Epithelioid Subtype Gastrointestinal Stromal Tumors of Stomach in an Endoscopic Biopsy: A Potential Diagnostic Pitfall.

Background: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract with a broad morphological spectrum. Although epithelioid GISTs account for 20% of GISTs, their morphological features may pose a diagnostic pitfall for pathologists due to their morphological similarities to poorly differentiated adenocarcinoma and lymphoma. Case Presentation: Herein, we report a 65-year-old male patient with gastric epithelioid GIST misdiagnosed as adenocarcinoma for four years. During this period, he was treated with chemotherapy combined with PD-L1 immunotherapy. The clinicians thought the treatments were effective. However, there was no significant change in tumor size. The patient's clinical symptoms did not improve significantly as well. Finally, an endoscopic biopsy was performed again and gastric epithelioid GIST was confirmed in our hospital through morphology, immunohistochemistry, and whole-genome sequencing. Conclusion: A broad morphological spectrum and diverse immunophenotypic changes of GISTs could represent a pitfall for pathologists. However, predisposed anatomical sites, morphology, and corresponding immunohistochemical markers are of great significance for the diagnosis of GISTs and the differential diagnosis from other diseases. On the other hand, clinicians should diagnose and comprehensively evaluate treatment effects based on the patient's clinical symptoms and relevant laboratory examinations, instead of over-reliance on pathological diagnosis.

Interferon regulatory factor 4 binding protein is a novel p53 target gene and suppresses cisplatin-induced apoptosis of breast cancer cells.

BACKGROUND: Our previous work demonstrated that ectopic expression of interferon regulatory factor 4 binding protein (IBP) was correlated with the malignant behaviour of human breast cancer cells. The mechanisms controlling differential expression of IBP in breast cancer still remain unknown. RESULTS: To investigate the mechanism of IBP dysregulation in breast cancer, we identified IBP was a novel p53 target gene. IBP expression was negatively regulated by wild-type p53 and was p53 dependently suppressed by DNA damage agent cisplatin. Furthermore, high levels of IBP were found to decrease cisplatin-induced growth suppression and apoptotic cell death, which was associated with decreased p53 activity and imbalanced Bcl-2 family member expression. CONCLUSIONS: IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy.