Sun-Seog Kweon

Youjin Hong, Soseul Sung, Woojin Lim, Sungji Moon, Kwang-Pil Ko, Jung Eun Lee, Inah Kim, Sun Ha Jee, Sun-Seog Kweon, Min-Ho Shin, Sangmin Park, Seung-Ho Ryu, Sun Young Yang, Jeongseon Kim, Sang-Wook Yi, Sue K. Park. J Cancer Prev 2026;31:20-7. https://doi.org/10.15430/JCP.25.042

Yang JH, et al. Korean Circ J. 2025 Nov;56:e20. https://doi.org/10.4070/kcj.2025.0246

OBJECTIVES:Korea is becoming a multiethnic society, with immigrants comprising nearly 5% of the population. Evidence on cardiovascular disease (CVD) risk among immigrants remains limited.METHODS: We conducted a population-based study of 582 immigrants in Gwangju and 2,328 age-matched and gender-matched native Koreans (2022-2023). Immigrant data were obtained from direct health assessments, while native Korean data were drawn from the Korea National Health and Nutrition Examination Survey. CVD risk was estimated using the Framingham risk score (FRS) and pooled cohort equations (PCE). Logistic regression was employed to compare the odds of elevated risk (10-year CVD risk ≥7.5%), adjusting for socio-demographic and behavioral factors.RESULTS: Immigrants had a higher prevalence of hypertension (37.3 vs. 16.1%), diabetes (11.5 vs. 5.6%), poor self-rated health (69.6 vs. 61.3%), and unmet medical needs (30.9 vs. 8.9%), as well as lower rates of health checkups and cancer screening (all p<0.001), compared to native Koreans. Elevated CVD risk was more frequent in immigrants (FRS, 31.4 vs. 20.8%; PCE, 33.6 vs. 22.8%). The adjusted odds ratios (95% confidence intervals) were 1.47 (1.14 to 1.88) for FRS and 1.49 (1.07 to 2.08) for PCE. Disparities were greatest among women, adults ≥40 years, uninsured people, low-income groups, and migrants from Central Asia, Russia, and Africa.CONCLUSIONS: Immigrants in Korea face substantially higher CVD risk than native Koreans, particularly within socioeconomically vulnerable subgroups. Targeted prevention and policies addressing structural barriers are urgently needed.

OBJECTIVES: Dietary factors play an important role in modifying cancer risk. This study aimed to assess the proportion of cancer incidence and mortality in Korea attributable to dietary factors from 2015 to 2030.METHODS: We estimated the population-attributable fraction (PAF) of cancer incidence and mortality using dietary intake levels, exposure rates, and relative risks (RRs). Intake and exposure rates were derived from the Korean National Health and Nutrition Examination Survey, assuming a 15-year latency. RRs were obtained from meta-analyses of Korean cohort and case- control studies.RESULTS: In 2020, 6.08% of cancer cases and 5.70% of deaths in Korea were attributable to dietary factors. High salted vegetable intake (2.12% for incidence and 1.78% for deaths) and low intake of non-starchy vegetables and fruits (1.92 and 2.34%, respectively) were major contributors. However, high intakes of red meat and processed meat showed low PAFs, each less than 1%. The projected PAF for cancer attributable to high salted vegetable intake is expected to decrease substantially to 1.17% in 2030. In contrast, the PAF linked to low intake of non-starchy vegetables and fruits is projected to remain relatively stable.CONCLUSIONS: Our findings provide evidence that dietary factors make a substantial contribution to cancer incidence and mortality in Korea. This study highlights that reducing salted vegetable intake and encouraging a diet rich in non-starchy vegetables and fruits may support cancer prevention efforts. Continuous monitoring of dietary trends remains crucial for reducing the cancer burden.

Background: C-reactive protein (CRP) is a widely used inflammatory biomarker that has been related to colorectal cancer risk. However, observational studies are prone to confounding and reverse causality. Methods: We conducted a two-sample Mendelian randomization using CRP genome-wide association study (GWAS) data from 59,605 Korean individuals and colorectal cancer GWAS data from 23,572 cases and 48,700 controls from an East Asia population. The analysis had 80% power to detect an OR of 1.12 for colorectal cancer risk per twofold increase in CRP levels. Results: Genetically predicted serum CRP levels (per twofold increase) were not significantly associated with colorectal cancer risk (inverse-variance weighted OR, 0.995; 95% confidence interval, 0.893–1.109; P value, 0.929). Null findings remained consistent in sensitivity analyses excluding the horizontally pleiotropic effect. Conclusions: Despite sufficient statistical power, little evidence supported a causal association between CRP and colorectal cancer risk in East Asians. Impact: Our findings suggest that CRP is unlikely to be a key determinant of colorectal carcinogenesis, aligning with prior studies in European populations.

Background: Lung adenocarcinoma in never-smokers is a major public health burden, especially among East Asian women. Polygenic risk scores (PRSs) are promising for risk stratification but are primarily developed in European-ancestry populations. We aimed to develop and validate single- and multi-ancestry PRSs for East Asian never-smokers to improve lung adenocarcinoma risk prediction. Methods: PRSs were developed using genome-wide association study summary statistics from East Asian (8002 cases; 20 782 controls) and European (2058 cases; 5575 controls) populations. Single-ancestry models included a PRS with 25 single nucleotide variants (PRS-25), PRS clumping and thresholding (CT), and LDpred2; multi-ancestry models included LDpred2 plus European PRS-128, PRS-CSx, and clumping and thresholding, super learning, empirical Bayes (CT-SLEB). Performance was evaluated in independent East Asian data from the Female Lung Cancer Consortium and externally validated in the Nanjing Lung Cancer Cohort. We assessed predictive accuracy via area under the curve operating procedure (AUC), with 10-year and (ages 30-80 years) absolute risks estimates. Results: The best multi-ancestry PRS, using East Asian and European data via CT-SLEB, outperformed the best East Asian-only (LDpred2; AUC = 0.629, 95% confidence interval [CI] = 0.618 to 0.641), achieving an AUC of 0.640 (95% CI = 0.629 to 0.653) and odds ratio of 1.71 (95% CI = 1.61 to 1.82) per standard deviation increase. Nanjing Lung Cancer Cohort validation confirmed robust performance (AUC = 0.649, 95% CI = 0.623 to 0.676). The top 20% PRS group had a 3.92-fold higher lung adenocarcinoma risk than the bottom 20%. Further, the top 5% PRS group reached a 6.69% lifetime absolute risk. Notably, this group reached the average population 10-year lung adenocarcinoma risk at age 50 years (0.42%) by age 41 years, 9 years earlier. Conclusions: Multi-ancestry PRS approaches enhance lung adenocarcinoma risk stratification in East Asian never-smokers, with consistent external validation, suggesting future clinical utility.

Genome-wide association studies (GWAS) and subsequent functional interpretation have been used to identify susceptible genes and potential drug-repositioning candidates. This study aimed to identify genes associated with colorectal cancer (CRC) and potential drug-repositioning candidates. Patients with CRC at Seoul National University Hospital (SNUH, discovery study) and Chonnam National University Hospital (CNUH, replication study) were included as case groups. The Korean Genome and Epidemiology Study (KoGES) participants were included as a control group. Single-nucleotide polymorphisms (SNPs) were extracted from blood-derived DNA (N = 409,063). A SNP-based logistic regression model was applied. Furthermore, post-GWAS analysis was conducted. Drug-repositioning candidates were identified using a pre-trained deep neural network and the druggability assessment tool. In the discovery study, we conducted a 1:3 age- and sex-matched case–control study that included 500 CRC cases (mean age 63.0 ± 7.15 years) and 1,500 healthy controls (mean age 62.9 ± 7.07 years), each group comprising 50% males and 50% females. The replication study enrolled 4,860 patients with CRC and 46,384 healthy controls. The two-stage GWAS revealed statistically significant associations among MKLN1 (rs75170436, 7q32.3, beta (log odds ratio) = − 0.90, Pmeta = 5.90 × 10–13), MMP14 (rs3751489, 14q11.2, beta (log odds ratio) = − 1.91, Pmeta = 2.31 × 10–12). Post-GWAS functional analysis revealed strong associations on two genes highlighting deleterious effects and increased gene expression. Drug-repositioning analysis identified GW0742 (PPARβ/δ agonist) with the highest binding score and druggability score for MMP14 with a reference allele (12.06, 0.85). Using GWAS, MKLN1 and MMP14 were found to be associated with CRC development and we identified GW0742 (PPARβ/δ agonist) as a potential drug-repositioning candidate for CRC based on MKLN1 and MMP14. These findings improve the understanding of CRC development and provide insights into novel therapeutic targets and candidates for CRC treatment.

Supplementary Table 4 shows the genome-wide significant variants related to (a) allergic diseases (asthma, hay fever, or eczema), (b) early-onset asthma, (c) later-onset asthma, (d) atopic asthma, and (e) hay fever or eczema and their association with other traits in previous genome-wide association studies.

Supplementary Table 2 shows the genetic variant overlap (same variants or variants in LD R2>0.001 between exposures) for the three exposures tested in our Mendelian randomization analyses (i.e., genetic liability to allergic diseases and their overlap with variants associated with asthma-related phenotypes and hay fever/allergic rhinitis or eczema).

Supplementary Table 7 shows the Mendelian randomization estimates for the potential causal effect of genetic liability to allergic diseases and asthma on colorectal cancer risk; leave one genetic variant out sensitivity analyses.