize the FAT/FRY molecular subtype, evaluate prognosis, and select potential beneficiaries of ICIs in ESCC.
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.