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  • American Association for Cancer Research (AACR)  (42)
  • Park, Sue K.  (42)
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  • 1
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 18 ( 2018-09-15), p. 5419-5430
    Abstract: Large-scale genome-wide association studies (GWAS) have identified approximately 35 loci associated with epithelial ovarian cancer (EOC) risk. The majority of GWAS-identified disease susceptibility variants are located in noncoding regions, and causal genes underlying these associations remain largely unknown. Here, we performed a transcriptome-wide association study to search for novel genetic loci and plausible causal genes at known GWAS loci. We used RNA sequencing data (68 normal ovarian tissue samples from 68 individuals and 6,124 cross-tissue samples from 369 individuals) and high-density genotyping data from European descendants of the Genotype-Tissue Expression (GTEx V6) project to build ovarian and cross-tissue models of genetically regulated expression using elastic net methods. We evaluated 17,121 genes for their cis-predicted gene expression in relation to EOC risk using summary statistics data from GWAS of 97,898 women, including 29,396 EOC cases. With a Bonferroni-corrected significance level of P & lt; 2.2 × 10−6, we identified 35 genes, including FZD4 at 11q14.2 (Z = 5.08, P = 3.83 × 10−7, the cross-tissue model; 1 Mb away from any GWAS-identified EOC risk variant), a potential novel locus for EOC risk. All other 34 significantly associated genes were located within 1 Mb of known GWAS-identified loci, including 23 genes at 6 loci not previously linked to EOC risk. Upon conditioning on nearby known EOC GWAS-identified variants, the associations for 31 genes disappeared and three genes remained (P & lt; 1.47 × 10−3). These data identify one novel locus (FZD4) and 34 genes at 13 known EOC risk loci associated with EOC risk, providing new insights into EOC carcinogenesis. Significance: Transcriptomic analysis of a large cohort confirms earlier GWAS loci and reveals FZD4 as a novel locus associated with EOC risk. Cancer Res; 78(18); 5419–30. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 2
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 28, No. 24 ( 2022-12-15), p. 5383-5395
    Abstract: Advanced-stage mucinous ovarian carcinoma (MOC) has poor chemotherapy response and prognosis and lacks biomarkers to aid stage I adjuvant treatment. Differentiating primary MOC from gastrointestinal (GI) metastases to the ovary is also challenging due to phenotypic similarities. Clinicopathologic and gene-expression data were analyzed to identify prognostic and diagnostic features. Experimental Design: Discovery analyses selected 19 genes with prognostic/diagnostic potential. Validation was performed through the Ovarian Tumor Tissue Analysis consortium and GI cancer biobanks comprising 604 patients with MOC (n = 333), mucinous borderline ovarian tumors (MBOT, n = 151), and upper GI (n = 65) and lower GI tumors (n = 55). Results: Infiltrative pattern of invasion was associated with decreased overall survival (OS) within 2 years from diagnosis, compared with expansile pattern in stage I MOC [hazard ratio (HR), 2.77; 95% confidence interval (CI), 1.04–7.41, P = 0.042]. Increased expression of THBS2 and TAGLN was associated with shorter OS in MOC patients (HR, 1.25; 95% CI, 1.04–1.51, P = 0.016) and (HR, 1.21; 95% CI, 1.01–1.45, P = 0.043), respectively. ERBB2 (HER2) amplification or high mRNA expression was evident in 64 of 243 (26%) of MOCs, but only 8 of 243 (3%) were also infiltrative (4/39, 10%) or stage III/IV (4/31, 13%). Conclusions: An infiltrative growth pattern infers poor prognosis within 2 years from diagnosis and may help select stage I patients for adjuvant therapy. High expression of THBS2 and TAGLN in MOC confers an adverse prognosis and is upregulated in the infiltrative subtype, which warrants further investigation. Anti-HER2 therapy should be investigated in a subset of patients. MOC samples clustered with upper GI, yet markers to differentiate these entities remain elusive, suggesting similar underlying biology and shared treatment strategies.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 3
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    Online Resource
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2163-2163
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2163-2163
    Abstract: BACKGROUND: Incidence of thyroid cancer has been rapidly increased, in not only small sizes with improved detection devices but also large size of tumors whose underlying mechanisms remain unclear. Body size and weight change in adulthood were examined as the potential risk factors for thyroid cancer development. METHODS: A large scale case-control study was conducted with constructed questionnaire for their height, weight (current, 2 years ago, at the age of 20 and 35 years old) and confounders. Medical charts were reviewed for cancer histology, tumor aggressiveness and BRAF mutation status. A total of 2,003 cases (1,611 females and 392 males) and individually matched 17,700 controls (13,983 females and 3,717 males) by age, sex, 12-year education and birth year were included. Logistic regression model were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Having a tall height and heavy weight was associated with increased risk in both females [OR and 95%CI for height and weight: 1.46 (1.25-1.71) and 2.66 (2.24-3.15), respectably] and males [OR and 95%CI for height and weight: 1.71 (1.25-2.34) and 2.80 (2.00-3.92), respectably] compared to those in the lowest quartile for the body sizes. This study observed approximated tripled the risk of thyroid cancer [OR and 95%CI: 3.03 (2.10-4.37)] when female subjects gained 10kg or more within recent 2 years. Males who gained 10 kg or more after 35 years old were more likely to have a greater tumor size [ & lt;1cm vs. ≥1cm: 3.76 (2.62-5.38) vs. 6.87 (4.38-10.77)]. However, other factors were not significantly related to increased tumor aggressiveness (tumor size, lymph node metastasis, and mutlifocality) and BRAF mutation affected carriers. CONCLUSION: The results support plausible hormonal and metabolic factors related height, weight, and rapid weight gain in adulthood increase thyroid carcinogenesis. Citation Format: Yunji Hwang, Kyu-Eun Lee, Young Joo Park, Do Joon Park, Yeo-Kyu Youn, Yohwan Yeo, Seung-Hyun Ma, Daehee Kang, Keun-Young Yoo, Sue K. Park. Height, weight and weight changes during adulthood and thyroid cancer risk. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2163. doi:10.1158/1538-7445.AM2014-2163
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 3 ( 2020-02-01), p. 624-638
    Abstract: Pathogenic sequence variants (PSV) in BRCA1 or BRCA2 (BRCA1/2) are associated with increased risk and severity of prostate cancer. We evaluated whether PSVs in BRCA1/2 were associated with risk of overall prostate cancer or high grade (Gleason 8+) prostate cancer using an international sample of 65 BRCA1 and 171 BRCA2 male PSV carriers with prostate cancer, and 3,388 BRCA1 and 2,880 BRCA2 male PSV carriers without prostate cancer. PSVs in the 3′ region of BRCA2 (c.7914+) were significantly associated with elevated risk of prostate cancer compared with reference bin c.1001-c.7913 [HR = 1.78; 95% confidence interval (CI), 1.25–2.52; P = 0.001], as well as elevated risk of Gleason 8+ prostate cancer (HR = 3.11; 95% CI, 1.63–5.95; P = 0.001). c.756-c.1000 was also associated with elevated prostate cancer risk (HR = 2.83; 95% CI, 1.71–4.68; P = 0.00004) and elevated risk of Gleason 8+ prostate cancer (HR = 4.95; 95% CI, 2.12–11.54; P = 0.0002). No genotype–phenotype associations were detected for PSVs in BRCA1. These results demonstrate that specific BRCA2 PSVs may be associated with elevated risk of developing aggressive prostate cancer. Significance: Aggressive prostate cancer risk in BRCA2 mutation carriers may vary according to the specific BRCA2 mutation inherited by the at-risk individual.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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    detail.hit.zdb_id: 410466-3
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  • 5
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    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-432-LB-432
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-432-LB-432
    Abstract: Background: A model for predicting breast cancer risk has been developed in Korea. Associated risk factors included in the model were 1st degree relatives with breast cancer, age at menarche, menopausal status, number of children, age at first fullterm pregnancy, mammography, and exercise for patients less than 50 years of age and 1st degree relatives with breast cancer, age at menarche, age at menopause, number of children, BMI, mammography, and exercise for patients greater than 50 years of age. The area under the curve among over 50 year olds was 0.655 and 0.611 among under 50 year old. Objectives: The objective of the study was validation of an absolute risk prediction model for breast cancer in Korea by using a large, population cohort and patient registry. Method: The Korean Multi-center Cancer Cohort (KMCC) and registry data of breast cancer patients constructed by the Korean Breast Cancer Society were used to validate the model. 12221 women more than 30 years of age at baseline answered questions about demographic characteristics, reproductive factors, lifestyle, family history since 1993 and we identified 11 and 5 incident breast cancer patient more than 50 and less than 50 years of age, respectively. Age, resident area, and included year were matched to select controls; women aged less than 50 were matched 1:20 while women aged greater than 50 were matched 1:10. In the breast cancer registry, clinical, demographic characteristics and reproductive factors of breast cancer patients were collected since 1980. We selected 2727 patients under 50 years old and 2000 patients over 50 years old matched by age and diagnostic year and calculated their 10, 20, 30, and 40 year absolute risk. Result: In the KMCC data, 10 year absolute risk was 0.39 (95% CI 0.36-0.42) among cases and 0.36 (95% CI 0.35-0.37) among controls under 50 years old and 0.16 (95% CI 0.10-0.22) among cases and 0.08 (0.07-0.09) among controls over 50 years old and it was significantly different in the median test (P-value: 0.02 in both groups). Among breast cancer patient group over 50 years old, 10, 20, 30 and 40 year absolute risk were 0.22 (95% CI 0.21-0.23), 0.35 (95% CI 0.34-0.36), 0.43 (95% CI 0.42-0.45), 0.46 (95% CI 0.44-0.48) respectively and 0.56 (95% CI 0.55-0.57), 1.18 (95% CI 1.15-1.21), 1.53 (95% CI 1.50-1.57), 1.74 (95% CI 1.70-1.78). Conclusion: Due to the short follow up time and small number of cancer incidence in the KMCC cohort, although absolute risk was small, a significant difference was confirmed. Future validation study with a large number and enough follow up cohort time is needed. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-432.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 6
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 21, No. 8 ( 2012-08-01), p. 1371-1380
    Abstract: Background: Matrix metalloproteinase-2 (MMP-2) has been thought of as a predictor of recurrence or metastasis risk or prognostic markers in cancer. We evaluated whether preoperative serum levels of MMP-2 work as a prognostic biomarker in breast cancer prognosis. Methods: Preoperative serum levels of MMP-2 were measured with ELISA in 303 patients with histologically confirmed breast cancer. The median follow-up time for all patients was 4.24 years. The relationship of MMP-2 to survival was investigated using Cox proportional hazard regression model adjusted for the tumor–node–metastasis (TNM) stage and estrogen receptor (ER) status. Results: In the multivariate analysis, disease-free survival (DFS) was worse among patients with the third tertile of MMP-2 level than with the first tertile of MMP-2 level [hazard ratio, 1.80; 95% confidence interval (CI), 1.04–3.11; P = 0.04]. However, when the patients were stratified by age, ER status, histologic grade, and nuclear grade, inverse correlation was shown between serum MMP-2 levels and prognostic factors, and the associations between MMP-2 and DFS were only significant among patients with poor prognostic factors (HR, 2.75; 95% CI, 1.32–5.73 in ER-negative; HR, 2.90; 95% CI, 1.42–5.92 in histologic grade III; and HR, 2.61; 95% CI, 1.26–5.39 in nuclear grade III). Conclusions: Our results suggest that the preoperative serum levels of MMP-2 were associated with the survival in patients with breast cancer in ER-negative, higher histologic grade, or higher nuclear grade breast cancers. Impact: Our results indicate that serum levels of MMP-2 may play a role as prognostic biomarker in breast cancer survival. Cancer Epidemiol Biomarkers Prev; 21(8); 1371–80. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 632-632
    Abstract: Background Epidemiological studies investigating the associations of coffee and tea intake with lung cancer risk have yielded inconsistent results. These previous studies included mostly lung cancer patients diagnosed among smokers. Because coffee and tea consumption are closely related to smoking behavior, these previous studies could suffer from biases due to residual confounding of smoking. To better characterize the relationship, a large study with a large number of lung cancer cases diagnosed among never smokers and detailed information on tea and coffee consumption, is needed. Using data from a large-scale pooled analysis that consists of over 1.2 million participants in the U.S. and Asia, we carried out a comprehensive evaluation on the association of coffee and tea intake with lung cancer risk. Methods Individual-level data from seven prospective cohort studies conducted in the U.S., and ten studies conducted in Asia, were included. Demographic, lifestyle, coffee and tea intake data were collected at the baseline survey for each study. Multivariable-adjusted Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). The first 2 years of follow-up time was excluded to minimize potential influence of reverse causality on study results. Subgroup analyses by smoking status, sex, race, histologic subtype and coffee type (caffeinated or decaffeinated) were also conducted to assess potential effect modification, as well as heterogeneity of the association. Results After a median follow-up of 8.6 years, 20,519 incident lung cancer cases were identified. Both coffee and tea consumption were associated with an increased risk of lung cancer. Comparing non-coffee and non-tea consumption, HRs for lung cancer associated with exclusive coffee drinkers (≥2 cups/day) among current, former and never smokers were 1.30 (95% CI, 1.15-1.47), 1.49 (1.27-1.74) and 1.41 (95% CI, 1.21-1.63), respectively. Similar positive associations were observed for caffeinated and decaffeinated coffee. The HRs associated with exclusive tea drinkers ( & gt;2 cups/day) were 1.16 (95% CI, 1.02-1.32), 1.10 (0.92, 1.32) and 1.37 (95% CI, 1.17-1.60) for current, former and never smokers, respectively. These associations did not differ significantly by sex, race or histologic subtypes. Conclusion A high consumption of coffee or tea was both associated with an increased risk of lung cancer regardless of race or smoking status. Our study included a large number of never-smoker lung cancer patients, which minimized potential confounding effects due to smoking. The positive association observed for both caffeinated and decaffeinated coffee suggests that compounds other than caffeine may play a role in the etiology of lung cancer. Citation Format: Jingjing Zhu, Wei Zheng, Rashimi Sinha, Stephanie A. Smith-Warner, Yong-Bing Xiang, Yikyung Park, Shoichiro Tsugane, Emily White, Woon-Puay Koh, Sue K. Park, Norie Sawada, Seiki Kanemura, Yumi Sugawara, Ichiro Tsuji, Kim Robien, Yasutake Tomata, Keun-Young Yoo, Jeongseon Kim, Jian-Min Yuan, Yu-Tang Gao, Yumie Takata, Eiko Saito, William Blot, Xiao-Ou Shu. Associations of coffee and tea consumption with lung cancer risk: A pooled analysis of 17 cohort studies involving over 1.2 million participants [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 632.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 8
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    Online Resource
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4675-4675
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4675-4675
    Abstract: Objectives: To examine the association between alcohol consumption, types of beverages, alcohol amount and total and some diseases mortality among Korean adults. Methods: Patients included 16,257 subjects of the Korean Multi-center Cancer Cohort who were cancer-free at baseline enrollment reported their lifestyle factors between 1993 and 2008, including the status of alcohol consumption primarily from the national death certificate. Alcohol consumption (ie, soju, beer, raw rice wine) was assessed at cohort entry using a questionnaire. Two hundred sixty-eight were excluded on the grounds that they were founded out as having no data about alcohol consumption. Final study populations are 15,989. Cox proportional hazard regression model was used to estimate the hazard ratio (HR) of alcohol consumption for total mortality as adjusted for age, gender, the geographic area and the smoking status, the education level and the body mass index (BMI). Results: The number of total death was one Thousand ninety-three after an average follow-up of 8.8 years. During the follow-up period, including 483 cancer mortality cases with a total of 151,150 person-years, 6,736 subjects (42.1%) were considered as drinkers (the sum of current and past drinkers) and the majority drank soju (90.9%). Alcohol consumption was significantly associated with an increased risk of total mortality (p-trend, & lt; 0.05, & lt;0.005, & lt;0.05, respectively). Past and current drinkers compared with no drinkers was associated with an increased risk of total mortality (past drinker: HR, 1.40; 95% CI: 1.1 to 1.7, current drinker: HR, 1.20; 95% CI, 1.0 to 1.4). The risk of mortality appeared to be increased among current smoking (HR, 1.51; 95% CI, 1.27 to 1.79) and old (HR, 1.08; 95% CI, 1.07 to 1.09) and lived women in some specific areas. The amount of alcohol intake was associated with total mortality ( & lt;25g/wk; HR: 0.3, 95% CI: 0.3-0.5, & gt;504g/wk; HR: 1.3; 95% CI: 1.1 to 1.6) and disease-specific mortalities which were included total cancer, lung cancer, stomach cancer and esophageal cancer and liver disease. Added to this, it was founded that liver cancer, pancreas and colon cancer might have significant relationship with mortality and it was depended on alcohol amount. And soju was founded out as having an increased risk of mortality regardless of drinking with other beverages together. Also, drinkers had increased risk of mortality due to liver cancer and liver disease. In addition to, soju drinking only without any other beverages had the increased risk of mortality with liver disease. Conclusions: Consuming alcohol may increase the risk of total mortality and mortality of liver cancer and liver disease, particularly among soju drinkers, yet the significant relationship between alcohol amount and mortality of some specific diseases were suggested. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4675. doi:10.1158/1538-7445.AM2011-4675
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 19, No. 5 ( 2010-05-01), p. 1292-1300
    Abstract: Background: The role of soybean products in gastric cancer risk is not clear in epidemiologic studies due to measurement error from dietary intake questionnaires and due to different degrees of bias according to study design. To examine the association between soybean products and gastric cancer risk, we measured phytoestrogen biological markers in a nested case-control study. Methods: The study population was composed of 131 cases and 393 matched controls within the Korean Multicenter Cancer Cohort. The concentrations of the four biomarkers in the plasma samples were measured using time-resolved fluoroimmunoassay. Conditional and unconditional logistic regression models were used to compute the odds ratio (OR) and 95% confidence intervals (CI). Results: Median plasma concentrations of genistein (229 nmol/L for controls, 181.8 nmol/L for cases; P = 0.07) and daidzein (131.2 nmol/L for controls, 80.5 nmol/L for cases; P = 0.04) in cases were lower than in controls, whereas equol concentrations were similar. Compared with the reference group, gastric cancer risk decreased in the highest groups for genistein (OR, 0.54; 95% CI, 0.31-0.93) and daidzein (OR, 0.21; 95% CI, 0.08-0.58). Higher equol concentrations were associated with a decreased risk for gastric cancer (OR, 0.50; 95% CI, 0.27-0.90). The combination of the highest concentrations for each isoflavone category was associated with a 0.09-fold decreased risk for gastric cancer compared with the combination of the lowest concentrations for each category. There was no association between plasma lignan concentrations and gastric cancer. Conclusions: High serum concentrations of isoflavones were associated with a decreased risk for gastric cancer. Impact: These results suggest a beneficial effect of high soybean product intake for gastric cancer risk. Cancer Epidemiol Biomarkers Prev; 19(5); 1292–300. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 10
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 26, No. 1 ( 2017-01-01), p. 126-135
    Abstract: Background: Common cancers develop through a multistep process often including inherited susceptibility. Collaboration among multiple institutions, and funding from multiple sources, has allowed the development of an inexpensive genotyping microarray, the OncoArray. The array includes a genome-wide backbone, comprising 230,000 SNPs tagging most common genetic variants, together with dense mapping of known susceptibility regions, rare variants from sequencing experiments, pharmacogenetic markers, and cancer-related traits. Methods: The OncoArray can be genotyped using a novel technology developed by Illumina to facilitate efficient genotyping. The consortium developed standard approaches for selecting SNPs for study, for quality control of markers, and for ancestry analysis. The array was genotyped at selected sites and with prespecified replicate samples to permit evaluation of genotyping accuracy among centers and by ethnic background. Results: The OncoArray consortium genotyped 447,705 samples. A total of 494,763 SNPs passed quality control steps with a sample success rate of 97% of the samples. Participating sites performed ancestry analysis using a common set of markers and a scoring algorithm based on principal components analysis. Conclusions: Results from these analyses will enable researchers to identify new susceptibility loci, perform fine-mapping of new or known loci associated with either single or multiple cancers, assess the degree of overlap in cancer causation and pleiotropic effects of loci that have been identified for disease-specific risk, and jointly model genetic, environmental, and lifestyle-related exposures. Impact: Ongoing analyses will shed light on etiology and risk assessment for many types of cancer. Cancer Epidemiol Biomarkers Prev; 26(1); 126–35. ©2016 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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