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Articles by E. L Goode
Total Records ( 2 ) for E. L Goode
  L. E Kelemen , X Wang , Z. S Fredericksen , V. S Pankratz , P. D.P Pharoah , S Ahmed , A. M Dunning , D. F Easton , R. A Vierkant , J. R Cerhan , E. L Goode , J. E Olson and F. J. Couch
 

Background: Gene amplification leading to overexpression is a common event in breast tumors that is linked to tumor development and progression. The 17q23 region is amplified in >40% of breast tumors and contains several candidate oncogenes. Because common genetic variation in several oncogenes has been associated with cancer risk, we assessed the relevance of common variants in the 17q23 candidate oncogenes to breast cancer.

Methods: We investigated 60 polymorphisms in the TUBD1, SEPT4, PRKCA, TBX2, TBX4, TEX14, TLK2, YPEL2, and PPM1E genes from this amplicon for association with breast cancer risk among 798 Caucasian breast cancer cases and 843 unaffected Caucasian controls from the Mayo Clinic.

Results: Eight polymorphisms in PRKCA, TBX4, TLK2, and YPEL2 displayed significant dose-response associations with breast cancer risk (Ptrend < 0.05). Of these, PRKCA rs7342847 and TLK2 rs2245092 and rs733025 were also associated with hormone receptor–positive breast cancer: PRKCA rs7342847 (odds ratio, 0.7; 95% confidence interval, 0.6-0.9; Ptrend = 0.002) and TLK2 rs733025 and rs2245092 (both: odds ratio, 0.8; 95% confidence interval, 0.7-1.0; Ptrend = 0.03). Interactions between SEPT4 rs758377 and TEX14 rs302864 (Pinteraction = 0.0003) and between TLK2 rs733025 and YPEL2 rs16943468 (Pinteraction = 0.05) for risk of breast cancer were also observed.

Conclusion: These findings suggest that single polymorphisms and combinations of polymorphisms within candidate oncogenes from the 17q23 amplicon may influence risk of breast cancer overall and possibly specific molecular subtypes of breast tumors. The findings are discussed within the context of the results from two independent data sets. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1864–8)

  H Song , S. J Ramus , S. K Kjaer , R. A DiCioccio , G Chenevix Trench , C. L Pearce , E Hogdall , A. S Whittemore , V McGuire , C Hogdall , J Blaakaer , A. H Wu , D. J Van Den Berg , D. O Stram , U Menon , A Gentry Maharaj , I. J Jacobs , P. M Webb , J Beesley , X Chen , The Australian Ovarian Cancer Study Group the Australian Cancer (Ovarian) Study , J. A Doherty , J Chang Claude , S Wang Gohrke , M. T Goodman , G Lurie , P. J Thompson , M. E Carney , R. B Ness , K Moysich , E. L Goode , R. A Vierkant , J. M Cunningham , S Anderson , J. M Schildkraut , A Berchuck , E. S Iversen , P. G Moorman , M Garcia Closas , S Chanock , J Lissowska , L Brinton , H Anton Culver , A Ziogas , W. R Brewster , B. A.J Ponder , D. F Easton , S. A Gayther , P. D.P Pharoah and on behalf of the Ovarian Cancer Association Consortium (OCAC)
 

Because both ovarian and breast cancer are hormone-related and are known to have some predisposition genes in common, we evaluated 11 of the most significant hits (six with confirmed associations with breast cancer) from the breast cancer genome-wide association study for association with invasive ovarian cancer. Eleven SNPs were initially genotyped in 2927 invasive ovarian cancer cases and 4143 controls from six ovarian cancer case–control studies. Genotype frequencies in cases and controls were compared using a likelihood ratio test in a logistic regression model stratified by study. Initially, three SNPs (rs2107425 in MRPL23, rs7313833 in PTHLH, rs3803662 in TNRC9) were weakly associated with ovarian cancer risk and one SNP (rs4954956 in NXPH2) was associated with serous ovarian cancer in non-Hispanic white subjects (P-trend < 0.1). These four SNPs were then genotyped in an additional 4060 cases and 6308 controls from eight independent studies. Only rs4954956 was significantly associated with ovarian cancer risk both in the replication study and in combined analyses. This association was stronger for the serous histological subtype [per minor allele odds ratio (OR) 1.07 95% CI 1.01–1.13, P-trend = 0.02 for all types of ovarian cancer and OR 1.14 95% CI 1.07–1.22, P-trend = 0.00017 for serous ovarian cancer]. In conclusion, we found that rs4954956 was associated with increased ovarian cancer risk, particularly for serous ovarian cancer. However, none of the six confirmed breast cancer susceptibility variants we tested was associated with ovarian cancer risk. Further work will be needed to identify the causal variant associated with rs4954956 or elucidate its function.

 
 
 
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