Increased Risk for CRC in Diabetic Patients with the Nonrisk Allele of SNPs at 8q24
Background Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated. Methods A multi-institutional collaborative study with 1511 CRC patie...
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Published in | Annals of surgical oncology Vol. 19; no. 9; pp. 2853 - 2858 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Springer-Verlag
01.09.2012
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
ISSN | 1068-9265 1534-4681 1534-4681 |
DOI | 10.1245/s10434-012-2278-6 |
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Abstract | Background
Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated.
Methods
A multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures.
Results
Variants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06–1.27,
P
= 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM.
Conclusions
We confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present. |
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AbstractList | Background: Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated. Methods: A multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures. Results: Variants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06-1.27, P = 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM. Conclusions: We confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present. Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated. A multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures. Variants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06-1.27, P = 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM. We confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present.[PUBLICATION ABSTRACT] Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated. A multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures. Variants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06-1.27, P = 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM. We confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present. Background Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated. Methods A multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures. Results Variants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06–1.27, P = 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM. Conclusions We confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present. Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated.BACKGROUNDColorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors that influence CRC morbidity have yet to be fully investigated.A multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures.METHODSA multi-institutional collaborative study with 1511 CRC patients and 2098 control subjects was used to compare the odds ratios for the occurrence of polymorphisms at 11 known single nucleotide polymorphisms (SNPs). TaqMan PCR and questionnaires were used to evaluate the effects of environmental exposures.Variants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06-1.27, P = 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM.RESULTSVariants of rs6983267 on 8q24 were the most significant markers of risk for CRC (odds ratio 1.16, 95% confidence interval 1.06-1.27, P = 0.0015). Non-insulin-dependent diabetes mellitus (DM), a higher body mass index at age 20, and meat consumption were environmental risk factors, whereas a tuna-rich diet and vitamin intake were protective factors. The cohort of rs6983267 SNP major (T) allele at 8q24 and DM had a 1.66-fold higher risk ratio than the cohort of major allele patients without DM.We confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present.CONCLUSIONSWe confirmed that interactions between the genetic background and environmental factors are associated with increased risk for CRC. There is a robust risk of the minor G allele at the 8q24 rs6983267 SNP; however, a major T allele SNP could more clearly reveal a correlation with CRC specifically when DM is present. |
Author | Toh, Hiroyuki Mori, Masaki Yamamoto, Ken Maeda, Toyoki Kusunoki, Masato Kudo, Shin-ei Mimori, Koshi Miyano, Satoru Yamada, Kazutaka Imoto, Seiya Ishii, Hideshi Sato, Tetsuya Yamaguchi, Rui Shimada, Yasuhiro Hase, Kazuo Barnard, Graham F. Inoue, Hiroshi Kawano, Shuichi Watanabe, Masahiko Suzuki, Sadao Sugihara, Ken-ichi Moriya, Yoshihiro Ishimaru, Shinya Tanaka, Jun-ichi Mochizuki, Hidetaka Tokudome, Shinkan Iinuma, Hisae |
Author_xml | – sequence: 1 givenname: Shinya surname: Ishimaru fullname: Ishimaru, Shinya organization: Department of Surgery, Kyushu University Beppu Hospital, Department of Surgery, Tokyo Medical and Dental University – sequence: 2 givenname: Koshi surname: Mimori fullname: Mimori, Koshi organization: Department of Surgery, Kyushu University Beppu Hospital – sequence: 3 givenname: Ken surname: Yamamoto fullname: Yamamoto, Ken organization: Department of Molecular and Cellular Biology, Kyushu University – sequence: 4 givenname: Hiroshi surname: Inoue fullname: Inoue, Hiroshi organization: Department of Surgery, Kyushu University Beppu Hospital – sequence: 5 givenname: Seiya surname: Imoto fullname: Imoto, Seiya organization: Laboratory of DNA Information Analysis, Human Genome Center Institute of Medical Science, University of Tokyo – sequence: 6 givenname: Shuichi surname: Kawano fullname: Kawano, Shuichi organization: Laboratory of DNA Information Analysis, Human Genome Center Institute of Medical Science, University of Tokyo – sequence: 7 givenname: Rui surname: Yamaguchi fullname: Yamaguchi, Rui organization: Laboratory of DNA Information Analysis, Human Genome Center Institute of Medical Science, University of Tokyo – sequence: 8 givenname: Tetsuya surname: Sato fullname: Sato, Tetsuya organization: Division of Molecular Design, Kyushu University – sequence: 9 givenname: Hiroyuki surname: Toh fullname: Toh, Hiroyuki organization: Division of Molecular Design, Kyushu University – sequence: 10 givenname: Hisae surname: Iinuma fullname: Iinuma, Hisae organization: Department of Surgery, Teikyo University – sequence: 11 givenname: Toyoki surname: Maeda fullname: Maeda, Toyoki organization: Department of Surgery, Kyushu University Beppu Hospital – sequence: 12 givenname: Hideshi surname: Ishii fullname: Ishii, Hideshi organization: Department of Surgery, Kyushu University Beppu Hospital – sequence: 13 givenname: Sadao surname: Suzuki fullname: Suzuki, Sadao organization: Department of the Public Health, Nagoya City University – sequence: 14 givenname: Shinkan surname: Tokudome fullname: Tokudome, Shinkan organization: Department of the Public Health, Nagoya City University – sequence: 15 givenname: Masahiko surname: Watanabe fullname: Watanabe, Masahiko organization: Department of Surgery, Kitazato University – sequence: 16 givenname: Jun-ichi surname: Tanaka fullname: Tanaka, Jun-ichi organization: Digestive Disease Center, Northern Yokohama Hospital, Showa University – sequence: 17 givenname: Shin-ei surname: Kudo fullname: Kudo, Shin-ei organization: Digestive Disease Center, Northern Yokohama Hospital, Showa University – sequence: 18 givenname: Ken-ichi surname: Sugihara fullname: Sugihara, Ken-ichi organization: Department of Surgery, Tokyo Medical and Dental University – sequence: 19 givenname: Kazuo surname: Hase fullname: Hase, Kazuo organization: Department of Surgery, National Defense University – sequence: 20 givenname: Hidetaka surname: Mochizuki fullname: Mochizuki, Hidetaka organization: Department of Surgery, National Defense University – sequence: 21 givenname: Masato surname: Kusunoki fullname: Kusunoki, Masato organization: Department of Surgery, Mie University – sequence: 22 givenname: Kazutaka surname: Yamada fullname: Yamada, Kazutaka organization: Department of Surgery, Takano Hospital – sequence: 23 givenname: Yasuhiro surname: Shimada fullname: Shimada, Yasuhiro organization: Department of Surgery and Digestive Tract Medicine, National Cancer Center – sequence: 24 givenname: Yoshihiro surname: Moriya fullname: Moriya, Yoshihiro organization: Department of Surgery and Digestive Tract Medicine, National Cancer Center – sequence: 25 givenname: Graham F. surname: Barnard fullname: Barnard, Graham F. organization: Department of Medicine, University of Massachusetts Medical School – sequence: 26 givenname: Satoru surname: Miyano fullname: Miyano, Satoru organization: Laboratory of DNA Information Analysis, Human Genome Center Institute of Medical Science, University of Tokyo – sequence: 27 givenname: Masaki surname: Mori fullname: Mori, Masaki email: mmori@gesurg.med.osaka-u.ac.jp organization: Department of Gastroenterological Surgery, Osaka University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22434246$$D View this record in MEDLINE/PubMed |
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Keywords | Nonrisk Allele Vitamin Intake Environmental Risk Factor Unconditional Logistic Regression Risk Allele |
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Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting... Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting factors... Background: Colorectal cancer (CRC) oncogenesis was considered to be determined by interactions between genetic and environmental factors. Specific interacting... |
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SubjectTerms | Age Factors Alleles Animals Body Mass Index Case-Control Studies Chromosomes, Human, Pair 8 Colorectal Neoplasms - epidemiology Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Confidence Intervals Diabetes Complications - epidemiology Female Genetic Predisposition to Disease - epidemiology Humans Logistic Models Male Meat - adverse effects Medicine Medicine & Public Health Odds Ratio Oncology Polymorphism, Single Nucleotide Risk Factors Surgery Surgical Oncology Surveys and Questionnaires Translational Research and Biomarkers Tuna Vitamins |
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Title | Increased Risk for CRC in Diabetic Patients with the Nonrisk Allele of SNPs at 8q24 |
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