Advances in the study of disulfidptosis in digestive tract tumors.

Disulfidptosis, a recently identified cell death mechanism, plays a pivotal role in the development, progression, and treatment of digestive tract tumors, including gastric cancer, hepatocellular cancer, esophageal cancer, colorectal cancer, pancreatic cancer, cholangiocarcinoma, and neuroendocrine tumors, which have high global incidence and mortality rates. Analyzing the expression of disulfidptosis-related gene expression within the tumor microenvironment enhances our understanding of tumor biology and facilitates novel diagnostic and therapeutic strategies. Research on immune infiltration and checkpoints can identify therapeutic targets linked to disulfidptosis, thereby improving immunotherapy efficacy. Targeting genes such as SLC7A11, which are essential for maintaining glutathione levels and regulating oxidative stress, may overcome chemoresistance and enhance existing treatments. Disulfidptosis could complement current therapies as it induces cytoskeletal collapse and selective tumor cell death, especially in chemoresistant cancers. Additionally, genes like SLC7A11, RPN1, and NCKAP1 in gastric cancer correlate with poor prognosis, highlighting their potential as prognostic biomarkers. Personalized medicine approaches utilizing disulfidptosis-related biomarkers could identify patients who would benefit from therapies targeting oxidative stress regulation, leading to more precise treatments and improved outcomes. This review summarizes disulfidptosis mechanisms, advancements in digestive cancers, and the potential of related genes for prognosis, immune response evaluation, and targeted therapies, providing novel perspectives for diagnosis and personalized treatment.