Publications by authors named "A I Zaĭka"
Chronic Gastroesophageal Reflux Dysregulates Proteostasis in Esophageal Epithelial Cells.
Cell Mol Gastroenterol Hepatol
December 2024
Article Synopsis
- GERD is a common digestive disorder that causes damage to the esophagus due to stomach acid exposure, which can lead to serious complications like esophageal tumors and is characterized by oxidative stress and reactive byproducts known as isoLGs.
- The study examined how isoLGs interact with and cause misfolding and aggregation of proteins, using various assays and animal models to analyze esophageal tissues affected by GERD.
- The findings reveal that GERD leads to protein misfolding and cell death through mechanisms involving isoLG adduction, suggesting it shares features with other diseases related to protein aggregation.
Article Synopsis
- Aberrant cell fate transitions can lead to cancer, and p63 is identified as a key factor in determining cell type in esophageal development, specifically between squamous and neuroendocrine lineages.
- Deleting p63 in developing mice and human stem cells leads to increased neuroendocrine differentiation, suggesting that this transcription factor is crucial for maintaining proper cell identity.
- In esophageal neuroendocrine carcinoma, p63 is silenced by EZH2-mediated trimethylation, but reactivating p63 can promote a return to squamous cell characteristics, highlighting its role in cancer progression.
Helicobacter pylori (H. pylori) infection is the main risk factor for gastric cancer. The SRY-Box Transcription Factor 9 (SOX9) serves as a marker of stomach stem cells.
View Article and Find Full Text PDFPurpose: TGFβ signaling is implicated in the progression of most cancers, including esophageal adenocarcinoma (EAC). Emerging evidence indicates that TGFβ signaling is a key factor in the development of resistance toward cancer therapy.
Experimental Design: In this study, we developed patient-derived organoids and patient-derived xenograft models of EAC and performed bioinformatics analysis combined with functional genetics to investigate the role of SMAD family member 3 (SMAD3) in EAC resistance to oxaliplatin.