Researchers from a leading medical university have discovered a potential new marker for prognosis and individualized treatment of ccRCC, which causes 14,000 deaths annually in the United States. The study focused on oxidative stress, which occurs when there is an imbalance between oxidative and antioxidant activities in the body, leading to inflammation and increased protease secretion. Cancer cells, especially ccRCC cells, have higher levels of reactive oxygen species (ROS) than normal cells.

The researchers screened and enriched 136 differentially expressed genes (DEGs) associated with oxidative stress, including 95 up-regulated genes and 41 down-regulated genes. Further analysis using Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analysis showed that the DEGs were mainly enriched in pathways associated with cancer, lipid and atherosclerosis, cytokine-cytokine receptor interactions, and signaling receptor activator activity.

In addition, the researchers filtered 1479 oxidative stress-related lncRNAs and identified seven OS-associated lncRNAs that constructed a predictive signature for ccRCC, including SPART-AS1, AL162586.1, LINC00944, LINC01550, HOXB-AS4, LINC02027, and DOCK9-DT. The risk scores of these lncRNAs were calculated, and patients were divided into high-risk and low-risk groups based on the median risk score. The overall survival rate was significantly lower in the high-risk group than that in the low-risk group.

The researchers hypothesize that oxidative stress plays a key role in ccRCC, and this study provides a reliable prognostic signature for ccRCC based on differentially expressed OS-related lncRNAs. Further research is needed to explore the potential of these lncRNAs as therapeutic targets for ccRCC.

This study, which is a step towards individualized treatment of kidney cancer, has been published in a leading medical journal and has been well received by the medical community.

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