Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Online Resource  (6)
  • American Association for Cancer Research (AACR)  (6)
  • Han, Wonshik  (6)
  • Park, Sue K.  (6)
Type of Medium
  • Online Resource  (6)
Publisher
  • American Association for Cancer Research (AACR)  (6)
Language
Years
Subjects(RVK)
  • 1
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4720-4720
    Abstract: Background: DNA copy number variation (CNV) is a common phenomenon in human genome and some CNVs have been associated with susceptibility or resistance to disease. It has been suggested that gene copy number can be elevated in cancer cells. To evaluate potential role of CNV in breast cancer development, we conducted genome-wide association study of CNV in Seoul Breast Cancer Study. Methods: Cases were diagnosed with breast cancer and underwent curative surgery at two teaching hospitals located in Seoul, Korea, between 2001 and 2007 (n=2,386). Control subjects were selected from multi-center based cohort study in 2007 (n=2,386). The Affymetrix SNP assay 6.0 array, which includes 946,000 probes for the detection of copy number variation, was used. Nexus Copy Number version 4.1 was used for detecting CNVs (significance threshold=10−6; minimum number of probes per segment=4), and statistical analysis. After quality control step (i.e., robust variance sample QC), total 2,315 cases and 2,039 controls were compared for the difference of each CNV. In this study, we selected the CNVs that were different between cases and controls by at least 5% (P adjusted for multiple comparison & lt;0.01). Adjacent CNVs were grouped into CNV regions ranging 10 kb to 300 kb. Results: Between case and controls, thirteen CNV regions including chr115q11.2, chr3q26.1, chr6q16.3, chr17q31.1 were significantly different for copy number. We note that those regions include genes such as UGT2B17 (UDP glucuronosyltransferase 2 family, polypeptide B18), OR4C11 (olfactory receptor, family 4, subfamily C, member 11), LRRC37A2 (leucine rich repeat containing 37, member A2), ARL17P1 (ADP-ribosylation factor-like 17 pseudogene 1), LOC644974, and the others. We are planning validation study for the regions by quantitative PCR to verify the association with breast cancer risk found in this study. Conclusion: Our results suggest that common CNVs may be associated with breast cancer in Korean women. However, further variation study is essential to support our observation and underlying biological mechanisms for the associations needs to be elucidated. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 4720.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 21, No. 11_Supplement ( 2012-11-01), p. 60-60
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 21, No. 11_Supplement ( 2012-11-01), p. 60-60
    Abstract: Background: Although several low-penetrance loci associated with breast cancer risk were identified and confirmed, knowledge of the effect of multiple risk alleles is limited especially in Asian women. Therefore we evaluated the association between the polygenic risk scores and breast cancer risk in Korean women using the most recent list of breast cancer susceptibility loci. Methods: We analyzed 51 single-nucleotide polymorphisms (SNPs) located in 34 loci in 1,774 cases and age-frequency matched 1,774 control subjects participating in Seoul Breast Case-Control Study. The fourteen independent SNPs associated with breast cancer risk were selected based on the results of single SNP analysis. The genetic risk score (GRS) were calculated using simple count method and weighted method. Tests of association were conducted using the logistic regression for quintiles of each GRS with or without adjustment. The c-statistic was estimated to evaluate the contribution of GRS to risk prediction model including non-genetic factors (age, family history of breast cancer, education, BMI, menopausal status, age at menarche, age at first full-term pregnancy, and number of children). Results: Fourteen SNPs (rs13393577, rs4973768, rs7716600, rs1092913, rs889312, rs9485372, rs2046210, rs1562430, rs704010, rs10736303, rs7107217, rs10771399, rs3803662, and rs4784227), each of which reflected a genetically independent locus, were found to be associated with breast cancer risk. A highly significant trend was observed between the GRS and the risk of breast cancer. The adjusted odds ratios for women in the highest quintile of count GRS or weighted GRS vs. those in the lowest were 2.64 (95% confidence interval (95% CI), 2.09- 3.35; Ptrend=9.3E-19) and 2.76 (95% CI, 2.18- 3.50; Ptrend=5.9E-21), respectively. The c-statistic for model including the GRS in additional to the conventional risk factors was 0.6389 (95% CI, 0.620-0.658) vs. 0.6041 (95% CI, 0.585-0.623) with the conventional risk factors only. Conclusions: Supporting the polygenic inheritance model of breast cancer, our study showed that GRS based on low-penetrance SNPs adds very modest improvement to risk prediction models. Citation Format: Hyuna Sung, Ji-Yeob Choi, Sue K. Park, Wonshik Han, Keun-Young Yoo, Sei-Hyun Ahn, Dong-Young Noh, Daehee Kang. Combined effects of low-penetrance variants on breast cancer risk: Results from the Seoul Breast Cancer Study. [abstract]. In: Proceedings of the AACR Special Conference on Post-GWAS Horizons in Molecular Epidemiology: Digging Deeper into the Environment; 2012 Nov 11-14; Hollywood, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(11 Suppl):Abstract nr 60.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 22, No. 7 ( 2013-07-01), p. 1297-1303
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 22, No. 7 ( 2013-07-01), p. 1297-1303
    Abstract: Background: Recently, 41 new genetic susceptibility loci for breast cancer risk were identified in a genome-wide association study (GWAS) conducted in European descendants. Most of these risk variants have not been directly replicated in Asian populations. Methods: We evaluated nine of those nonreplication loci in East Asians to identify new risk variants for breast cancer in these regions. First, we analyzed single-nucleotide polymorphisms (SNP) in these regions using data from two GWAS conducted among Chinese and Korean women, including 5,083 cases and 4,376 controls (stage 1). In each region, we selected an SNP showing the strongest association with breast cancer risk for replication in an independent set of 7,294 cases and 9,404 controls of East Asian descents (stage 2). Logistic regression models were used to calculate adjusted ORs and 95% confidence intervals (CI) as a measure of the association of breast cancer risk and genetic variants. Results: Two SNPs were replicated in stage 2 at P & lt; 0.05: rs1419026 at 6q14 [per allele OR, 1.07; 95% confidence interval (CI), 1.03–1.12; P = 3.0 × 10−4] and rs941827 at 10q25 (OR, 0.92, 95% CI, 0.89–0.96; P = 5.3 × 10−5). The association with rs941827 remained highly statistically significant after adjusting for the risk variant identified initially in women of European ancestry (OR, 0.88; 95% CI, 0.82–0.97; P = 5.3 × 10−5). Conclusion: We identified a new breast cancer risk variant at 10q25 in East Asian women. Impact: Results from this study improve the understanding of the genetic basis for breast cancer. Cancer Epidemiol Biomarkers Prev; 22(7); 1297–303. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 128-128
    Abstract: Lifestyle factors have been chronologically changed into western-style in Korea, which may result in the rapid increase of breast cancer incidence. It is plausible reproductive factors through hormonal mechanisms are differentially related to risk of breast cancer subtypes defined estrogen receptor (ER) and progesterone receptor (PR) status. We investigated the differential association of reproductive risk factors on such subtypes and also evaluated the temporal trends between those factors and the subtypes. Using data of Seoul Breast Cancer Study (SeBCS), a multicenter based case-control study, 3,689 breast cancer patients and 3,870 control subjects were analyzed in this study. The distribution of subtypes among cases was 62.7% of ER+, 37.3% ER-, 53.2% of PR+ and 46.8% PR-, respectively. Reproductive factors including age at menarche, pregnancy history, age at first full term pregnancy, number of children, duration of estrogen exposure before first full term pregnancy (EEBF), duration of lifetime estrogen exposure (LEED), breast feeding history and duration of breast feeding were evaluated on breast cancer risk by hormone receptor status. Multinomial logistic regression and Wald tests for heterogeneity across the subtypes were conducted. The frequency of PR-positive breast cancer significantly was higher among the women born in 1960s (56.4%) compared to women born in 1940s (41.9%) (p for trend & lt;0.0001). However, there was no significant trend of the distribution in ER-defined breast cancer subtype. Breast cancer risks associated with number of children, EEBF, LEED, duration of breast feeding were different between ER or PR status (all p for heterogeneity & lt;0.05). Those reproductive factors showed a chronological trend according to the birth year groups. EEBF was longer among the women born in 1960s group than women born in 1940s. As the EEBF increased, the risk of breast cancer increased significantly; this association was stronger among PR-positive (OR= 1.96, 95% CI= 1.65 - 2.33 for Q4 vs Q1) than among PR-negative cancer (OR= 1.48, 95% CI= 1.24 - 1.77 for Q4 vs Q1) (p for heterogeneity= 0.0100). LEED was shorter among the women born in 1960s group than women born in 1940s. As the LEED increased, the risk of breast cancer decreased significantly, which is stronger among PR-negative (OR= 0.67, 95% CI= 0.57 - 0.79 for Q4 vs Q1) than among PR-positive cancer (OR= 0.89, 95% CI= 0.76 - 1.05 for Q4 vs Q1) (p for heterogeneity= 0.0014). Our results suggest that association between the reproductive risk factors and breast cancer risk differs appreciably for breast cancer defined by hormone receptor status. Increasing distribution of PR-positive breast cancer might be attributed to changes of EEBF and LEED. Citation Format: Seokang Chung, Nan Song, Hyuna Sung, Sue K. Park, Wonshik Han, Dong-Young Noh, Sei-Hyun Ahn, Keun-Young Yoo, Daehee Kang, Ji-Yeob Choi. Chronological changes of hormone receptor status in breast cancer by reproductive factors: results from Seoul Breast Cancer Study (SeBCS). [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 128. doi:10.1158/1538-7445.AM2013-128
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 3273-3273
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 3273-3273
    Abstract: Many previous association studies have been addressed genetic variations in obesity related genes on breast cancer risk, however, limited consideration of genes and gene-environmental interaction was involved. We investigated the associations of known obesity-related genes on breast cancer risk by comprehensive assessment based on individual SNP analysis and gene-based pathway-analysis. This study was conducted in 1,786 cases and 1,789 controls from Seoul Breast Cancer Study (SEBCS), a multicenter case-control study. The selection of 1,561 candidate obesity-related gene for this study was involved based on GWAS catalog and previous published data associated with obesity. Associations of single-nucleotide polymorphism (SNP) with BMI were assessed by linear regression models under an additive genetic model adjusting for age and disease status to identify genetic loci for obesity. 2,366 BMI-related significant SNPs including additional significant 449 SNPs which independently associated with BMI in our data (p & lt;10-4) were evaluated for the genetic effect on breast cancer risk. Per-allele odds ratio for breast cancer risk was assessed using logistic regression models adjusting for age and 1st family history of breast cancer. Gene-based pathway significance was assessed by the adaptive rank-truncated product (ARTP) method with 1,000 permutations for association between BMI-related genes and breast cancer risk. Among available 227,197 SNPs from candidate genes and additional significant SNPs in SEBCS data, 12,388 SNPs in 890 genes were found to be associated with BMI (p & lt;0.05): 495 genes (55.7%) from GWAS catalog and 281 genes (48.4%) from published candidate genes for obesity were identified, respectively. Rs17804012 in RBFOX1 and rs2014791 in LINC00317 showed the most significant association with BMI (p & lt;5E-6), which observed null association with breast cancer risk. In contrast, the gene-based pathway analysis including less significantly associated genes with BMI (N=644, p & lt;0.05) showed significant association with breast cancer risk (the pathway p=0.003). Especially, the effect of THRB gene on breast cancer risk has highly significant value (p=9E-04) and the association was confined to premenopausal women with BMI above 23.2 (p & lt;0.01). The group of BMI-related genes including THRB was significantly associated with breast cancer risk in pathway analysis and the associations were different depending on the menopausal status and/or BMI levels. Our results suggest that consideration of the complex genetic pathway related to environmental factors might reveal additional breast cancer susceptibility loci. Citation Format: Seokang Chung, Nan Song, Hyuna Sung, Sue K. Park, Wonshik Han, Dong-Young Noh, Sei-Hyun Ahn, Keun-Young Yoo, Daehee Kang, Ji-Yeob Choi. Genetic variation in obesity-related genes and breast cancer risk in the Seoul Breast Cancer Study. [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 3273. doi:10.1158/1538-7445.AM2014-3273
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 18, No. 2 ( 2009-02-01), p. 508-515
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 18, No. 2 ( 2009-02-01), p. 508-515
    Abstract: High-density lipoprotein cholesterol (HDL-C) has been suggested to be associated with breast cancer. However, the roles of HDL-C and hypertriglyceridemia on breast cancer still have been controversial. The goal of this study was to investigate the association between HDL-C with breast cancer risk, stratifying by menopausal status, and body mass index. The hormonal receptor status of breast has been proposed to modify the effect of HDL-C on breast cancer. Multicenter hospital-based case-control study was conducted from November 2004 to December 2005 in Korea. After one to two individual matchings by age (±5 years) and menopausal status, 690 cases and 1,380 controls were included in the analysis. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by conditional, unconditional, and multinomial logistic regressions. Protective effect of HDL-C on breast cancer was only observed among premenopausal women with an OR (95% CI) of 0.49 (0.33-0.72) for HDL-C ≥60 versus & lt;50 mg/dL (Ptrend & lt; 0.01). Only nonobese premenopausal women had a significant decreased risk (OR, 0.34; 95% CI, 0.22-0.53). OR (95% CI) of low HDL-C ( & lt;50 mg/dL) and high triglyceride (TG; ≥150 mg/dL) category was 2.20 (1.32-3.67) on estrogen receptor-negative and progesterone receptor-negative breast cancer compared with high HDL-C (≥50 mg/dL) and low TG ( & lt;150 mg/dL) category. This study suggests that higher level of HDL-C may reduce breast cancer risk among premenopausal women. Estrogen receptor-negative and progesterone receptor-negative breast cancer was associated with dyslipidemia, which implicates that association among HDL-C, TG, and breast cancer may be modified by receptor status. (Cancer Epidemiol Biomarkers Prev 2009;18(2):508–15)
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages