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  • American Association for Cancer Research (AACR)  (84)
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  • 1
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3764-3764
    Abstract: To date, genome-wide association studies (GWAS) have identified fourteen SNPs that influence risk of developing colorectal cancer (CRC) in Caucasians. None of these tagging SNPs is within coding region of a candidate gene. Only five of these SNPs were associated with CRC risk in Chinese population. We aimed to perform GWAS to identify new susceptibility loci associated with differential response to environmental insults in sporadic Chinese CRC patients. A total of 1,000 cases (aged 50 years or more) and 1,000 age- and gender-matched healthy controls were genotyped with Affymetrix SNP 6 array, a newer microarray platform which includes the ability to interrogate structural variants. Over 90% of the arrays have call rate of 99% or more. Thirty five arrays with call rate less than 97% and either null QC or negative QC (enzyme) values were replicated. Principal component analysis performed together with 270 HapMap and 92 Singapore Genome Variant Project (SGVP) samples indicate that there is no population substructure. Sixteen outliers were removed. SNPs with call rate less than 99% and minor allelic frequency less than 0.1, and control SNPs not in Hardy-Weinburg equilibrium were filtered. Subsequent quantile-quantile plot shows no evidence of allelic test statistic inflation. Twelve new chromosomal regions with SNPs having -log10 p-values greater than four and good clustering patterns were identified via Manhattan plot. Linkage disequilibrium (LD) analysis was performed to ascertain the LD blocks around these SNPs. SNPs in three chromosomal regions within the vicinity of promising CRC candidate genes were prioritized and currently being validated in a replication panel consisting of another 2,000 cases and controls. 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 3764. doi:10.1158/1538-7445.AM2011-3764
    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
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  • 2
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    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2189-2189
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2189-2189
    Abstract: Colorectal cancer (CRC) is one of the most frequent cancers and leading cause of cancer mortality in the developed world. Twin study has attributed about 35% of the etiology of sporadic CRC to genes. Structural variations in the human genome have recently been associated with complex neurological diseases. Their role in CRC, however, is unclear. We performed genome-wide association study (GWAS) on 2,000 ethnicity-, age-, and gender-matched Singapore Chinese CRC patients (aged 50 or more and with no dominant family history of CRC) and healthy controls. Genome-wide genotyping was performed using Affymetrix SNP 6 platform, and rare copy number variants (CNV) were interrogated in 1830 samples that passed the quality assurance tests. A 400 kb region at chromosome 14q11 was identified to be significantly associated (-log10 p-value = 11) with sporadic CRC risk. A chromatin modifier implicated in the β-catenin/Wnt signalling pathway is one of the candidate genes found in the region. Primers unique for this gene applied to an optimal real-time copy number assay verified the CNV region in an independent replication panel comprising another 1,000 sporadic CRC cases. About 6% of the cases exhibit copy number alterations at this region compared to 1% in the healthy controls. A second gene, a small guanosine triphosphatase (GTPase) involved in protein trafficking and preferentially up-regulated in colonic tumors , was shown by long-range polymerase chain reaction to have more structural variations in the cases compared to the controls. Furthermore, expression of the H1 binding domain of the chromatin modifier was positively correlated to the expressions of Cyclin D1 and C-myc. The data suggest that the rare CNV in 14q11 was dynamically associated with the activation of genes implicated in sporadic CRC in the Singapore Chinese. Citation Format: Peh Yean Cheah, Lai Fun Thean, Yik-Ying Teo, Woon-Puay Koh, Jian-Min Yuan, Poh Koon Koh, Min Hoe Chew, Choong Leong Tang. A rare copy number variant at chromosome 14q11 was associated with sporadic colorectal cancer risk in Singapore Chinese. [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 2189. doi:10.1158/1538-7445.AM2014-2189
    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
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Prevention Research Vol. 4, No. 10_Supplement ( 2011-10-01), p. B97-B97
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 4, No. 10_Supplement ( 2011-10-01), p. B97-B97
    Abstract: Background: Cervical cancer incidence is highest in developing countries in Asia and South America and is associated with relatively poor survival in these high-risk populations. Diet may influence susceptibility to and/or persistence of human papillomavirus infection, a necessary cause of cervical cancer. Soy isoflavones and green tea catechins have immunomodulating properties that may protect against cervical cancer. Methods: We investigated the relationship between soy, green tea and black tea intake and risk of cervical cancer in the well-established prospective population-based Singapore Chinese Health Study. Soy and tea consumption data were collected at baseline using a validated food frequency questionnaire. Cervical cancer cases (n=257) were identified from 34,028 women followed for an average of 11.7 years. Proportional hazards regression methods were used to assess the associations between soy and tea intake and cervical cancer risk. Hazard ratios (HRs) and 95% confidence intervals (CIs) were adjusted for Papanicolaou (Pap) test history, education level, parity, use of oral contraceptives, and other potential confounders. Results: A statistically significant inverse association was observed for highest versus lowest soy intake and cervical cancer risk (HR=0.71; 95% CI:0.53, 0.96; p for trend=0.03). Consumption of green tea on a weekly or more frequent basis, compared to no tea intake was inversely associated with cervical cancer risk (HR=0.80; 95% CI:0.56, 1.14; p for trend=0.2). There was no association with black tea. We observed interacting effects for soy and green tea intake on risk of cervical cancer. The inverse association with soy intake was stronger among women who drank green tea (HR=0.42; 95% CI:0.25, 0.69; p for trend=0.001). No association was observed for soy intake among non-tea drinkers (p for interaction=0.01). Conclusions: We provide the first human evidence for individual, as well as synergistic protective effects of soy and green tea intake on risk of cervical cancer. These findings were independent of self-reported frequency of Pap testing and education level. Our findings support experimental evidence for immunomodulating effects of green tea catechins and soy isoflavones as a possible mechanism underlying the protective effect of these dietary factors on cervical cancer risk. Citation Information: Cancer Prev Res 2011;4(10 Suppl):B97.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4695-4695
    Abstract: Chinese women in Asia have higher rates of lung cancer than in many other places in the world. In China, the age standardized incidence rate for female lung cancer is 19.9 per 100,000 and in Singapore it is 17.5, while rates are far lower (1.5-9.2) in countries such as Vietnam, Indonesia, India, and Russia. Cigarette smoking is not the major risk factor for lung cancer in these women, nor is secondhand tobacco smoke exposure. Some studies demonstrate the role of fumes from indoor heating under special circumstances. However, multiple epidemiologic studies document an association between lung cancer in Chinese women and Chinese-style cooking with oils heated at high temperatures. Carcinogens and toxicants have been identified in fumes generated during high temperature cooking with various oils but there have been no biomarker studies to assess carcinogen and toxicant uptake in Chinese women who regularly cook at home. We quantified urinary mercapturic acid biomarkers of exposure to the volatile compounds acrolein, crotonaldehyde, benzene, 1,3-butadiene, and ethylene oxide; and urinary metabolites of the non-volatile combustion products pyrene and phenanthrene in 54 non-smoking, non alcohol-drinking Chinese women who reported regularly doing home cooking and 50 non-smoking, non-alcohol drinking women randomly selected from the Singapore Chinese Health Study as controls. Compared with controls, women who engaged in regular home cooking had significantly higher levels of mercapturic acids of acrolein [geometric mean 1959 pmol/mg creatinine (95% CI 1554-2467) vs.1370 (95% CI 1077-1742), P = 0.038], crotonaldehyde [geometric mean 231.6 pmol/mg creatinine (95% CI 193-277) vs. 142.2 (95% CI 118-171) P = 0.0004] , and benzene [geometric mean 0.58 pmol/mg creatinine (95% CI 0.44-0.78) vs. 0.18 (95% CI 0.14-0.24) P & lt; 0.0001]. No significant differences were found in levels of mercapturic acids of 1,3-butadiene or metabolites of pyrene and phenanthrene between the two groups whereas levels of the ethylene oxide mercapturic acid were significantly higher in the controls than in the cooking group. The higher levels of the mercapturic acid of benzene, a multi-organ carcinogen, in the women who cooked, are particularly notable. The results of this study showing increased exposure to the volatile toxicants and carcinogens acrolein, crotonaldehyde, and benzene in Chinese women who regularly cook provide a plausible lead for further investigating the role of volatile compounds generated during cooking as causes of lung cancer. 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 4695.
    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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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
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    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 912-912
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 912-912
    Abstract: Epidemiologic studies among populations that consume moderate to high amount of soy have shown that soy isoflavones may reduce breast cancer risk, and the chemopreventive effects are postulated to be related to the anti-estrogenic properties of soy isoflavones. Recently, experimental studies have revealed that dietary isoflavones may also down-regulate the expression of the MDM2 oncogene, and the inhibition of the expression of the MDM2 oncoprotein has in turn been associated with antitumor activities in breast cancer models. Furthermore, a polymorphism in the promoter region of MDM2 SNP309 (T & gt;G change at nucleotide 309 in the first intron; rs2279744) leads to increased expression of the oncogene and has been associated with earlier onset of breast cancer. We have previously shown that postmenopausal women with a higher than median intake of soy have a reduced risk of breast cancer compared with those with a lower intake. If down-regulation of the MDM2 oncogene is one of the mechanistic pathways for the chemopreventive effects of soy isoflavones in breast cancer, we postulate that the protective effect of soy isoflavones on breast cancer will be stronger in those possessing the high-activity MDM2 genotype. To confirm this hypothesis, we conducted a nested case-control study among 281 incident, postmenopausal breast cancer cases and 462 postmenopausal control subjects within the Singapore Chinese Health Study Cohort. Overall, there was no significant association between MDM2 gene polymorphism and breast cancer risk. Postmenopausal women who had a higher than median intake of soy had a reduced risk of breast cancer [odds ratio (OR), 0.76; 95% confidence interval (CI), 0.56-1.03]. This inverse association was principally noted among women homozygous for the high activity MDM2 allele (GG genotype). There was a statistically significant, roughly 50% reduction in breast cancer risk between above versus below median level of soy consumption in this subgroup of women (OR, 0.52; 95% confidence interval, 0.28-0.98). On the other hand, a much weaker, and statistically nonsignificant association was noted among women possessing the lower-activity MDM2 genotypes (OR, 0.86, 95% CI, 0.59-1.24). Our findings suggest that the ability of soy isoflavones to down-regulate the MDM2 oncoprotein may be one etiologic mechanism through which the intake of soy is associated with breast cancer protection. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of th e 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 912.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    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
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  • 6
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    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4486-4486
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4486-4486
    Abstract: Background: Mitochondrial DNA (mtDNA) copy number variation is common in colorectal tumors and one case control study showed mtDNA copy number to be associated with increased colorectal cancer risk. Data on mtDNA copy number and colorectal cancer risk in prospective cohorts is lacking. Objectives: We evaluated the association between mtDNA copy number in peripheral blood and colorectal cancer risk among participants of the Singapore Chinese Health Study. Methods: We conducted a nested case-cohort study of 422 colorectal cancer cases (168 incident cases with pre-diagnostic blood and 254 prevalent cases with post-diagnostic blood) and 880 controls who were free of colorectal cancer at blood draw. The relative mtDNA copy number was measured using real time PCR. Analysis of covariance and logistic regression methods were employed to examine the association between mtDNA copy number and colorectal cancer risk. Results: mtDNA copy number was significantly higher among colorectal cancer cases than controls (geometric mean: 0.62 vs. 0.50, p & lt;0.0001). There was a U shaped relationship between the mtDNA copy number and colorectal cancer risk. Individuals in the low and high mtDNA copy numbers were at increased risk of colorectal cancer; odds ratios (95% confidence interval) for developing colorectal cancer for the lowest and highest quartile of mtDNA copy numbers were 1.83 (1.16-2.90) and 3.54 (2.25-5.55), respectively, compared to those in the second quartile of mtDNA after adjustment for potential confounders (p for curvilinear trend & lt;0.001). The lowest mtDNA copy number quartile was associated with colorectal cancer only in the pre-diagnostic blood samples (OR=3.22, 95% CI:1.51-6.85) but not in the post-diagnostic blood samples (OR=1.36, 95% CI:0.80-2.32), implying that cancer status impacts the mtDNA copy number-colorectal cancer risk association. Conclusions: This is the first study to show a prospective association between mtDNA copy number and colorectal cancer risk. Further studies are needed to confirm this association and understand the biological significance of these observations. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4486. doi:1538-7445.AM2012-4486
    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: 2012
    detail.hit.zdb_id: 2036785-5
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  • 7
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    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 677-677
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 677-677
    Abstract: ACKGROUND Recent prospective data from US and European populations was published showing no association between fish intake and lung cancer risk. High temperature cooking of meat, including fish, increases exposure to air pollutants, including volatile organic compounds (VOCs). Recently, we reported that nonsmoking Chinese women who cooked daily had statistically significant 3.7- to 21.6-fold greater risk of having urinary VOC metabolite levels in the third versus the first tertile, than a random sample of women (Hecht, et al., CEBP 2010). Exposure to these air pollutants may increase risk of certain histologic subtypes of lung cancer. METHODS We investigated the relationship between fish intake and risk of lung cancer in the well-established prospective population-based Singapore Chinese Health Study. Dietary consumption data were collected at baseline using a validated food frequency questionnaire. Lung cancer cases (n=1130) were identified from 61,321 men and women followed for an average of 11.5 years. Histology information was available for 87% of cases. Analyses were conducted separately for adenocarcinomas (n=419 cases) and combined squamous cell and small cell carcinomas (n=337 cases). Proportional hazards regression methods were used to assess the associations between dietary factors and lung cancer risk. Hazard ratios (HRs) and 95% confidence intervals (CIs) were adjusted for age, total caloric intake, education level, smoking (years smoked, number of cigarettes smoked per day and years since quitting smoking among former smokers), and other potential confounders. RESULTS Higher fish intake was positively associated with adenocarcinoma risk (HR=1.47; 95% CI: 1.08, 1.99, for fourth versus first quartile of intake). The association became stronger with greater fish intake (p for trend = 0.02), and when analyses were restricted to lifetime never smokers (HR=1.78; 95% CI:1.10, 2.87, for fourth versus first quartile of intake). The positive association between fish intake and risk of adenocarcinoma remained, but lost statistical significance after excluding cases diagnosed within the first two years of follow-up (HR=1.37; 95% CI:0.98, 1.90). Adenocarcinoma risk associated with fish intake was evaluated by cooking method. Positive associations were observed for greater intake of deep fried fish (HR=1.31; 95% CI: 1.01, 1.70) and pan fried fish (HR=1.34; 95% CI: 1.02, 1.77), but no association was observed for intake of steamed fish. Fish intake was not associated with squamous/small cell carcinoma risk, regardless of smoking history. CONCULSIONS We observed that fried fish intake was a risk factor specific for adenocarcinoma of the lung, among lifetime never smokers. Stir-frying cooking at a high temperature is the primary mode of food preparation in our study population. Our results for fish intake by cooking method support the notion that cooking fumes from stir-frying fish increase risk of adenocarcinoma of the lung. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 677. doi:1538-7445.AM2012-677
    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: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 632-632
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 632-632
    Abstract: Background: Tobacco smoking is an established risk factor for gastric cancer. Recently, reports have suggested high body mass index (BMI) as a significant risk factor for esophageal adenocarcinoma whereas the relationship with gastric cancer remains inconsistent. The aim of the current study is to evaluate two potentially modifiable factors, tobacco smoking and increased body mass index, as risk factors for gastric cancer among Singapore Chinese. Methods: We prospectively examined the association between smoking and BMI at baseline, and the risk of developing gastric cancer in the Singapore Chinese Health Study, a cohort of 63,257 middle-aged and older Chinese men and women enrolled between 1993 and 1998. Information on body weight, height, cigarette smoking and other lifestyle factors and diet was obtained through in-person interview at enrollment. BMI was calculated using weight in kg divided by height in meter squared (kg/m2). Incidence of cancer and death among cohort participants was obtained via linkage with nationwide registries. Results: As of 31 December 2009, 568 cohort participants who were free of cancer at baseline had developed gastric cancer. Compared to never smokers, current smokers had a 38% increase in risk of gastric cancer (95% confidence interval: 1.12-1.70), with a positive dose-response association between number of cigarettes per day (P for trend=0.002) and number of years of smoking (P for trend=0.005), and gastric cancer risk. After adjustment for cigarette smoking and other potential confounders, hazard ratios (95% confidence interval) of gastric cancer for subjects with BMI 20- & lt;24, 24- & lt;28 and 28+ kg/m2 were 1.30 (1.00-1.68), 1.19 (0.88-1.60), and 1.65 (1.14-2.40), respectively, relative to those with & lt;20 kg/m2 (P for trend=0.063). This dose-response association between increasing BMI and cancer risk was stronger for cardia cancer (P for trend =0.021) than for noncardia cancer (P for trend=0.19). In separate analyses in groups defined by BMI, hazard ratios (95% confidence interval) of gastric cancer for current smokers with BMI of β28, 24- & lt;28, 20- & lt;24, and & lt;20 kg/m2 were 1.11 (0.51-2.45), 1.08 (0.67-1.75), 1.52 (1.16-1.99), and 1.90 (1.05-3.43), respectively, as compared with nonsmokers. The positive dose-response associations between dose and duration of smoking, and gastric cancer risk were limited to lean subjects with BMI & lt;24 kg/m2 and not observed in the more obese subjects. Conclusion: Smokers with relatively low level of BMI had enhanced risk of gastric cancer compared to smokers with higher BMI. Our findings corroborate the hypothesis that lean smokers have increased oxidative DNA damage relative to their non-lean counterparts, which may in turn explain their heightened susceptibility to tobacco carcinogens-induced DNA damage in gastric carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 632. doi:1538-7445.AM2012-632
    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: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 6 ( 2013-03-15), p. 1876-1882
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 6 ( 2013-03-15), p. 1876-1882
    Abstract: TGF-β plays a critical role in normal mammary development and morphogenesis. Decreased TGF-β signaling has been associated with increased mammographic density. Percent mammographic density (PMD) adjusted for age and body mass index (BMI) is a strong risk factor and predictor of breast cancer risk. PMD is highly heritable, but few genetic determinants have been identified. We investigated the association between genetic variation in TGFB1 and PMD using a cross-sectional study of 2,038 women who were members of the population-based Singapore Chinese Health Study cohort. We assessed PMD using a computer-assisted method. We used linear regression to examine the association between nine tagging single-nucleotide polymorphisms (SNP) of TGFB1 and PMD and their interaction with parity, adjusting for age, BMI, and dialect group. We calculated P values adjusted for correlated tests (PACT) to account for multiple testing. The strongest association was observed for rs2241716. Adjusted PMD was higher by 1.5% per minor allele (PACT = 0.04). When stratifying by parity, this association was limited to nulliparous women. For nulliparous women, adjusted PMD was higher by 8.6% per minor allele (PACT = 0.003; P for interaction with parity = 0.002). Three additional TGFB1 tagging SNPs, which were in linkage disequilibrium with rs2241716, were statistically significantly associated with adjusted PMD (PACT & lt; 0.05) for nulliparous women. However, none of these three SNPs showed statistically significant association after adjusting for rs2241716. Our data support that TGFB1 genetic variation may be an important genetic determinant of mammographic density measure that predicts breast cancer risk, particularly in nulliparous women. Cancer Res; 73(6); 1876–82. ©2012 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: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1339-1339
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1339-1339
    Abstract: A previous case-control study reported a positive association between mitochondrial DNA (mtDNA) copy number in peripheral blood and breast cancer risk. However, data on mtDNA copy number and breast cancer risk in prospective cohorts is lacking. We evaluated the prospective association between mtDNA copy number and breast cancer risk in the Singapore Chinese Health Study. We conducted a nested case-control study of 183 incident breast cancer cases with pre-diagnostic blood samples and 529 individually matched control women who were free of breast cancer. The mtDNA copy number was measured using real time PCR. Conditional logistic regression methods were employed to examine the association between mtDNA copy number and breast cancer risk. Overall, there was no association between mtDNA copy number and breast cancer after adjustment for potential confounders (p=0.37). Among participants who donated a blood sample within 3 years of breast cancer diagnosis women in the second and third tertile of mtDNA copy number had a significantly increased breast cancer risk as compared to those in the lowest mtDNA copy number tertile (odds ratio (95% confidence interval): 1.84 (0.93-3.64) and 2.13 (1.09-4.17) respectively; p for trend = 0.03). There was no association between mtDNA copy number and breast cancer risk among women who donated a blood sample ≥ 3 years before breast cancer diagnosis (p for trend = 0.73). This study supports a prospective association between increased mtDNA copy number and breast cancer risk that is dependent on the time interval between blood collection and breast cancer diagnosis. Citation Format: Bharat Thyagarajan, Renwei Wang, Helene Barcelo, Heather Nelson, Woon Puay Koh, Jian Min Yuan. Mitochondrial DNA copy number is prospectively associated with breast cancer risk. [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 1339. doi:10.1158/1538-7445.AM2013-1339
    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: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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