Mechanistically, the knock-down/knock-out of UCK2 might decrease the expression levels of the p-AKT, cyclin D1, and cyclin E1 proteins in GC cells, leading to G1/S phase arrest. Our findings established UCK2 as a novel and clinically valuable biomarker, providing a potential tool for improving the diagnosis and prognosis evaluation of GC, and highlighted its potential as a therapeutic target for future anti-tumor strategies.
Diagnosis requires systematically excluding other primary squamous cell carcinoma sites (oesophagus, lung, head and neck) before confirming primary gastric squamous cell carcinoma (GSCC).Radical resection (R0) combined with aggressive adjuvant chemotherapy is the optimal treatment strategy, offering the best survival chance even in advanced disease (pT4bN3aM0, LVI+/PNI+).Treatment must be individualised due to a lack of standardised protocols: for this extremely rare malignancy, the decision between upfront surgery versus neoadjuvant chemotherapy should be based on tumour resect ability, biological characteristics and multidisciplinary tumour board discussion.
SIRT2 is upregulated in GC tissues and is associated with poor prognosis. It may serve as a promising biomarker for predicting GC progression and evaluating patient outcomes.
This review summarizes the cooperative roles of these inflammatory mediators in the progression from gastritis to gastric cancer and discusses their potential as therapeutic targets. A better understanding of these mechanisms may facilitate the development of novel strategies for the prevention and treatment of gastric cancer.
Finally, we identify current limitations in the field, including inconsistent CLDN18.2 testing criteria, and outline prioritized future directions to optimize integration of CLDN18.2-directed therapies across gastrointestinal cancers. By looking beyond zolbetuximab and incorporating cross-platform comparison, immuno-oncology considerations, and multi-tumor context, this review provides a broad and forward-looking framework to guide clinical application and next-generation research in CLDN18.2-targeted therapy.
ACC and DLBC shared a consensus expression program, whereas STAD diverged; chromatin analysis showed AP-2 motifs near microbe-responsive genes in ACC and DLBC but not STAD, supporting cohort-specific regulation. Collectively, AP-2 family members emerge as plausible mediators of tumor microbiota-host interplay, warranting further mechanistic and translational research.
This review provides a comprehensive overview of the evolving therapeutic landscape of GEC. It emphasizes the growing role of precision medicine and the integration of emerging clinical data into practice.
These findings suggest that TGFBR1 inhibition could provide a strategic approach to reduce the dosage of 5FU, thereby minimizing its severe side effects in gastric cancer patients. Furthermore, these results underscore the potential of TGFBR1 as both a prognostic biomarker and a therapeutic target, warranting further investigation in aggressive forms of gastric cancer.
P=N/A, N=239, Terminated, University Hospital, Gasthuisberg | Trial completion date: May 2025 --> Dec 2025 | Active, not recruiting --> Terminated; halted prematurely due to futility finding at te occasion of an unplanned interm analysis at 200 participants
Our study provides a prognostic assessment tool for GC based on EMT-related genes and offers novel insights into understanding the roles of EMT in GC progression and treatment resistance. These findings may aid in the development of precision therapy strategies for GC.