Author
So Yeon Kong
Bio: So Yeon Kong is an academic researcher from International Agency for Research on Cancer. The author has contributed to research in topics: European Prospective Investigation into Cancer and Nutrition & Cancer. The author has an hindex of 7, co-authored 7 publications receiving 306 citations.
Papers
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Emory University1, Charité2, Newcastle University3, Imperial College London4, University of Paris-Sud5, French Institute of Health and Medical Research6, German Cancer Research Center7, Academy of Athens8, National and Kapodistrian University of Athens9, University of Tromsø10, University of Granada11, Umeå University12, University of Oxford13, Prevention Institute14, Aarhus University15
TL;DR: The findings indicate that Se status is suboptimal in many Europeans and suggest an inverse association between CRC risk and higher serum Se status, which is more evident in women.
Abstract: Suboptimal intakes of the micronutrient selenium (Se) are found in many parts of Europe. Low Se status may contribute to colorectal cancer (CRC) development. We assessed Se status by measuring seru ...
155 citations
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Imperial College London1, International Agency for Research on Cancer2, Institut Gustave Roussy3, French Institute of Health and Medical Research4, University of Paris-Sud5, German Cancer Research Center6, Aarhus University7, University of Cambridge8, Medical Research Council9, University of Oxford10, National and Kapodistrian University of Athens11, Academy of Athens12, Harvard University13, University of Naples Federico II14, Utrecht University15, Lund University16, Umeå University17, University of Tromsø18, University of Ioannina19
TL;DR: The results support the idea that individuals with the metabolically healthy/overweight phenotype (with normal insulin levels) are at lower colorectal cancer risk than those with hyperinsulinaemia.
Abstract: The coordination of EPIC is financially
supported by the European Commission (DGSANCO);
and the International Agency for Research
on Cancer. The national cohorts are supported by
Danish Cancer Society (Denmark); Ligue Contre le
Cancer; Institut Gustave Roussy; Mutuelle Generale
de l’Education Nationale; and Institut National de la
Sante et de la Recherche Medicale (INSERM)
(France); Deutsche Krebshilfe, Deutsches
Krebsforschungszentrum; and Federal Ministry of
Education and Research (Germany); Hellenic Health
Foundation; Stavros Niarchos Foundation; and the
Hellenic Ministry of Health and Social Solidarity
(Greece); Italian Association for Research on Cancer
(AIRC); National Research Council; and
Associazione Iblea per la Ricerca Epidemiologica
(AIRE-ONLUS) Ragusa, Associazione Volontari
Italiani Sangu (AVIS) Ragusa, Sicilian Government
(Italy); Dutch Ministry of Public Health, Welfare and
Sports (VWS); Netherlands Cancer Registry (NKR);
LK Research Funds; Dutch Prevention Funds; Dutch
ZON (Zorg Onderzoek Nederland); World Cancer
Research Fund (WCRF); and Statistics Netherlands
(the Netherlands); European Research Council
(ERC) (grant number ERC-2009-AdG 232997) and
Nordforsk; and Nordic Center of Excellence
Programme on Food, Nutrition and Health (Norway);
Health Research Fund (FIS); Regional Governments
of Andalucia, Asturias, Basque Country, Murcia (No.
6236) and Navarra; and the Centro de Investigacion
Biomedica en Red en Epidemiologia y Salud Publica
and Instituto de Salud Carlos II (ISCIII RETIC) (RD06/
0020) (Spain); Swedish Cancer Society; Swedish
Scientific Council; and Regional Government of
Skane and Vasterbotten (Sweden); Cancer Research
UK; Medical Research Council; Stroke Association;
British Heart Foundation; Department of Health; Food
Standards Agency; Wellcome Trust (UK); and
National Cancer Institute (USA) (grant number:
1RO1CA102460) (PI, Professor Rudolf Kaaks). The
funders had no role in study design, data collection
and analysis, decision to publish, or preparation of
the manuscript.
83 citations
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German Cancer Research Center1, Harvard University2, French Institute of Health and Medical Research3, University of Freiburg4, Academy of Athens5, Harokopio University6, University of Cambridge7, University of Oxford8, University of Naples Federico II9, Imperial College London10, Utrecht University11, Lund University12, Umeå University13, Karolinska Institutet14, University of Tromsø15, International Agency for Research on Cancer16
TL;DR: The results of this study do not support LTL as a uniform and strong predictor of pancreatic cancer risk and can provide insights into telomere dynamics and highlight the complex relationship between LTL and Pancreas cancer risk.
Abstract: Background: Several studies have examined leukocyte telomere length (LTL) as a possible predictor for cancer at various organ sites. The hypothesis originally motivating many of these studies was that shorter telomeres would be associated with an increase in cancer risk, the results of epidemiologic studies have been inconsistent, however, and suggested positive, negative, or null associations. Two studies have addressed the association of LTL in relation to pancreatic cancer risk and the results are contrasting. Methods: we measured LTL in a prospective study of 331 pancreatic cancer cases and 331 controls in the context of the European Prospective Investigation into Cancer and Nutrition (EPIC). Results: We observed that the mean LTL was higher in cases (0.59±0.20) than in controls (0.57±0.17), although this difference was not statistically significant (p=0.07), and a basic logistic regression model showed no association of LTL with pancreas cancer risk. When adjusting for levels of HbA1c and C-Peptide, however, there was a weakly positive association between longer LTL and pancreatic cancer risk , OR=1.13 (1.01-1.27). Additional analyses by cubic spline regression suggested a possible non-linear relationship between RTL and pancreatic cancer risk (P=0.022), with a statistically non-significant increase in risk at very low LTL, as well as a significant increase at high LTL. Conclusion: Taken together, the results from our study do not support LTL as a uniform and strong predictor of pancreatic cancer. Impact: The results of this manuscript can provide insights into telomere dynamics and highlight the complex relationship between LTL and pancreatic cancer risk.
38 citations
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Utrecht University1, Imperial College London2, Emory University3, International Agency for Research on Cancer4, Aarhus University5, Institut Gustave Roussy6, German Cancer Research Center7, Academy of Athens8, Harvard University9, University of Naples Federico II10, Karolinska Institutet11, University of Tromsø12, University of Oslo13, Lund University14, Umeå University15, University of Oxford16, University of Cambridge17
TL;DR: The prediagnostic reported intake of dairy products and dietary calcium is not associated with disease-specific or all-cause risk of death in patients diagnosed with colorectal cancer.
Abstract: Background We investigated whether prediagnostic reported intake of dairy products and dietary calcium are associated with colorectal cancer (CRC) survival. Methods Data from 3,859 subjects with CRC (42.1% male, mean age at diagnosis 64.2 ± 8.1 years) in the European Investigation into Cancer and Nutrition (EPIC) cohort were analyzed. Intake of dairy products and dietary calcium was assessed at baseline (1992-2000) using validated, country-specific dietary questionnaires. Multivariable Cox regression models were used to calculate hazard ratios (HR) and corresponding 95% confidence intervals (95%-CI) for CRC specific death (n=1,028) and all-cause death (n=1,525) for different quartiles of intake. Results The consumption of total dairy products was not statistically significantly associated with risk of CRC-specific death (adjusted HR Q4 vs. Q1: 1.17 95%-CI 0.97-1.43) nor of all-cause death (Q4 vs. Q1: 1.16 95%-CI 0.98-1.36). Multivariable adjusted HRs for CRC-specific death (Q4 vs. Q1) were 1.21 (95%-CI 0.99-1.48) for milk, 1.09 (95%-CI 0.88-1.34) for yoghurt and 0.93 (95%-CI 0.76-1.14) for cheese. The intake of dietary calcium was not associated with the risk of CRC-specific (adjusted HR Q4 vs. Q1: 1.01 95%-CI 0.81-1.26) nor of all-cause death (Q4 vs. Q1: 1.01 95%-CI 0.84-1.21). Conclusions The prediagnostic reported intake of dairy products and dietary calcium are not associated with disease-specific or all-cause risk of death in patients diagnosed with CRC. Impact The impact of diet on cancer survival is largely unknown. This study shows that despite it's inverse association with CRC risk, the prediagnostic intake of dairy and dietary calcium do not affect CRC survival.
34 citations
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International Agency for Research on Cancer1, Kanazawa Medical University2, Hiroshima University3, University of Toronto4, Kurume University5, Aarhus University6, Institut Gustave Roussy7, German Cancer Research Center8, National and Kapodistrian University of Athens9, Academy of Athens10, Harvard University11, University of Naples Federico II12, Imperial College London13, Utrecht University14, Umeå University15, Cambridge University Hospitals NHS Foundation Trust16, University of Cambridge17, University of Oxford18, Medical University of Vienna19
TL;DR: A large proportion of colorectal cancers are associated with unhealthy dietary and lifestyle exposures, particularly energy excess, obesity, hyperinsulinemia, and hypergly....
Abstract: Background: A large proportion of colorectal cancers are thought to be associated with unhealthy dietary and lifestyle exposures, particularly energy excess, obesity, hyperinsulinemia, and hypergly ...
31 citations
Cited by
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Mayo Clinic1, National Institutes of Health2, Harvard University3, Science Applications International Corporation4, New York University5, Utrecht University6, University of Toronto7, University of Minnesota8, Mercy Medical Center (Baltimore, Maryland)9, University of California, San Francisco10, American Cancer Society11, Johns Hopkins University12, Fred Hutchinson Cancer Research Center13, University of Texas MD Anderson Cancer Center14, Yale University15, Vanderbilt University16, University of Paris-Sud17, German Cancer Research Center18, Veterans Health Administration19, Umeå University20, Georgetown University21, Memorial Sloan Kettering Cancer Center22, University of Pittsburgh23, Imperial College London24, French Institute of Health and Medical Research25, Academy of Athens26, Kaiser Permanente27, National Institute for Health and Welfare28, University at Buffalo29, Group Health Cooperative30
TL;DR: This study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies and identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.1 that are associated with multiple cancers.
Abstract: We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.
494 citations
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TL;DR: Diet modification has the promise of reducing colorectal cancer incidence and emerging evidence also implicates the gut microbiota as an important effector in the relationship between diet and cancer.
466 citations
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TL;DR: Findings have limitations due to study design, quality and heterogeneity that complicate interpretation of the summary statistics, and some studies suggested that genetic factors may modify the relation between selenium and cancer risk-a hypothesis that deserves further investigation.
Abstract: Background
This review is an update of the first Cochrane publication on selenium for preventing cancer (Dennert 2011).
Selenium is a metalloid with both nutritional and toxicological properties. Higher selenium exposure and selenium supplements have been suggested to protect against several types of cancers.
455 citations