478 Background: The disruption of redox balance is increasingly thought to be one of the most important underlying factors contributing to the development, progression, and metastasis of cancers in human cells. This imbalance in redox homeostasis has been shown to be induced by the generation of free radicals, predominantly reactive oxygen species (ROS). Emerging data have established ROS as a new potential therapeutic target. Understanding the mechanisms associated with tumorigenesis is important to integrate novel potential therapeutic targets and understand which tumors or patient populations may benefit from ongoing research. Shortcomings in oncologists’ knowledge and confidence can hamper the integration of new treatments into the care of patients with cancer. Methods: An online continuing education (CME) activity consisted of a multi-media 30-minute video panel of two panelists discussing the mechanism, pathophysiology, and the premises for novel anti-cancer therapies. Educational effect was assessed using a repeated paired pre-/post-assessment study design. A McNemar’s test was used to identify differences between pre- and post-assessment responses. Effect size was calculated using Cohen’s d test by determining the strength of the association between the activity and the outcomes (d < .20 is modest and d ≥ .80 is large). P values were calculated and those < .05 were considered statistically significant. The activity launched 5/14/2020 and data are represented through 8/6/2020. Results: A total of 1,033 learners, of which there are 656 physicians, participated in the activity. Participating in education resulted in statistically significant improvements and noticeable educational effect and data for oncologists that answered all pre- and post-assessment questions are represented below (n = 45, p < .001, Cohen’s d = .454). Percentages represent relative rates of improvement The role of ROS on cancer cell proliferation, cancer cell toxicity, and the tumor microenvironment (67%, p < .05) The interplay of antioxidants to aid in the development of therapies to induce DNA-damaged cell death (100%; p < .001) The potential biomarkers to aid in the development of therapies to induce DNA-damaged cell death (34%; p < .05). Conclusions: This online, interactive, expert-led, CME-certified educational activity resulted in significant gains in oncologist knowledge and confidence regarding the ROS pathway and associated clinical pipeline developments Upon completion of the initiative, only 11% of oncologists were able to answer all 3 matched pre/post questions correctly, signifying the need for further education The novelty of the information to many learners demonstrate the need to continue highlighting clinical advances and molecular pathways that may have potential implications in cancer therapy progress.
Trichosanthin-induced autophagy in gastric cancer cell MKN-45 is dependent on reactive oxygen species (ROS) and NF-κB/p53 pathway
