On a global scale, pancreatic cancer is a leading cause of cancer-related death. According to the GLOBOCAN data, approximately half a million people were diagnosed and died from pancreatic cancer in 2018. 1 The most prevalent histological subtype of pancreatic cancer is adenocarcinoma, with the cancer of the pancreatic head accounting for a majority of cases (60-70%). At the time of diagnosis, approxi-mately 80-85% of individuals with pancreatic adenocarcinoma are ineligible for curative treatment. 2 Survival and response rates to treatment remain low due to the unique pathological features of pancreatic adenocarcinoma. Targeted therapies and immune checkpoint inhibitors that have shown efficacy in other types of cancer have not been significantly beneficial in advanced pancreatic cancer, except in indi-69 69 69

This study aimed to assess two oxidative stress (OxS) markers, thiol-disulfide (TD) homeostasis and ischemia-modified albumin (IMA), in newly diagnosed metastatic pancreatic cancer (PC) patients. Material and Methods: This was a prospective casecontrol study including two groups: 30 cases each of histopathologically confirmed metastatic PC patients and healthy controls. Serum TD and IMA levels were measured and compared in both groups. Moreover, the association between TD and IMA levels, as well as overall survival (OS) in the patient group, were investigated. Results: Both native thiol (NT) and total thiol (TT) levels significantly decreased in the patient group than in the control group (p=0.016 and p=0.009, respectively). However, disulfide (D) and IMA levels were similar between the two groups (p=0.056 and p=0.068, respectively). Both the D/NT and D/TT ratios were significantly higher in the patient group (p=0.005 and p=0.004, respectively) than in the control group. Additionally, no association was observed between IMA, TD homeostasis, and OS. Conclusion: Our results showed that increased OxS levels affected PC progression. With the development of newer targeted therapeutics for OxS, the progression of PC in individuals with higher genetic risk may be prevented.

No abstract