ArticleOncogene2004
Gastrointestinal stromal tumors (GISTs) with KIT and PDGFRA mutations have distinct gene expression profiles.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 148 citations in OpenAlex.
- Gene expression signatures and response to imatinib mesylate in gastrointestinal stromal tumor.Molecular cancer therapeutics · 2009Trial
- Laparoscopic resection for high-risk gastric gastrointestinal stromal tumors: safety and oncological outcome.Surgical endoscopy · 2026Article
- Targeted Therapy for Advanced Gastrointestinal Stromal Tumors: Evolution and Future Directions.Drug design, development and therapy · 2026Review
- 18F-Fluorodeoxyglucose Uptake in PDGFRA-Mutant Gastrointestinal Stromal Tumors.JAMA network open · 2025Article
- Retroperitoneal extra gastrointestinal stromal tumor: A case report.International journal of surgery case reports · 2023Article
- Emerging Targeted Therapeutic Strategies to Overcome Imatinib Resistance of Gastrointestinal Stromal Tumors.International journal of molecular sciences · 2023Review
- Article
- Identification of Wee1 as a target in combination with avapritinib for gastrointestinal stromal tumor treatment.JCI insight · 2021Article
- Renal Clearable Theranostic Nanoplatforms for Gastrointestinal Stromal Tumors.Advanced materials (Deerfield Beach, Fla.) · 2020Article
- The new horizon of liquid biopsy in sarcoma: the potential utility of circulating tumor nucleic acids.Journal of Cancer · 2020Review
- Multiple gastrointestinal stromal tumors with exon 11 mutation of the c-KIT gene in a young male without family history.International journal of clinical and experimental pathology · 2020Article
- Stomatin plays a suppressor role in non-small cell lung cancer metastasis.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019Article
- Targeted therapy and personalized medicine in gastrointestinal stromal tumors: drug resistance, mechanisms, and treatment strategies.OncoTargets and therapy · 2019Review
- Gastrointestinal stromal tumor enhancers support a transcription factor network predictive of clinical outcome.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Insights into the Proteome of Gastrointestinal Stromal Tumors-Derived Exosomes Reveals New Potential Diagnostic Biomarkers.Molecular & cellular proteomics : MCP · 2018Article
- Genetic progression in gastrointestinal stromal tumors: mechanisms and molecular interventions.Oncotarget · 2017Review
- Novel Insights into the Treatment of Imatinib-Resistant Gastrointestinal Stromal Tumors.Targeted oncology · 2017Review
- Revisiting a dogma: similar survival of patients with small bowel and gastric GIST. A population-based propensity score SEER analysis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2017Article
- Efficacy of Imatinib in Patients with Platelet-Derived Growth Factor Receptor Alpha-Mutated Gastrointestinal Stromal Tumors.Cancer research and treatment · 2016Article
- Gene expression identifies heterogeneity of metastatic behavior among gastrointestinal stromal tumors.Journal of translational medicine · 2016Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 3 countries.
Funding
Abstract
Most GISTs require oncogenic activation of the KIT or PDGFRA receptor tyrosine kinase proteins, and the genomic mechanisms of oncogene activation are heterogeneous. Notably, the kinase mutation type correlates with both tumor biology and imatinib response. For example, GISTs with KIT exon 11 mutations are typically gastric and have excellent imatinib response, whereas those with KIT exon 9 mutations generally arise in the small bowel and are less responsive to imatinib. To identify genes that might contribute to these biological differences, we carried out gene expression profiling of 26 GISTs with known KIT and PDGFRA mutational status. Expression differences were then evaluated further by RNA in situ hybridization, immunohistochemistry, and immunoblotting. Unsupervised hierarchical clustering grouped tumors with similar mutations together, but the distinction between the different groups was not absolute. Differentially expressed genes included ezrin, p70S6K, and PKCs, which are known to have key roles in KIT or PDGFRA signaling, and which might therefore contribute to the distinctive clinicopathological features in GISTs with different mutation types. These gene products could serve as highly selective therapeutic targets in GISTs containing the KIT or PDGFRA mutational types with which they are associated.
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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.