Polymorphisms in Inflammation Pathway Genes and Endometrial Cancer Risk

被引：28

作者：

Delahanty, Ryan J. ^{[1
,2
]}

Xiang, Yong-Bing ^{[3
]}

Spurdle, Amanda ^{[5
]}

Beeghly-Fadiel, Alicia ^{[1
,2
]}

Long, Jirong ^{[1
,2
]}

Thompson, Deborah ^{[7
]}

Tomlinson, Ian ^{[8
,9
]}

Yu, Herbert ^{[10
]}

Lambrechts, Diether ^{[11
]}

Doerk, Thilo ^{[12
]}

Goodman, Marc T. ^{[13
]}

Zheng, Ying ^{[4
]}

Salvesen, Helga B. ^{[14
,15
]}

Bao, Ping-Ping ^{[4
]}

Amant, Frederic ^{[11
]}

Beckmann, Matthias W. ^{[16
]}

Coenegrachts, Lieve ^{[11
]}

Coosemans, An ^{[11
]}

Dubrowinskaja, Natalia ^{[12
]}

Dunning, Alison ^{[8
,9
]}

Runnebaum, Ingo B. ^{[18
]}

Easton, Douglas ^{[7
]}

Ekici, Arif B. ^{[17
]}

Fasching, Peter A. ^{[17
,19
]}

Halle, Mari K. ^{[14
,15
]}

Hein, Alexander ^{[16
]}

Howarth, Kimberly ^{[8
,9
]}

Gorman, Maggie ^{[8
,9
]}

Kaydarova, Dylyara ^{[20
]}

Krakstad, Camilla ^{[14
,15
]}

Lose, Felicity ^{[5
]}

Lu, Lingeng ^{[10
]}

Lurie, Galina ^{[13
]}

O'Mara, Tracy ^{[5
,6
]}

Matsuno, Rayna K. ^{[13
]}

Pharoah, Paul ^{[7
]}

Risch, Harvey ^{[10
]}

Corssen, Madeleine ^{[12
]}

Trovik, Jone ^{[14
,15
]}

Turmanov, Nurzhan ^{[12
]}

Wen, Wanqing ^{[1
,2
]}

Lu, Wei ^{[4
]}

Cai, Qiuyin ^{[1
,2
]}

Zheng, Wei ^{[1
,2
]}

Shu, Xiao-Ou ^{[1
,2
]}

机构：

[1] Vanderbilt Univ, Sch Med, Div Epidemiol, Dept Med, Nashville, TN 37212 USA

[2] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Nashville, TN 37212 USA

[3] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China

[4] Shanghai Inst Prevent Med, Shanghai, Peoples R China

[5] Queensland Univ Technol, Queensland Inst Med Res, Div Genet & Populat Hlth, Brisbane, Qld 4001, Australia

[6] Queensland Univ Technol, Canc Program, Inst Hlth & Biomed Innovat, Brisbane, Qld 4001, Australia

[7] Univ Cambridge, Dept Oncol, Strangeways Res Lab, Cambridge CB2 1TN, England

[8] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England

[9] Univ Oxford, NIHR Comprehens Biomed Res Ctr, Oxford, England

[10] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, Yale Canc Ctr, New Haven, CT 06510 USA

[11] Katholieke Univ Leuven, Div Gynaecol Oncol, Louvain, Belgium

[12] Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany

[13] Univ Hawaii, Ctr Canc, Epidemiol Program, Honolulu, HI 96822 USA

[14] Haukeland Hosp, Dept Obstet & Gynecol, N-5021 Bergen, Norway

[15] Univ Bergen, Dept Clin Med, Bergen, Norway

[16] Univ Erlangen Nurnberg, Dept Gynecol & Obstet, Univ Hosp Erlangen, Comprehens Canc Ctr Erlangen Nuremberg, D-91054 Erlangen, Germany

[17] Univ Erlangen Nurnberg, Inst Human Genet, D-91054 Erlangen, Germany

[18] Jena Univ Hosp, Dept Gynecol, Jena, Germany

[19] Univ Calif Los Angeles, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90024 USA

[20] State Oncol Inst, Almaty Oncol Ctr, Alma Ata, Kazakhstan

来源：

CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION | 2013年 / 22卷 / 02期

基金：

英国医学研究理事会; 英国惠康基金;

关键词：

GENOME-WIDE ASSOCIATION; BREAST-CANCER; SUSCEPTIBILITY LOCUS; REPRODUCTIVE FACTORS; EXPRESSION; OVARIAN; CELLS; METAANALYSIS; ACTIVATION; CARCINOMA;

D O I：

10.1158/1055-9965.EPI-12-0903

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Background: Experimental and epidemiologic evidence have suggested that chronic inflammation may play a critical role in endometrial carcinogenesis. Methods: To investigate this hypothesis, a two-stage study was carried out to evaluate single-nucleotide polymorphisms (SNP) in inflammatory pathway genes in association with endometrial cancer risk. In stage I, 64 candidate pathway genes were identified and 4,542 directly genotyped or imputed SNPs were analyzed among 832 endometrial cancer cases and 2,049 controls, using data from the Shanghai Endometrial Cancer Genetics Study. Linkage disequilibrium of stage I SNPs significantly associated with endometrial cancer (P < 0.05) indicated that the majority of associations could be linked to one of 24 distinct loci. One SNP from each of the 24 loci was then selected for follow-up genotyping. Of these, 21 SNPs were successfully designed and genotyped in stage II, which consisted of 10 additional studies including 6,604 endometrial cancer cases and 8,511 controls. Results: Five of the 21 SNPs had significant allelic odds ratios (ORs) and 95% confidence intervals (CI) as follows: FABP1, 0.92 (0.85-0.99); CXCL3, 1.16 (1.05-1.29); IL6, 1.08 (1.00-1.17); MSR1, 0.90 (0.82-0.98); and MMP9, 0.91 (0.87-0.97). Two of these polymorphisms were independently significant in the replication sample (rs352038 in CXCL3 and rs3918249 in MMP9). The association for the MMP9 polymorphism remained significant after Bonferroni correction and showed a significant association with endometrial cancer in both Asian- and European-ancestry samples. Conclusions: These findings lend support to the hypothesis that genetic polymorphisms in genes involved in the inflammatory pathway may contribute to genetic susceptibility to endometrial cancer. Impact statement: This study adds to the growing evidence that inflammation plays an important role in endometrial carcinogenesis. Cancer Epidemiol Biomarkers Prev; 22(2); 216-23. (c) 2012 AACR.

引用

页码：216 / 223

页数：8

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