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Pancreatic Neoplasms: HELP
Articles by Mitsuru Mori
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, Mitsuru Mori wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review An overview of genetic polymorphisms and pancreatic cancer risk in molecular epidemiologic studies. 2011

Lin, Yingsong / Yagyu, Kiyoko / Egawa, Naoto / Ueno, Makoto / Mori, Mitsuru / Nakao, Haruhisa / Ishii, Hiroshi / Nakamura, Kozue / Wakai, Kenji / Hosono, Satoyo / Tamakoshi, Akiko / Kikuchi, Shogo. ·Department of Public Health, Aichi Medical University School of Medicine, Nagakute, Japan. ·J Epidemiol · Pubmed #21071884.

ABSTRACT: BACKGROUND: Although pancreatic cancer has been extensively studied, few risk factors have been identified, and no validated biomarkers or screening tools exist for early detection in asymptomatic individuals. We present a broad overview of molecular epidemiologic studies that have addressed the relationship between pancreatic cancer risk and genetic polymorphisms in several candidate genes and suggest avenues for future research. METHODS: A comprehensive literature search was performed using the PubMed database. RESULTS: Overall, individual polymorphisms did not seem to confer great susceptibility to pancreatic cancer; however, interactions of polymorphisms in carcinogen-metabolizing genes, DNA repair genes, and folate-metabolizing genes with smoking, diet, and obesity were shown in some studies. The major problem with these studies is that, due to small sample sizes, they lack sufficient statistical power to explore gene-gene or gene-environment interactions. Another important challenge is that the measurement of environmental influence needs to be improved to better define gene-environment interaction. It is noteworthy that 2 recent genome-wide association studies of pancreatic cancer have reported that variants in ABO blood type and in 3 other chromosomal regions are associated with risk for this cancer, thus providing new insight into pancreatic cancer etiology. CONCLUSIONS: As is the case in other complex diseases, common, low-risk variants in different genes may act collectively to confer susceptibility to pancreatic cancer in individuals with repeated environmental exposures, such as smoking and red meat intake. Clarification of gene-gene and gene-environmental interaction is therefore indispensable for future studies. To address these issues, a rigorously designed molecular epidemiologic study with a large sample is desirable.

2 Article Prediction model for pancreatic cancer risk in the general Japanese population. 2018

Nakatochi, Masahiro / Lin, Yingsong / Ito, Hidemi / Hara, Kazuo / Kinoshita, Fumie / Kobayashi, Yumiko / Ishii, Hiroshi / Ozaka, Masato / Sasaki, Takashi / Sasahira, Naoki / Morimoto, Manabu / Kobayashi, Satoshi / Ueno, Makoto / Ohkawa, Shinichi / Egawa, Naoto / Kuruma, Sawako / Mori, Mitsuru / Nakao, Haruhisa / Wang, Chaochen / Nishiyama, Takeshi / Kawaguchi, Takahisa / Takahashi, Meiko / Matsuda, Fumihiko / Kikuchi, Shogo / Matsuo, Keitaro. ·Division of Data Science, Data Coordinating Center, Department of Advanced Medicine, Nagoya University Hospital, Nagoya, Japan. · Department of Public Health, Aichi Medical University School of Medicine, Nagakute, Japan. · Division of Cancer Information and Control, Aichi Cancer Center Research Institute, Nagoya, Japan. · Department of Gastroenterology, Aichi Cancer Center Hospital, Nagoya, Japan. · Clinical Research Center, National Hospital Organization Shikoku Cancer Center, Matsuyama, Japan. · Department of Hepato-biliary-pancreatic Medicine, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan. · Hepatobiliary and Pancreatic Medical Oncology Division, Kanagawa Cancer Center Hospital, Kanagawa, Japan. · Tokyo Metropolitan Hiroo Hospital, Tokyo, Japan. · Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo, Japan. · Hokkaido Chitose College of Rehabilitation, Hokkaido, Japan. · Division of Hepatology and Pancreatology, Aichi Medical University School of Medicine, Nagakute, Japan. · Department of Public Health, Nagoya City University Graduate School of Medicine, Nagoya, Japan. · Center for Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan. · Division of Cancer Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya, Japan. ·PLoS One · Pubmed #30192808.

ABSTRACT: Genome-wide association studies (GWASs) have identified many single nucleotide polymorphisms (SNPs) that are significantly associated with pancreatic cancer susceptibility. We sought to replicate the associations of 61 GWAS-identified SNPs at 42 loci with pancreatic cancer in Japanese and to develop a risk model for the identification of individuals at high risk for pancreatic cancer development in the general Japanese population. The model was based on data including directly determined or imputed SNP genotypes for 664 pancreatic cancer case and 664 age- and sex-matched control subjects. Stepwise logistic regression uncovered five GWAS-identified SNPs at five loci that also showed significant associations in our case-control cohort. These five SNPs were included in the risk model and also applied to calculation of the polygenic risk score (PRS). The area under the curve determined with the leave-one-out cross-validation method was 0.63 (95% confidence interval, 0.60-0.66) or 0.61 (0.58-0.64) for versions of the model that did or did not include cigarette smoking and family history of pancreatic cancer in addition to the five SNPs, respectively. Individuals in the lowest and highest quintiles for the PRS had odds ratios of 0.62 (0.42-0.91) and 1.98 (1.42-2.76), respectively, for pancreatic cancer development compared with those in the middle quintile. We have thus developed a risk model for pancreatic cancer that showed moderately good discriminatory ability with regard to differentiation of pancreatic cancer patients from control individuals. Our findings suggest the potential utility of a risk model that incorporates replicated GWAS-identified SNPs and established demographic or environmental factors for the identification of individuals at increased risk for pancreatic cancer development.

3 Article Associations between polymorphisms in folate-metabolizing genes and pancreatic cancer risk in Japanese subjects. 2016

Nakao, Haruhisa / Wakai, Kenji / Ishii, Norimitsu / Kobayashi, Yuji / Ito, Kiyoaki / Yoneda, Masashi / Mori, Mitsuru / Nojima, Masanori / Kimura, Yasutoshi / Endo, Takao / Matsuyama, Masato / Ishii, Hiroshi / Ueno, Makoto / Kuruma, Sawako / Egawa, Naoto / Matsuo, Keitaro / Hosono, Satoyo / Ohkawa, Shinichi / Nakamura, Kozue / Tamakoshi, Akiko / Takahashi, Mami / Shimada, Kazuaki / Nishiyama, Takeshi / Kikuchi, Shogo / Lin, Yingsong. ·Division of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, 480-1195, Japan. · Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan. · Department of Public Health, Sapporo Medical University School of Medicine, Sapporo, 060-0061, Japan. · Department of Surgery, Surgical Oncology and Science, Sapporo Medical University, Sapporo, 060-8543, Japan. · Sapporo Shirakaba-dai Hospital, Sapporo, 062-0052, Japan. · Hepatobiliary and Pancreatic Section, Gastroenterological Division, Cancer Institute Hospital, Tokyo, 135-8550, Japan. · Clinical Research Center, National Hospital Organization Shikoku Cancer Center, Matsuyama, 791-0280, Japan. · Hepatobiliary and Pancreatic Medical Oncology Division, Kanagawa Cancer Center Hospital, Kanagawa, 241-8515, Japan. · Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo, 113-8677, Japan. · Tokyo Metropolitan Otsuka Hospital, Tokyo, 170-8476, Japan. · Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya, 762-6111, Japan. · Department of Epidemiology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan. · Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya, 762-6111, Japan. · Department of Food and Nutrition, Gifu City Women's College, Gifu, 501-2592, Japan. · Department of Public Health, Hokkaido University Graduate School of Medicine, Sapporo, 060-8638, Japan. · Central Animal Division, National Cancer Center Research Institute, Tokyo, 104-0045, Japan. · Department of Hepatobiliary and Pancreatic Surgery, National Cancer Center Hospital, Tokyo, 104-0045, Japan. · Department of Public Health, Aichi Medical University School of Medicine, Nagakute, 480-1195, Japan. · Department of Public Health, Aichi Medical University School of Medicine, Nagakute, 480-1195, Japan. linys@aichi-med-u.ac.jp. ·BMC Gastroenterol · Pubmed #27473058.

ABSTRACT: BACKGROUND: Evidence supporting the associations between folate metabolizing gene polymorphisms and pancreatic cancer has been inconclusive. We examined their associations in a case-control study of Japanese subjects. METHODS: Our case-control study involved 360 newly diagnosed pancreatic cancer cases and 400 frequency-matched, non-cancer control subjects. We genotyped four folate metabolizing gene polymorphisms, including two polymorphisms (rs1801133 and rs1801131) in the methylenetetrahydrofolate (MTHFR) gene, one polymorphism (rs1801394) in the 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene and one polymorphism (rs1805087) in the 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR) gene. Genotyping was performed using Fluidigm SNPtype assays. Unconditional logistic regression methods were used to estimate odds ratios (ORs) and 95 % confidence intervals (CIs) for the associations between folate metabolizing gene variants and pancreatic cancer risk. RESULTS: Overall we did not observe a significant association between these four genotypes and pancreatic cancer risk. For rs1801133, compared with individuals with the CC genotype of MTHFR C677T, the OR for those with the CT genotype and TT genotype was 0.87 (0.62-1.22) and 0.99 (0.65-1.51), respectively. For rs1801131, individuals with the CC genotype had approximately 1.2-fold increased risk compared with those with the AA genotype, but the association was not statistically significant. In analyses stratified by smoking and drinking status, no significant associations were noted for C677T genotypes. No significant interactions were observed with smoking and drinking with respect to pancreatic cancer risk. CONCLUSIONS: Our data did not support the hypothesis that MTHFR polymorphisms or other polymorphisms in the folate metabolizing pathway are associated with pancreatic cancer risk.

4 Article Genome-wide association study-identified SNPs (rs3790844, rs3790843) in the NR5A2 gene and risk of pancreatic cancer in Japanese. 2015

Ueno, Makoto / Ohkawa, Shinichi / Morimoto, Manabu / Ishii, Hiroshi / Matsuyama, Masato / Kuruma, Sawako / Egawa, Naoto / Nakao, Haruhisa / Mori, Mitsuru / Matsuo, Keitaro / Hosono, Satoyo / Nojima, Masanori / Wakai, Kenji / Nakamura, Kozue / Tamakoshi, Akiko / Takahashi, Mami / Shimada, Kazuaki / Nishiyama, Takeshi / Kikuchi, Shogo / Lin, Yingsong. ·Hepatobiliary and Pancreatic Medical Oncology Division, Kanagawa Cancer Center Hospital, Kanagawa 241-8515, Japan. · Hepatobiliary and Pancreatic Section, Gastroenterological Division, Cancer Institute Hospital, Tokyo 135-8550, Japan. · Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo 113-8677, Japan. · Tokyo Metropolitan Ohtsuka Hospital, Tokyo 170-8476, Japan. · Division of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan. · Department of Public Health, Sapporo Medical University School of Medicine, Sapporo 060-0061, Japan. · Division of Molecular Medicine, Aichi Cancer Center Research Insitute, Nagoya 762-6111, Japan. · Department of Epidemiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan. · Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya 762-6111, Japan. · Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan. · Department of Food and Nutrition, Gifu City Women's College, Gifu 501-2592, Japan. · Department of Public Health, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan. · Central Animal Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan. · Department of Hepatobiliary and Pancreatic Surgery, National Cancer Center Hospital, Tokyo 104-0045, Japan. · Department of Public Health, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan. ·Sci Rep · Pubmed #26592175.

ABSTRACT: We genotyped 2 SNPs (rs3790844 T/C and rs3790843 G/A) in the NR5A2 gene that were identified in a genome-wide association study (GWAS) of pancreatic cancer in populations of mainly European ancestry, and we examined their associations with pancreatic cancer risk in a case-control study of 360 patients and 400 control subjects in Japan. Unconditional logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). The SNPs were in linkage disequilibrium (r(2) = 0.80). For rs3790843, the multivariable-adjusted OR was 0.75 (95% CI: 0.41-1.36) and 0.60 (95%CI: 0.33-1.08) for subjects with the AG and AA genotype, respectively, compared to subjects with the GG genotype. The per allele OR was 0.78 (0.62-0.99) (P = 0.046). For rs3790844, the multivariable-adjusted OR was 0.65 (95% CI: 0.37-1.14) and 0.47 (95%CI: 0.27-0.83) for subjects with the CT and CC genotype, respectively, compared to subjects with the TT genotype. The per allele OR was 0.70 (0.56-0.89) (P = 0.003). Our case-control study found that rs3790843 and rs3790844 in the NR5A2 gene are associated with pancreatic cancer risk in Japanese subjects. The direction of association is consistent with the prior findings from GWASs.

5 Article Case-control study of diabetes-related genetic variants and pancreatic cancer risk in Japan. 2014

Kuruma, Sawako / Egawa, Naoto / Kurata, Masanao / Honda, Goro / Kamisawa, Terumi / Ueda, Junko / Ishii, Hiroshi / Ueno, Makoto / Nakao, Haruhisa / Mori, Mitsuru / Matsuo, Keitaro / Hosono, Satoyo / Ohkawa, Shinichi / Wakai, Kenji / Nakamura, Kozue / Tamakoshi, Akiko / Nojima, Masanori / Takahashi, Mami / Shimada, Kazuaki / Nishiyama, Takeshi / Kikuchi, Shogo / Lin, Yingsong. ·Sawako Kuruma, Terumi Kamisawa, Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo 113-8677, Japan. ·World J Gastroenterol · Pubmed #25516658.

ABSTRACT: AIM: To examine whether diabetes-related genetic variants are associated with pancreatic cancer risk. METHODS: We genotyped 7 single-nucleotide polymorphisms (SNPs) in PPARG2 (rs1801282), ADIPOQ (rs1501299), ADRB3 (rs4994), KCNQ1 (rs2237895), KCNJ11 (rs5219), TCF7L2 (rs7903146), and CDKAL1 (rs2206734), and examined their associations with pancreatic cancer risk in a multi-institute case-control study including 360 cases and 400 controls in Japan. A self-administered questionnaire was used to collect detailed information on lifestyle factors. Genotyping was performed using Fluidigm SNPtype assays. Unconditional logistic regression methods were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between these diabetes-associated variants and pancreatic cancer risk. RESULTS: With the exception of rs1501299 in the ADIPOQ gene (P = 0.09), no apparent differences in genotype frequencies were observed between cases and controls. Rs1501299 in the ADPIOQ gene was positively associated with pancreatic cancer risk; compared with individuals with the AA genotype, the age- and sex-adjusted OR was 1.79 (95%CI: 0.98-3.25) among those with the AC genotype and 1.86 (95%CI: 1.03-3.38) among those with the CC genotype. The ORs remained similar after additional adjustment for body mass index and cigarette smoking. In contrast, rs2237895 in the KCNQ1 gene was inversely related to pancreatic cancer risk, with a multivariable-adjusted OR of 0.62 (0.37-1.04) among individuals with the CC genotype compared with the AA genotype. No significant associations were noted for other 5 SNPs. CONCLUSION: Our case-control study indicates that rs1501299 in the ADIPOQ gene may be associated with pancreatic cancer risk. These findings should be replicated in additional studies.

6 Article Lack of associations between genetic polymorphisms in GSTM1, GSTT1 and GSTP1 and pancreatic cancer risk: a multi-institutional case-control study in Japan. 2014

Yamada, Ikuhiro / Matsuyama, Masato / Ozaka, Masato / Inoue, Dai / Muramatsu, Yusuke / Ishii, Hiroshi / Junko, Ueda / Ueno, Makoto / Egawa, Naoto / Nakao, Haruhisa / Mori, Mitsuru / Matsuo, Keitaro / Nishiyama, Takeshi / Ohkawa, Shinichi / Hosono, Satoyo / Wakai, Kenji / Nakamura, Kozue / Tamakoshi, Akiko / Kuruma, Sawako / Nojima, Masanori / Takahashi, Mami / Shimada, Kazuaki / Yagyu, Kiyoko / Kikuchi, Shogo / Lin, Yingsong. ·Hepatobiliary and Pancreatic Section, Gastroenterological Division, Cancer Institute Hospital, Tokyo, Japan E-mail : linys@aichi-med-u.ac.jp. ·Asian Pac J Cancer Prev · Pubmed #24528063.

ABSTRACT: BACKGROUND: We aimed to evaluate the role of genetic polymorphisms in tobacco carcinogen-metabolizing genes and their interactions with smoking in a hospital-based case-control study of Japanese subjects. MATERIALS AND METHODS: We examine the associations of pancreatic cancer risk with genetic polymorphisms in GSTM1, GSTT1 and GSTP1, phase II enzymes that catalyze the conjugation of toxic and carcinogenic electrophilic molecules. The study population consisted of 360 patients and 400 control subjects, who were recruited from several medical facilities in Japan. Unconditional logistic regression methods were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between genotypes and pancreatic cancer risk. RESULTS: Among the control subjects, the prevalence of the GSTM1-null genotype and the GSTT1-null genotype was approximately 56% and 48%, respectively. Cases and controls were comparable in terms of GSTM1 and GSTT1 genotype distributions. Neither of the deleted polymorphisms in GSTM1 and GSTT1 was associated with the risk of pancreatic cancer, with an age- and sex-adjusted OR of 0.99 (95%CI: 0.74-1.32) for the GSTM1-null genotype, and 0.98 (95%CI: 0.73-1.31) for the GSTT1-null genotype. The OR was 0.97 (95%CI: 0.64-1.47) for individuals with the GSTM1 and GSTT1-null genotypes compared with those with the GSTM1 and GSTT1- present genotypes. No synergistic effects of smoking or GST genotypes were observed. CONCLUSIONS: Our results indicate no overall association between the GSTM1 and GSTT1 deletion polymorphisms and pancreatic cancer risk in the Japanese subjects in our study.

7 Article Association between variations in the fat mass and obesity-associated gene and pancreatic cancer risk: a case-control study in Japan. 2013

Lin, Yingsong / Ueda, Junko / Yagyu, Kiyoko / Ishii, Hiroshi / Ueno, Makoto / Egawa, Naoto / Nakao, Haruhisa / Mori, Mitsuru / Matsuo, Keitaro / Kikuchi, Shogo. ·Department of Public Health, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan. ·BMC Cancer · Pubmed #23835106.

ABSTRACT: BACKGROUND: It is clear that genetic variations in the fat mass and obesity-associated (FTO) gene affect body mass index and the risk of obesity. Given the mounting evidence showing a positive association between obesity and pancreatic cancer, this study aimed to investigate the relation between variants in the FTO gene, obesity and pancreatic cancer risk. METHODS: We conducted a hospital-based case-control study in Japan to investigate whether genetic variations in the FTO gene were associated with pancreatic cancer risk. We genotyped rs9939609 in the FTO gene of 360 cases and 400 control subjects. An unconditional logistic model was used to estimate the odds ratio (OR) and 95% confidence interval (CI) for the association between rs9939609 and pancreatic cancer risk. RESULTS: The minor allele frequency of rs9939609 was 0.18 among control subjects. BMI was not associated with pancreatic cancer risk. Compared with individuals with the common homozygous TT genotype, those with the heterozygous TA genotype and the minor homozygous AA genotype had a 48% (OR=1.48; 95%CI: 1.07-2.04), and 66% increased risk (OR=1.66; 95%CI: 0.70-3.90), respectively, of pancreatic cancer after adjustment for sex, age, body mass index, cigarette smoking and history of diabetes. The per-allele OR was 1.41 (95%CI: 1.07-1.85). There were no significant interactions between TA/AA genotypes and body mass index. CONCLUSIONS: Our findings indicate that rs9939609 in the FTO gene is associated with pancreatic cancer risk in Japanese subjects, possibly through a mechanism that is independent of obesity. Further investigation and replication of our results is required in other independent samples.