ArticleJournal of experimental & clinical cancer research : CR2019
A subset of diffuse-type gastric cancer is susceptible to mTOR inhibitors and checkpoint inhibitors.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Targetable genes associated with hematogenous metastasis in gastric cancer using the TCGA database.Korean journal of clinical oncology · 2026Article
- Linc-ROR orchestrates autophagy suppression and marks gastric cancer via the miR-145-5p/CARMIL1 axis.Cell biology and toxicology · 2026Article
- Actionable Genes and Carcinogenic Pathways for Gastric Cancer in Latinos.Cancer medicine · 2025Article
- CNV-mediated dysregulation of the ceRNA network mechanism revealed heterogeneity in diffuse and intestinal gastric cancers.Journal of translational medicine · 2025Article
- A literature review of recent advances in gastric cancer treatment: exploring the cross-talk between targeted therapies.Cancer cell international · 2025Review
- Clinical outcomes and biomarker exploration of first-line PD-1 inhibitors plus chemotherapy in patients with low PD-L1-expressing of gastric or gastroesophageal junction adenocarcinoma.Cancer immunology, immunotherapy : CII · 2024Article
- E-cadherin loss drives diffuse-type gastric tumorigenesis via EZH2-mediated reprogramming.The Journal of experimental medicine · 2024Article
- Xenograft and organoid models in developing precision medicine for gastric cancer (Review).International journal of oncology · 2024Review
- Implementing an On-Slide Molecular Classification of Gastric Cancer: A Tissue Microarray Study.Cancers · 2023Article
- CDH1 loss promotes diffuse-type gastric cancer tumorigenesis via epigenetic reprogramming and immune evasion.bioRxiv : the preprint server for biology · 2023Article
- Patient-derived xenograft models in cancer therapy: technologies and applications.Signal transduction and targeted therapy · 2023Review
- Evaluation of pH-Sensitive Polymeric Micelles Using Citraconic Amide Bonds for the Co-Delivery of Paclitaxel, Etoposide, and Rapamycin.Pharmaceutics · 2023Article
- The phosphorylation level of Cofilin-1 is related to the pathological subtypes of gastric cancer.Medicine · 2022Article
- The dawn of precision medicine in diffuse-type gastric cancer.Therapeutic advances in medical oncology · 2022Review
- Dietary Intake of Soy Products, Vegetables, and Dairy Products and Gastric Cancer Survival according to Histological Subtype: a Long-term Prospective Cohort Study.Journal of gastric cancer · 2021Article
- Ferroptosis Patterns Correlate with Immune Microenvironment Characterization in Gastric Cancer.International journal of general medicine · 2021Article
- Gastric cancer: a comprehensive review of current and future treatment strategies.Cancer metastasis reviews · 2020Review
- Pan-cancer image-based detection of clinically actionable genetic alterations.Nature cancer · 2020Article
- PaccMann: a web service for interpretable anticancer compound sensitivity prediction.Nucleic acids research · 2020Article
- MEK inhibition overcomes everolimus resistance in gastric cancer.Cancer chemotherapy and pharmacology · 2020Article
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundMechanistic target of rapamycin (mTOR) pathway is essential for the growth of gastric cancer (GC), but mTOR inhibitor everolimus was not effective for the treatment of GCs. The Cancer Genome Atlas (TCGA) researchers reported that most diffuse-type GCs were genomically stable (GS). Pathological analysis suggested that some diffuse-type GCs developed from intestinal-type GCs.
methodsWe established patient-derived xenograft (PDX) lines from diffuse-type GCs, and searched for drugs that suppressed their growth. Diffuse-type GCs were classified into subtypes by their gene expression profiles.
resultsmTOR inhibitor temsirolimus strongly suppressed the growth of PDX-derived diffuse-type GC-initiating cells, which was regulated via Wnt-mTOR axis. These cells were microsatellite unstable (MSI) or chromosomally unstable (CIN), inconsistent with TCGA report. Diffuse-type GCs in TCGA cohort could be classified into two clusters, and GS subtype was major in cluster I while CIN and MSI subtypes were predominant in cluster II where PDX-derived diffuse-type GC cells were included. We estimated that about 9 and 55% of the diffuse-type GCs in cluster II were responders to mTOR inhibitors and checkpoint inhibitors, respectively, by identifying PIK3CA mutations and MSI condition in TCGA cohort. These ratios were far greater than those of diffuse-type GCs in cluster I or intestinal-type GCs. Further analysis suggested that diffuse-type GCs in cluster II developed from intestinal-type GCs while those in cluster I from normal gastric epithelial cells.
conclusionmTOR inhibitors and checkpoint inhibitors might be useful for the treatment of a subset of diffuse-type GCs which may develop from intestinal-type GCs.
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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.