This article reports the latest development in e-learning in Korean medical education. The Korean Consortium for e-Learning in Medical Education was formed for collaboration in providing quality online learning resources for medical schools around the nation. This e-learning strategy is aimed at improving the quality of medical education at the national level by providing students with equal access to quality learning resources and fostering students' self-directed learning and, in doing so, enhancing the effectiveness and efficiency of developing online learning resources by sharing necessary resources among the medical schools. The consortium also plans to share e-learning content with medical schools in other countries by engaging more medical schools in the consortium and also by sharing e-learning content developed by other institutions or consortiums. The consortium is also dedicated to the research and development of effective online learning strategies for medical education, including interactive virtual patient cases and other innovative pedagogies using Web 2.0 technologies.

Background To understand the molecular mechanisms involved in regulation of DNA methyltransferases (DNMTs) by metformin in non-small cell lung cancer (NSCLC) cells. Methods Expression levels of DNMTs in response to metformin were analyzed in NSCLC cells. MicroRNAs regulating expression of DNMTs at the post-transcriptional level were searched using miRNA-target databases (miRDB and miRTarBase), TCGA RNASeqV2 lung cancer data, and miRNA-seq. Results Metformin dose-dependently downregulated expression of DNMT1 and DNMT3a at the post-transcriptional level and expression of DNMT3b at the transcriptional level in A549 lung cancer cells. Activity of DNMTs was reduced by about 2.6-fold in A549 cells treated with 10 mM metformin for 72 h. miR-148/-152 family members (miR-148a, miR-148b, and miR-152) targeting the 3′UTR of DNMTs were associated with post-transcriptional regulation of DNMTs by metformin. Metformin upregulated expression of miR-148a, miR-148b, and miR-152 in A549 and H1650 cells. Transfection with an miR-148b plasmid or a mimic suppressed expression of DNMT1 and DNMT3b in A549 cells. Transfection with the miR-148a mimic in A549 and H1650 cells decreased the luciferase activity of DNMT1 3′UTR. A combination of metformin and cisplatin synergistically increased expression levels of miR-148/-152 family members but decreased expression of DNMTs in A549 cells. Low expression of miR-148b was associated with poor overall survival (HR = 2.56, 95% CI 1.09—6.47; P = 0.04) but not with recurrence-free survival. Conclusions The present study suggests that metformin inhibits expression of DNMTs by upregulating miR-148/-152 family members in NSCLC cells.

Purpose: In early-stage, Epidermal growth factor receptor mutation-positive (EGFR-M+) NSCLC, surgery remains the primary treatment, without personalized treatments. We aimed to identify risk factors for recurrence-free survival (RFS) to suggest personalized strategies. Patients and Methods: From January 2008 to August 2020, a total of 1,181 patients with pathological stage (pStage) IB–IIIA, non-squamous NSCLC. To identify clinicopathological risk factors, 1,181 patients with pStage IB–IIIA, common EGFR-M+ NSCLC were analyzed. Comprehensive genomic analysis was conducted in 56 matched case-control cases. Results: Among 1,181 patients, pStage IB, II, and IIIA comprised 48.9%, 28.0%, and 23.1% of subjects, respectively. Median RFS was 73.5 months, 48.7 months, and 22.7 months for each stage, respectively (P < 0.001). In multivariate analysis, pStage, micropapillary subtype, vascular invasion, pleural invasion, and pathological classification by cell of origin were associated with RFS. The non- terminal respiratory unit (non-TRU) of the RNA subtype (HR 3.49, 95%CI 1.72–7.09, P < 0.01) and TP53 mutation (HR 2.50, 95% CI 1.24–5.04, P = 0.01) were associated with poor RFS independent of pStage II or IIIA. After recurrence, patients with APOBEC mutation signature had inferior PFS of EGFR-TKI compared with that of patients without this signature (8.6 vs.·28.8 months, HR 4.16, 95%CI 1.28–13.46, P = 0.02). Conclusions: The low-risk group with TRU subtype and TP53 wild type without clinicopathological risk factors might not need adjuvant EGFR-TKIs. In the high-risk group with non-TRU subtype and/or TP 53 mutation, or clinicopathological risk factors, a novel adjuvant strategy including EGFR TKI and others needs to be investigated.

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