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Sei Hyun Ahn

Other affiliations: Asan Medical Center
Bio: Sei Hyun Ahn is an academic researcher from University of Ulsan. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 45, co-authored 351 publications receiving 10064 citations. Previous affiliations of Sei Hyun Ahn include Asan Medical Center.


Papers
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Journal ArticleDOI
Douglas F. Easton1, Karen A. Pooley1, Alison M. Dunning1, Paul D.P. Pharoah1, Deborah J. Thompson1, Dennis G. Ballinger, Jeffery P. Struewing2, Jonathan J. Morrison1, Helen I. Field1, Robert Luben1, Nicholas J. Wareham1, Shahana Ahmed1, Catherine S. Healey1, Richard Bowman, Kerstin B. Meyer1, Christopher A. Haiman3, Laurence K. Kolonel, Brian E. Henderson3, Loic Le Marchand, Paul Brennan4, Suleeporn Sangrajrang, Valerie Gaborieau4, Fabrice Odefrey4, Chen-Yang Shen5, Pei-Ei Wu5, Hui-Chun Wang5, Diana Eccles6, D. Gareth Evans7, Julian Peto8, Olivia Fletcher9, Nichola Johnson9, Sheila Seal, Michael R. Stratton10, Nazneen Rahman, Georgia Chenevix-Trench11, Georgia Chenevix-Trench12, Stig E. Bojesen13, Børge G. Nordestgaard13, C K Axelsson13, Montserrat Garcia-Closas2, Louise A. Brinton2, Stephen J. Chanock2, Jolanta Lissowska14, Beata Peplonska15, Heli Nevanlinna16, Rainer Fagerholm16, H Eerola16, Daehee Kang17, Keun-Young Yoo17, Dong-Young Noh17, Sei Hyun Ahn18, David J. Hunter19, Susan E. Hankinson19, David G. Cox19, Per Hall20, Sara Wedrén20, Jianjun Liu21, Yen-Ling Low21, Natalia Bogdanova22, Peter Schu¨rmann22, Do¨rk Do¨rk22, Rob A. E. M. Tollenaar23, Catharina E. Jacobi23, Peter Devilee23, Jan G. M. Klijn24, Alice J. Sigurdson2, Michele M. Doody2, Bruce H. Alexander25, Jinghui Zhang2, Angela Cox26, Ian W. Brock26, Gordon MacPherson26, Malcolm W.R. Reed26, Fergus J. Couch27, Ellen L. Goode27, Janet E. Olson27, Hanne Meijers-Heijboer24, Hanne Meijers-Heijboer28, Ans M.W. van den Ouweland24, André G. Uitterlinden24, Fernando Rivadeneira24, Roger L. Milne29, Gloria Ribas29, Anna González-Neira29, Javier Benitez29, John L. Hopper30, Margaret R. E. McCredie31, Margaret R. E. McCredie32, Margaret R. E. McCredie12, Melissa C. Southey12, Melissa C. Southey30, Graham G. Giles33, Chris Schroen30, Christina Justenhoven34, Christina Justenhoven35, Hiltrud Brauch35, Hiltrud Brauch34, Ute Hamann36, Yon-Dschun Ko, Amanda B. Spurdle11, Jonathan Beesley11, Xiaoqing Chen11, _ kConFab37, Arto Mannermaa37, Veli-Matti Kosma37, Vesa Kataja37, Jaana M. Hartikainen37, Nicholas E. Day1, David Cox, Bruce A.J. Ponder1 
28 Jun 2007-Nature
TL;DR: To identify further susceptibility alleles, a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls was conducted, followed by a third stage in which 30 single nucleotide polymorphisms were tested for confirmation.
Abstract: Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r2.0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P,1027). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P,0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach.

2,288 citations

Journal ArticleDOI
Angela Cox1, Alison M. Dunning2, Montserrat Garcia-Closas3, Sabapathy P. Balasubramanian1, Malcolm W.R. Reed1, Karen A. Pooley2, Serena Scollen2, Caroline Baynes2, Bruce A.J. Ponder2, Stephen J. Chanock3, Jolanta Lissowska4, Louise A. Brinton3, Beata Peplonska5, Melissa C. Southey6, John L. Hopper6, Margaret R. E. McCredie7, Graham G. Giles8, Olivia Fletcher9, Nichola Johnson9, Isabel dos Santos Silva9, Lorna Gibson9, Stig E. Bojesen10, Børge G. Nordestgaard10, C K Axelsson10, Diana Torres11, Ute Hamann11, Christina Justenhoven12, Christina Justenhoven13, Hiltrud Brauch12, Hiltrud Brauch13, Jenny Chang-Claude11, Silke Kropp11, Angela Risch11, Shan Wang-Gohrke14, Peter Schürmann15, Natalia Bogdanova15, Thilo Dörk15, Rainer Fagerholm16, Kirsimari Aaltonen16, Carl Blomqvist16, Heli Nevanlinna16, Sheila Seal, Anthony Renwick, Michael R. Stratton, Nazneen Rahman, Suleeporn Sangrajrang, David J. Hughes17, Fabrice Odefrey17, Paul Brennan17, Amanda B. Spurdle18, Georgia Chenevix-Trench18, Jonathan Beesley18, Arto Mannermaa19, Jaana M. Hartikainen19, Vesa Kataja19, Veli-Matti Kosma19, Fergus J. Couch20, Janet E. Olson20, Ellen L. Goode20, Annegien Broeks21, Marjanka K. Schmidt21, Frans B. L. Hogervorst21, Laura J. van't Veer21, Daehee Kang22, Keun-Young Yoo22, Dong Young Noh22, Sei Hyun Ahn23, Sara Wedrén24, Per Hall24, Yen-Ling Low25, Jianjun Liu25, Roger L. Milne26, Gloria Ribas26, Anna González-Neira26, Javier Benitez26, Alice J. Sigurdson27, Alice J. Sigurdson3, Denise L. Stredrick27, Denise L. Stredrick3, Bruce H. Alexander27, Bruce H. Alexander3, Jeffery P. Struewing27, Jeffery P. Struewing3, Paul D.P. Pharoah2, Douglas F. Easton2 
TL;DR: It is demonstrated that common breast cancer susceptibility alleles with small effects on risk can be identified, given sufficiently powerful studies, as well as the need for further studies to confirm putative genetic associations with breast cancer.
Abstract: The Breast Cancer Association Consortium (BCAC) has been established to conduct combined case-control analyses with augmented statistical power to try to confirm putative genetic associations with breast cancer. We genotyped nine SNPs for which there was some prior evidence of an association with breast cancer: CASP8 D302H (rs1045485), IGFBP3 -202 C --> A (rs2854744), SOD2 V16A (rs1799725), TGFB1 L10P (rs1982073), ATM S49C (rs1800054), ADH1B 3' UTR A --> G (rs1042026), CDKN1A S31R (rs1801270), ICAM5 V301I (rs1056538) and NUMA1 A794G (rs3750913). We included data from 9-15 studies, comprising 11,391-18,290 cases and 14,753-22,670 controls. We found evidence of an association with breast cancer for CASP8 D302H (with odds ratios (OR) of 0.89 (95% confidence interval (c.i.): 0.85-0.94) and 0.74 (95% c.i.: 0.62-0.87) for heterozygotes and rare homozygotes, respectively, compared with common homozygotes; P(trend) = 1.1 x 10(-7)) and weaker evidence for TGFB1 L10P (OR = 1.07 (95% c.i.: 1.02-1.13) and 1.16 (95% c.i.: 1.08-1.25), respectively; P(trend) = 2.8 x 10(-5)). These results demonstrate that common breast cancer susceptibility alleles with small effects on risk can be identified, given sufficiently powerful studies.

567 citations

Journal ArticleDOI
TL;DR: Tissue microarray analysis of basal cytokeratins and luminal CK and epidermal growth factor receptor, c-kit, hormone receptors (HRs), p53, and Her2/neu in 776 consecutive patients diagnosed with invasive breast carcinoma reveals that the Her2-neu status is the most important prognostic factor of breast cancers.

343 citations

Journal ArticleDOI
TL;DR: Younger patients (age < 35) showed worse prognosis than older patients ( age, 35 to 50 years) only in the hormone receptor-unknown or hormone receptors-positive subgroups, and adjuvant tamoxifen therapy might provide less survival benefit when added to chemotherapy in very young breast cancer patients.
Abstract: Purpose Breast cancer in very young women (age < 35 years) is uncommon and poorly understood. We sought to evaluate the prognosis and treatment response of these patients compared with women ages 35 to 50 years. Patients and Methods We analyzed data from 9,885 breast cancer patients age ≤ 50 years who were part of the Korean Breast Cancer Society registration program between 1992 and 2001. The overall survival (OS) and breast cancer-specific survival (BCSS) were compared between age groups. Results One thousand four hundred forty-four patients (14.6%) were younger than age 35 and 8,441 (85.4%) patients were between 35 and 50 years of age. Younger patients had significantly higher T-stage and higher lymph node positivity and lower hormone receptor expression than older patients. Younger patients had a greater probability of death than older patients, regardless of tumor size or lymph node status. The survival difference was significant for patients with positive or unknown hormone receptor status (P < .000...

219 citations

Journal ArticleDOI
TL;DR: This study provides strong evidence for a novel breast cancer susceptibility locus represented by rs9485372, near the TAB2 gene (6q25.1), and identifies two possible susceptibility loci located in the ESR1 gene and 11q24.3, respectively.
Abstract: 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-b activated kinase (TAB2) gene in chromosome 6q25.1, showed a consistent association with breast cancer risk across all four stages, with a P-value of 3.8610 212 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 (P=1.9610 26 from the combined analysis of all samples), located in intron 5 of the ESR1 gene, and SNP rs7107217 (P=4.6610 27 ), 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 TAB2 gene (6q25.1), and identifies two possible susceptibility loci located in the ESR1 gene and 11q24.3, respectively.

157 citations


Cited by
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TL;DR: The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors.
Abstract: The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors. While the organization of the book is similar to previous editions, major emphasis has been placed on disorders that affect multiple organ systems. Important advances in genetics, immunology, and oncology are emphasized. Many chapters of the book have been rewritten and describe major advances in internal medicine. Subjects that received only a paragraph or two of attention in previous editions are now covered in entire chapters. Among the chapters that have been extensively revised are the chapters on infections in the compromised host, on skin rashes in infections, on many of the viral infections, including cytomegalovirus and Epstein-Barr virus, on sexually transmitted diseases, on diabetes mellitus, on disorders of bone and mineral metabolism, and on lymphadenopathy and splenomegaly. The major revisions in these chapters and many

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TL;DR: This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process and the role of enzymatic and non-enzymatic antioxidants in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors.

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Journal ArticleDOI
21 Jul 1979-BMJ
TL;DR: It is suggested that if assessment of overdoses were left to house doctors there would be an increase in admissions to psychiatric units, outpatients, and referrals to social services, but for house doctors to assess overdoses would provide no economy for the psychiatric or social services.
Abstract: admission. This proportion could already be greater in some parts of the country and may increase if referrals of cases of self-poisoning increase faster than the facilities for their assessment and management. The provision of social work and psychiatric expertise in casualty departments may be one means of preventing unnecessary medical admissions without risk to the patients. Dr Blake's and Dr Bramble's figures do not demonstrate, however, that any advantage would attach to medical teams taking over assessment from psychiatrists except that, by implication, assessments would be completed sooner by staff working on the ward full time. What the figures actually suggest is that if assessment of overdoses were left to house doctors there would be an increase in admissions to psychiatric units (by 19°U), outpatients (by 5O°'), and referrals to social services (by 140o). So for house doctors to assess overdoses would provide no economy for the psychiatric or social services. The study does not tell us what the consequences would have been for the six patients who the psychiatrists would have admitted but to whom the house doctors would have offered outpatient appointments. E J SALTER

4,497 citations

Journal ArticleDOI
TL;DR: This Review highlights the knowledge gained, defines areas of emerging consensus, and describes the challenges that remain as researchers seek to obtain more complete descriptions of the susceptibility architecture of biomedical traits of interest and to translate the information gathered into improvements in clinical management.
Abstract: The past year has witnessed substantial advances in understanding the genetic basis of many common phenotypes of biomedical importance. These advances have been the result of systematic, well-powered, genome-wide surveys exploring the relationships between common sequence variation and disease predisposition. This approach has revealed over 50 disease-susceptibility loci and has provided insights into the allelic architecture of multifactorial traits. At the same time, much has been learned about the successful prosecution of association studies on such a scale. This Review highlights the knowledge gained, defines areas of emerging consensus, and describes the challenges that remain as researchers seek to obtain more complete descriptions of the susceptibility architecture of biomedical traits of interest and to translate the information gathered into improvements in clinical management.

2,908 citations