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Genome-Wide Association Study in East Asians Identifies Novel Susceptibility Loci for Breast Cancer
Long, Jirong,Cai, Qiuyin,Sung, Hyuna,Shi, Jiajun,Zhang, Ben,Choi, Ji-Yeob,Wen, Wanqing,Delahanty, Ryan J.,Lu, Wei,Gao, Yu-Tang,Shen, Hongbing,Park, Sue K.,Chen, Kexin,Shen, Chen-Yang,Ren, Zefang,Haima Public Library of Science 2012 PLoS genetics Vol.8 No.2
<P>Genetic factors play an important role in the etiology of both sporadic and familial breast cancer. We aimed to discover novel genetic susceptibility loci for breast cancer. We conducted a four-stage genome-wide association study (GWAS) in 19,091 cases and 20,606 controls of East-Asian descent including Chinese, Korean, and Japanese women. After analyzing 690,947 SNPs in 2,918 cases and 2,324 controls, we evaluated 5,365 SNPs for replication in 3,972 cases and 3,852 controls. Ninety-four SNPs were further evaluated in 5,203 cases and 5,138 controls, and finally the top 22 SNPs were investigated in up to 17,423 additional subjects (7,489 cases and 9,934 controls). SNP rs9485372, near the TGF-β activated kinase (<I>TAB2</I>) gene in chromosome 6q25.1, showed a consistent association with breast cancer risk across all four stages, with a <I>P</I>-value of 3.8×10<SUP>−12</SUP> in the combined analysis of all samples. Adjusted odds ratios (95% confidence intervals) were 0.89 (0.85–0.94) and 0.80 (0.75–0.86) for the A/G and A/A genotypes, respectively, compared with the genotype G/G. SNP rs9383951 (<I>P</I> = 1.9×10<SUP>−6</SUP> from the combined analysis of all samples), located in intron 5 of the <I>ESR1</I> gene, and SNP rs7107217 (<I>P</I> = 4.6×10<SUP>−7</SUP>), located at 11q24.3, also showed a consistent association in each of the four stages. This study provides strong evidence for a novel breast cancer susceptibility locus represented by rs9485372, near the <I>TAB2</I> gene (6q25.1), and identifies two possible susceptibility loci located in the <I>ESR1</I> gene and 11q24.3, respectively.</P><P><B>Author Summary</B></P> <P>Breast cancer is one of the most common malignancies among women worldwide. Genetic factors play an important role in the etiology of breast cancer. To identify common genetic susceptibility alleles for breast cancer, we performed a four-stage genome-wide association study in 19,091 cases and 20,606 controls among East-Asian women. Single nucleotide polymorphism (SNP) rs9485372, near the TGF-beta activated kinase 1 (<I>TAB2</I>) gene at chromosome 6q25.1, was associated with breast cancer risk (<I>P</I> = 3.8×10<SUP>−12</SUP>). SNPs rs9383951, located in intron 5 of the estrogen receptor 1 (<I>ESR1</I>) gene, and rs7107217, located at 11q24.3, were also consistently associated with breast cancer risk in all four stages with a combined <I>P</I> of 1.9×10<SUP>−6</SUP> and 4.6×10<SUP>−7</SUP>, respectively. This study provides strong evidence for a novel breast cancer susceptibility locus represented by rs9485372, near the <I>TAB2</I> gene (6q25.1), and identifies two possible susceptibility loci located in the <I>ESR1</I> gene and 11q24.3, respectively.</P>
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Zheng, Wei,Zhang, Ben,Cai, Qiuyin,Sung, Hyuna,Michailidou, Kyriaki,Shi, Jiajun,Choi, Ji-Yeob,Long, Jirong,Dennis, Joe,Humphreys, Manjeet K.,Wang, Qin,Lu, Wei,Gao, Yu-Tang,Li, Chun,Cai, Hui,Park, Sue K Oxford University Press 2013 Human Molecular Genetics Vol.22 No.12
<P>In a consortium including 23 637 breast cancer patients and 25 579 controls of East Asian ancestry, we investigated 70 single-nucleotide polymorphisms (SNPs) in 67 independent breast cancer susceptibility loci recently identified by genome-wide association studies (GWASs) conducted primarily in European-ancestry populations. SNPs in 31 loci showed an association with breast cancer risk at <I>P</I> < 0.05 in a direction consistent with that reported previously. Twenty-one of them remained statistically significant after adjusting for multiple comparisons with the Bonferroni-corrected significance level of <0.0015. Eight of the 70 SNPs showed a significantly different association with breast cancer risk by estrogen receptor (ER) status at <I>P</I> < 0.05. With the exception of rs2046210 at 6q25.1, the seven other SNPs showed a stronger association with ER-positive than ER-negative cancer. This study replicated all five genetic risk variants initially identified in Asians and provided evidence for associations of breast cancer risk in the East Asian population with nearly half of the genetic risk variants initially reported in GWASs conducted in European descendants. Taken together, these common genetic risk variants explain ∼10% of excess familial risk of breast cancer in Asian populations.</P>
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Han, Mi-Ryung,Zheng, Wei,Cai, Qiuyin,Gao, Yu-Tang,Zheng, Ying,Bolla, Manjeet K.,Michailidou, Kyriaki,Dennis, Joe,Wang, Qin,Dunning, Alison M.,Brennan, Paul,Chen, Shou-Tung,Choi, Ji-Yeob,Hartman, Mikae Oxford University Press 2017 Carcinogenesis Vol.38 No.5
<P>Over the past 20 years, high-penetrance pathogenic mutations in genes BRCA1, BRCA2, TP53, PTEN, STK11 and CDH1 and moderate-penetrance mutations in genes CHEK2, ATM, BRIP1, PALB2, RAD51C, RAD50 and NBN have been identified for breast cancer. In this study, we investigated whether there are additional variants in these 13 genes associated with breast cancer among women of Asian ancestry. We analyzed up to 654 single nucleotide polymorphisms (SNPs) from 6269 cases and 6624 controls of Asian descent included in the Breast Cancer Association Consortium (BCAC), and up to 236 SNPs from 5794 cases and 5529 controls included in the Shanghai Breast Cancer Genetics Study (SBCGS). We found three missense variants with minor allele frequency (MAF) < 0.05: rs80358978 (Gly2508Ser), rs80359065 (Lys2729Asn) and rs11571653 (Met784Val) in the BRCA2 gene, showing statistically significant associations with breast cancer risk, with P-values of 1.2 x 10(-4), 1.0 x 10(-3) and 5.0 x 10(-3), respectively. In addition, we found four low-frequency variants (rs8176085, rs799923, rs8176173 and rs8176258) in the BRCA1 gene, one common variant in the CHEK2 gene (rs9620817), and one common variant in the PALB2 gene (rs13330119) associated with breast cancer risk at P < 0.01. Our study identified several new risk variants in BRCA1, BRCA2, CHEK2, and PALB2 genes in relation to breast cancer risk in Asian women. These results provide further insights that, in addition to the high/moderate penetrance mutations, other low-penetrance variants in these genes may also contribute to breast cancer risk.</P>
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Shin, Aesun,Shrubsole, Martha J,Rice, Jeffrey M,Cai, Qiuyin,Doll, Mark A,Long, Jirong,Smalley, Walter E,Shyr, Yu,Sinha, Rashmi,Ness, Reid M,Hein, David W,Zheng, Wei American Association for Cancer Research 2008 Cancer Epidemiology, Biomarkers & Prevention Vol.17 No.2
<P>Most colorectal cancers arise from adenomatous polyps or certain hyperplastic polyps. Only a few studies have investigated potential genetic modifiers of the associations between meat intake and polyp risk, and results are inconsistent. Using data from the Tennessee Colorectal Polyp Study, a large colonoscopy-based study, including 1,002 polyp cases (557 adenoma only, 250 hyperplastic polyp only, 195 both polyps) and 1,493 polyp-free patients, we evaluated the association of colorectal polyp risk with carcinogen exposure from meat and genetic polymorphisms in enzymes involved in heterocyclic amine (HCA) metabolism, including N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2), cytochrome P450 1A2 (CYP1A2), and aryl hydrocarbon receptor (AhR). Data on intake levels of meats by preparation methods, doneness preferences, and other lifestyle factors were obtained. Fourteen single nucleotide polymorphisms in the AhR, CYP1A2, NAT1, and NAT2 genes were evaluated. No clear association was found for any polymorphisms with polyp risk. However, apparent interactions were found for intake of meat and HCAs with AhR, NAT1, and NAT2 genotypes, and the interactions were statistically significant for the group with both adenomatous and hyperplastic polyps. Dose-response relationships with meat or HCA intake were found only among those with the AhR GA/AA (rs2066853) genotype, NAT1 rapid, or NAT2 rapid/intermediate acetylators but not among those with other genotypes of these genes. This dose-response relationship was more evident among those with both AhR GA/AA and the NAT1 rapid acetylator than those without this genotype combination. These results provide strong evidence for a modifying effect of metabolizing genes on the association of meat intake and HCA exposure with colorectal polyp risk.</P>
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Lu, Yingchang,Kweon, Sun-Seog,Tanikawa, Chizu,Jia, Wei-Hua,Xiang, Yong-Bing,Cai, Qiuyin,Zeng, Chenjie,Schmit, Stephanie L.,Shin, Aesun,Matsuo, Keitaro,Jee, Sun Ha,Kim, Dong-Hyun,Kim, Jeongseon,Wen, Wa Elsevier 2019 Gastroenterology Vol.156 No.5
<P><B>Background & Aims</B></P> <P>Genome-wide association studies (GWASs) have associated approximately 50 loci with risk of colorectal cancer (CRC)—nearly one third of these loci were initially associated with CRC in studies conducted in East Asian populations. We conducted a GWAS of East Asians to identify CRC risk loci and evaluate the generalizability of findings from GWASs of European populations to Asian populations.</P> <P><B>Methods</B></P> <P>We analyzed genetic data from 22,775 patients with CRC (cases) and 47,731 individuals without cancer (controls) from 14 studies in the Asia Colorectal Cancer Consortium. First, we performed a meta-analysis of 7 GWASs (10,625 cases and 34,595 controls) and identified 46,554 promising risk variants for replication by adding them to the Multi-Ethnic Global Array (MEGA) for genotype analysis in 6445 cases and 7175 controls. These data were analyzed, along with data from an additional 5705 cases and 5961 controls genotyped using the OncoArray. We also obtained data from 57,976 cases and 67,242 controls of European descent. Variants at identified risk loci were functionally annotated and evaluated in correlation with gene expression levels.</P> <P><B>Results</B></P> <P>A meta-analyses of all samples from people of Asian descent identified 13 loci and 1 new variant at a known locus (10q24.2) associated with risk of CRC at the genome-wide significance level of <I>P</I> < 5 × 10<SUP>–8</SUP>. We did not perform experiments to replicate these associations in additional individuals of Asian ancestry. However, the lead risk variant in 6 of these loci was also significantly associated with risk of CRC in European descendants. A strong association (44%–75% increase in risk per allele) was found for 2 low-frequency variants: rs201395236 at 1q44 (minor allele frequency, 1.34%) and rs77969132 at 12p11.21 (minor allele frequency, 1.53%). For 8 of the 13 associated loci, the variants with the highest levels of significant association were located inside or near the protein-coding genes <I>L1TD1</I>, <I>EFCAB2</I>, <I>PPP1R21</I>, <I>SLCO2A1</I>, <I>HLA-G</I>, <I>NOTCH4</I>, <I>DENND5B</I>, and <I>GNAS</I>. For other intergenic loci, we provided evidence for the possible involvement of the genes <I>ALDH7A1</I>, <I>PRICKLE1</I>, <I>KLF5</I>, <I>WWOX</I>, and <I>GLP2R</I>. We replicated findings for 41 of 52 previously reported risk loci.</P> <P><B>Conclusions</B></P> <P>We showed that most of the risk loci previously associated with CRC risk in individuals of European descent were also associated with CRC risk in East Asians. Furthermore, we identified 13 loci significantly associated with risk for CRC in Asians. Many of these loci contained genes that regulate the immune response, Wnt signaling to β-catenin, prostaglandin E2 catabolism, and cell pluripotency and proliferation. Further analyses of these genes and their variants is warranted, particularly for the 8 loci for which the lead CRC risk variants were not replicated in persons of European descent.</P>
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Wu, Ying,Gao, He,Li, Huaixing,Tabara, Yasuharu,Nakatochi, Masahiro,Chiu, Yen-Feng,Park, Eun Jung,Wen, Wanqing,Adair, Linda S.,Borja, Judith B.,Cai, Qiuyin,Chang, Yi-Cheng,Chen, Peng,Croteau-Chonka, Da Oxford University Press 2014 Human Molecular Genetics Vol.23 No.4
<P>Blood levels of adiponectin, an adipocyte-secreted protein correlated with metabolic and cardiovascular risks, are highly heritable. Genome-wide association (GWA) studies for adiponectin levels have identified 14 loci harboring variants associated with blood levels of adiponectin. To identify novel adiponectin-associated loci, particularly those of importance in East Asians, we conducted a meta-analysis of GWA studies for adiponectin in 7827 individuals, followed by two stages of replications in 4298 and 5954 additional individuals. We identified a novel adiponectin-associated locus on chromosome 10 near <I>WDR11-FGFR2</I> (<I>P</I> = 3.0 × 10<SUP>−14</SUP>) and provided suggestive evidence for a locus on chromosome 12 near <I>OR8S1-LALBA</I> (<I>P</I> = 1.2 × 10<SUP>−7</SUP>). Of the adiponectin-associated loci previously described, we confirmed the association at <I>CDH13</I> (<I>P</I> = 6.8 × 10<SUP>−165</SUP>), <I>ADIPOQ</I> (<I>P</I> = 1.8 × 10<SUP>−22</SUP>), <I>PEPD</I> (<I>P</I> = 3.6 × 10<SUP>−12</SUP>), <I>CMIP</I> (<I>P</I> = 2.1 × 10<SUP>−10</SUP>), <I>ZNF664</I> (<I>P</I> = 2.3 × 10<SUP>−7</SUP>) and <I>GPR109A</I> (<I>P</I> = 7.4 × 10<SUP>−6</SUP>). Conditional analysis at <I>ADIPOQ</I> revealed a second signal with suggestive evidence of association only after conditioning on the lead SNP (<I>P</I><SUB>initial</SUB> = 0.020; <I>P</I><SUB>conditional</SUB> = 7.0 × 10<SUP>−7</SUP>). We further confirmed the independence of two pairs of closely located loci (<2 Mb) on chromosome 16 at <I>CMIP</I> and <I>CDH13</I>, and on chromosome 12 at <I>GPR109A</I> and <I>ZNF664</I>. In addition, the newly identified signal near <I>WDR11-FGFR2</I> exhibited evidence of association with triglycerides (<I>P</I> = 3.3 × 10<SUP>−4</SUP>), high density lipoprotein cholesterol (HDL-C, <I>P</I> = 4.9 × 10<SUP>−4</SUP>) and body mass index (BMI)-adjusted waist–hip ratio (<I>P</I> = 9.8 × 10<SUP>−3</SUP>). These findings improve our knowledge of the genetic basis of adiponectin variation, demonstrate the shared allelic architecture for adiponectin with lipids and central obesity and motivate further studies of underlying mechanisms.</P>
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