ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2025
Targeting yes-associated protein to overcome imatinib resistance in gastrointestinal stromal tumor drug-tolerant persister cells.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2025. 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.
- Estrogen-related receptor alpha (ERRα) promotes gastrointestinal stromal tumor progression and epithelial-mesenchymal transition through Wnt/β-catenin.Research square · 2026Article
- Targeting tumor dormancy: the next frontier in gastrointestinal stromal tumor therapy.Neoplasia (New York, N.Y.) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
backgroundThe tyrosine kinase inhibitor (TKI) imatinib targets KIT and PDGFRA, offering significant therapeutic benefits in advanced gastrointestinal stromal tumors (GISTs). However, the high rate of recurrence following treatment discontinuation suggests that drug-tolerant persister cells (DTPs) may contribute to therapy resistance. Elucidating the mechanisms underlying DTP survival is critical for the development of curative strategies. This study aimed to investigate the role of yes-associated protein (YAP) in DTP survival and to evaluate the efficacy of combining imatinib with YAP inhibitors as a potential therapeutic approach.
methodsImatinib-sensitive GIST cell lines were treated with imatinib to generate DTPs. YAP activity was assessed via western blotting, fluorescence immunostaining, and nuclear-cytoplasmic fractionation. Proliferation and apoptosis assays were conducted to evaluate sensitivity to YAP inhibitors, such as verteporfin. Xenograft mouse models were used to assess the efficacy of combination therapy with imatinib and verteporfin.
resultsDTPs exhibited increased nuclear localization and activity of YAP, which was reversible upon imatinib withdrawal. YAP inhibitors reduced nuclear YAP levels and showed greater efficacy in DTPs than in parental cells. Combination therapy with imatinib and verteporfin significantly suppressed DTP proliferation and induced apoptosis in vitro. In xenograft models, the combination therapy delayed tumor regrowth after treatment cessation compared to imatinib monotherapy.
conclusionsYAP activity was elevated in GIST DTPs, and YAP inhibitors effectively suppressed this activity. The combination of imatinib and YAP inhibitors enhanced tumor growth suppression. These findings underscore the pivotal role of YAP in DTP survival and demonstrate the therapeutic potential of combining imatinib with YAP inhibitors.
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.