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Purpose: Knowledge on the potential association between differential gene expression and risk of gastrointestinal stromal tumors (GISTs) is currently limited. We used bioinformatics tools to identify differentially expressed genes in GIST samples and the related signaling pathways of these genes.
Patients And Methods: The GSE136755 dataset was obtained from the GEO database and differentially expressed genes () were screened using String and Cytoscape bioinformatics tools. Then, three groups of eight patients at high, intermediate and low risk of GIST were selected from patients diagnosed with GIST by immunohistochemistry in our hospital from October 2020 to March 2021. Differential expression of and was verified by comparing the amount of expressed p21-Activated kinase 4 (PAK4) protein in pathological sections.
Results: SPSS26.0 analysis showed that the expression level of PAK4 in GISTs was significantly higher than in normal tissues and paratumoral tissues and there was significant difference among the three groups of patients (P < 0.01). PAK4 levels in paratumoral and normal tissues were negligible with no significant difference between the tissues.
Conclusion: and gene expression can be used as biomarkers to assess the risk of gastrointestinal stromal tumors whereby expression increases gradually with the increased risk of GIST formation. The genes encode proteins that regulate the division, proliferation and apoptosis of gastrointestinal stromal tumors mainly through PI3K/AKT, MARK, P53, WNT and other signaling pathways.
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http://dx.doi.org/10.2147/IJGM.S357224 | DOI Listing |
Neuro Endocrinol Lett
September 2025
Department of Radiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, China.
Background: Pheochromocytomas and paragangliomas (PPGLs) are rare catecholamine-secreting neuroendocrine tumors originating from the embryonic neural crest. Approximately 30% of PPGLs are hereditary and are frequently associated with genetic syndromes, including neurofibromatosis type 1 (NF1). Composite PPGLs, which include components of both PPGLs and related tumors such as ganglioneuromas, are extremely rare in NF1 patients.
View Article and Find Full Text PDFJ Immunother Precis Oncol
August 2025
Department of Medicine, Sylvester Comprehensive Cancer Center/University of Miami, Miami, FL, USA.
The combination of targeted therapies and immunotherapies for advanced and metastatic sarcomas has been proposed owing to the enhanced effect of antiangiogenic therapies on the tumor microenvironment. We found eight studies published to date assessing the effectiveness of combined multitargeted vascular endothelial growth factor (VEGF)-tyrosine kinase inhibitors with immune checkpoint inhibitors (ICIs) in sarcoma. It is difficult to draw conclusions owing to limited data and primarily single-arm studies, although initial literature appears promising and requires further study.
View Article and Find Full Text PDFOncogene
September 2025
Department of Molecular Medicine and Biochemistry, Akita University Graduate School of Medicine, Akita, Japan.
Forkhead-box-protein P3 (FOXP3) is a key transcription factor in T regulatory cells (Tregs). However, its expression and significance in non-immune stromal cells in the tumor microenvironment remain unclear. Here, we demonstrated FOXP3 expression in stromal fibroblasts of mouse and human gastrointestinal tumors.
View Article and Find Full Text PDFSurg Case Rep
September 2025
Department of Pathology, Self-Defense Forces Central Hospital, Tokyo, Japan.
Introduction: Solitary fibrous tumor (SFT) is a rare mesenchymal neoplasm that most commonly originates in the pleura but can also occur at extrapleural sites, including the abdominal cavity. Among these, primary SFT of the stomach is exceptionally rare. Due to overlapping clinical, endoscopic, and radiologic characteristics, distinguishing SFT from gastrointestinal stromal tumor (GIST) can be particularly challenging.
View Article and Find Full Text PDFGastric Cancer
September 2025
Department of Gastroenterological Surgery, The University of Osaka Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Background: The 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.
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