Ferroptosis represents a form of programmed cell death that is propelled by iron-dependent lipid peroxidation, thereby being distinguished by the prominent features of iron accumulation and lipid peroxidation. Ferroptosis has been implicated in numerous physiological and pathological phenomena, with mounting indications that it holds significant implications for cancer and other medical conditions. On one side, it demonstrates anti-cancer properties by triggering ferroptosis within malignant cells, and on the other hand, it damages normal cells causing other diseases. Therefore, in this paper, we propose to review the paradoxical regulation of ferroptosis in tumors and other diseases. First, we introduce the development history, concept and mechanism of ferroptosis. The second part focuses on the methods of inducing ferroptosis in tumors. The third section emphasizes the utilization of ferroptosis in different medical conditions and strategies to inhibit ferroptosis. The fourth part elucidates the key contradictions in the control of ferroptosis. Finally, potential research avenues in associated domains are suggested.

Colorectal cancer (CRC) is a common life-threatening disease that often requires surgical intervention, such as laparoscopic radical resection. However, despite successful surgeries, some patients experience disease relapse. Identifying the risk factors for CRC relapse can help guide clinical interventions and improve patient outcomes.

To determine the risk factors that may lead to CRC relapse after laparoscopic radical resection.

We performed a retrospective analysis using the baseline data of 140 patients with CRC admitted to our hospital between January 2018 and January 2020. All included participants were followed up until death or for 3 years. The baseline data and laboratory indicators were compared between the patients who experienced relapse and those who did not experienced relapse.

Among the 140 patients with CRC, 30 experienced relapse within 3 years after laparoscopic radical resection and 110 did not experience relapse. The relapse group had a higher frequency of rectal tumors with low differentiation and lymphatic vessel invasion than that of the non-relapse group. The expression of serum markers and the prognostic nutritional index were lower, whereas the neutrophil-to-lymphocyte ratio, expression of cytokeratin 19 fragment antigen 21-1, vascular endothelial growth factor, and Chitinase-3-like protein 1 were significantly higher in the relapse group than those in the non-relapse group. The groups did not differ significantly based on other parameters. Logistic regression analysis revealed that all the above significantly altered factors were independent risk factors for CRC relapse.

We identified multiple risk factors for CRC relapse following surgery, which can be considered for the clinical monitoring of patients to reduce disease recurrence and improve patient survival.

Circulating tumor DNA (ctDNA) has emerged as a promising non-invasive source to characterize genetic alterations related to the tumor. Upper gastrointestinal cancers, including gastroesophageal adenocarcinoma (GEC), biliary tract cancer (BTC) and pancreatic ductal adenocarcinoma (PADC) are poor prognostic malignancies, usually diagnosed at advanced stages when no longer amenable to surgical resection and show a poor prognosis even for resected patients. In this sense, ctDNA has emerged as a promising non-invasive tool with different applications, from early diagnosis to molecular characterization and follow-up of tumor genomic evolution. In this manuscript, novel advances in the field of ctDNA analysis in upper gastrointestinal tumors are presented and discussed. Overall, ctDNA analyses can help in early diagnosis, outperforming current diagnostic approaches. Detection of ctDNA prior to surgery or active treatment is also a prognostic marker that associates with worse survival, while ctDNA detection after surgery is indicative of minimal residual disease, anticipating in some cases the imaging-based detection of progression. In the advanced setting, ctDNA analyses characterize the genetic landscape of the tumor and identify patients for targeted-therapy approaches, and studies show variable concordance levels with tissue-based genetic testing. In this line, several studies also show that ctDNA serves to follow responses to active therapy, especially in targeted approaches, where it can detect multiple resistance mechanisms. Unfortunately, current studies are still limited and observational. Future prospective multi-center and interventional studies, carefully designed to assess the value of ctDNA to help clinical decision-making, will shed light on the real applicability of ctDNA in upper gastrointestinal tumor management. This manuscript presents a review of the evidence available in this field up to date.