Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention AACR Conference on Molecular Diagnostics - 2008
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhu, Y.
Right arrow Articles by Wu, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhu, Y.
Right arrow Articles by Wu, X.
[Cancer Research 64, 2251-2257, March 15, 2004]
© 2004 American Association for Cancer Research

Regular Articles

An Evolutionary Perspective on Single-Nucleotide Polymorphism Screening in Molecular Cancer Epidemiology

Yong Zhu, Margaret R. Spitz, Christopher I. Amos, Jie Lin, Matthew B. Schabath and Xifeng Wu

Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas


   ABSTRACT
Top
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Given that there are millions of single-nucleotide polymorphisms (SNPs) in the entire human genome, a major difficulty faced by scientists in planning costly population-based genotyping is to choose target SNPs that are most likely to affect phenotypic functions and ultimately contribute to disease development. Although it is widely accepted that sequences with important functionality tend to be less variable across species because of selective pressure, to what extent evolutionary conservation is mirrored by epidemiological outcome has never been demonstrated. In this study, we surveyed odds ratios detected for 46 SNPs in 39 different cancer-related genes from 166 molecular epidemiological studies. The conservation levels of amino acid that these SNPs affected were calculated as a tolerance index by comparing sequences from different species. Our results provide evidence of a significant relationship between the detected odds ratios associated with cancer risk and the conservation levels of the SNP-affected amino acids (P = 0.002; R2 = 0.06). Tolerance indices were further calculated for 355 nonsynonymous SNPs identified in 90 human DNA repair genes, of which 103 caused amino acid changes in very conserved positions. Our findings support the concept that SNPs altering the conserved amino acids are more likely to be associated with cancer susceptibility. Using such a molecular evolutionary approach may hold great promise for prioritizing SNPs to be genotyped in future molecular epidemiological studies.


   INTRODUCTION
Top
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
In this post-genomic era, single-nucleotide polymorphisms (SNPs) are being intensively studied to understand the biological basis of complex traits and diseases. Besides numerous ongoing efforts to identify millions of these SNPs, there is now also a focus on studying associations between disease risk and these genetic variations using a molecular epidemiological approach. Indeed, it has been estimated that each person has about 24,000–40,000 nonsynonymous SNPs and that there are 100,000–300,000 nonsynonymous SNPs constituting about 1% of the total SNPs in the entire human genome (1) . This plethora of SNPs points out a major difficulty faced by scientists in planning costly population-based genotyping, which is to choose target SNPs that are most likely to affect phenotypic functions and ultimately contribute to disease development. Currently, most molecular epidemiological studies are focusing on SNPs located in coding and regulatory regions, yet many of these studies have been unable to detect significant associations between SNPs and disease susceptibility.

To develop a coherent approach for prioritizing SNP selection for genotyping in molecular epidemiological studies, we applied an evolutionary perspective to SNP screening in molecular epidemiological studies. We correlated findings from molecular epidemiological studies of cancer with the evolutionary conservation levels of nonsynonymous SNPs using a sequence homology-based tool. Our hypothesis was that amino acids conserved across species are more likely to be functionally significant; therefore, SNPs that change these amino acids might be more likely to be associated with cancer susceptibility.


   MATERIALS AND METHODS
Top
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
For this analysis, we used the keyword combinations "polymorphism + cancer" and "genotype + cancer" limited to the field of title/abstract to search the literature for epidemiological studies investigating SNPs in the PubMed database.1 The studies selected for our analysis had to meet the following criteria: (a) be case-control studies; (b) examine SNPs in the coding region and alterered amino acids; and (c) investigate the association between SNPs and cancer risk. We chose the overall adjusted odds ratio (OR) for the homozygous variant allele if ORs were reported for heterozygous and homozygous variant alleles separately in a study.

The conservation level of a particular position in a protein was determined by using a sequence homology-based tool, SIFT, which sorts intolerant from tolerant amino acid substitutions (2) . Briefly, SIFT searches for similar protein sequences from different species in the database, obtains the multiple alignments of these sequences, and then calculates from the alignment the tolerance index (from 0 to 1) for all possible substitutions at each position. The sequences in the alignment are restricted to those homologous sequences that are available in the protein database; therefore, the resulting alignment information is expected to vary from protein to protein. The higher a tolerance index, the less functional impact a particular amino acid substitution is likely to have. We then correlated the tolerance index of an amino acid change caused by a SNP to the overall OR of the corresponding variant genotype detected in molecular epidemiological studies of cancer. If a SNP had been found to be protective (OR < 1) in a study, we re-expressed the OR in terms of the risk genotypes (OR > 1) to facilitate the comparisons.

We also estimated tolerance indices for SNPs in human DNA repair and repair-related genes included in two popular databases2 that contain up-to-date SNP information for the DNA repair and repair-related genes being sequenced. The definition of conserved SNPs was based on the tolerance index, a score representing the normalized probability that the amino acid change is tolerated. SIFT predicts substitutions with scores of <0.05 as deleterious. However, we included SNPs with scores <= 0.1 in this study to provide more SNPs for exploration.

Spearman’s rank correlation coefficient was calculated to assess the correlation between ORs and tolerance indices. Linear regression analysis was performed to further quantify the relationship between these two variables. Because small studies tend to report larger OR due to publication bias, we applied weighted linear regression by specifying sample size as a weighting variable in the model. All statistical analyses were done using the SAS system (version 8.0). All tests were two-sided with a significance level of 0.05.


   RESULTS
Top
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
By using both keywords "polymorphism" and "cancer" limited to the field of title and abstract, we identified 3386 articles in the database from the literature search. A similar search using the keywords "genotype" and "cancer" gave us 1836 articles. Following the selection criteria, we chose 165 case-control studies and 1 cohort study with a nested case-control component on SNPs that resulted in amino acid changes in our analysis (Table 1)Citation . These studies examined a total of 46 SNPs in 39 different genes for risk estimates at 16 different cancer sites. All of these SNPs were located in cancer-related genes, such as those involved in DNA repair, metabolism, and cell cycle checkpoints.


View this table:
[in this window]
[in a new window]
  		Table 1 Single-nucleotide polymorphisms investigated in cancer case-control studies

 
There was considerable variation in sample sizes of these studies, ranging from 50 cases and 50 controls to 1534 cases and 1504 controls. The majority of these studies investigated SNPs in a specific ethnicity, including Asian, Caucasian, African American, Jewish, Brazilian, Portuguese, and Egyptian, whereas a few others included ethnically heterogeneous populations. The 16 cancer types included lung, esophageal, colon, breast, ovarian, head and neck, gastric, oral, prostate, endometrial, hepatocellular, stomach, cervical, bladder, skin, and non-Hodgkin’s lymphoma. The overall ORs retrieved from these studies were adjusted by different factors across studies. However, age and gender were the two most common factors adjusted, whereas smoking status was adjusted for in most of the smoking-related cancers. There are a variety of other confounding factors adjusted in some specific studies, such as family history of cancer, family income, menopausal status, and so forth.

Overall, there was a significant inverse correlation between the ORs and tolerance indices (Spearman rank correlation coefficient r = -0.247; P = 0.001). Further analysis revealed a significant linear regression relationship between these two variables with a regression coefficient of -0.763 (R2 = 0.06; P = 0.002). The OR showed a negative correlation with sample size (r = -0.27; P = 0.0004), which might be due to some publication bias in the studies, with the smaller studies having higher ORs. The OR was skewed, and log2 transformation resulted in an approximately normal distribution. Specifically, the skewness and kurtosis for ORs were 4.81 and 35.47 for the untransformed ORs, whereas skewness and kurtosis for the log-transformed ORs were 1.29 and 2.47, respectively. We therefore also performed linear regression analysis of the log-transformed ORs and tolerance index weighted by sample size, an approach that gives the most weight to the largest and therefore most reliable studies. One cohort study and one case-control study with an unspecified sample size were not included in the weighted regression analyses. Again, we found a highly significant result (regression coefficient = -0.448; R2 = 0.08; P = 0.0002). Moreover, the weighted mean ORs from different studies examining the same SNPs were calculated and correlated with the corresponding tolerance indices. This approach revealed similar results.

Fig. 1Citation shows the linear relationship between the log2 ORs and the tolerance index. When we included ethnicity as a covariate using three coding groups (white, Asian, and other), we found no significant effect of ethnicity and again highly significant correlation between log OR and the tolerance index.



View larger version (12K):
[in this window]
[in a new window]
  		Fig. 1. The relationship between cancer risk (log2-transformed odds ratios) and tolerance index. Symbols are scaled by sample size of the corresponding studies.

 
To apply our finding in prioritizing SNPs for future genotyping in molecular cancer epidemiological studies, we also estimated tolerance indices for SNPs in human DNA repair and repair-related genes. In 90 repair-related genes included in the above two SNP databases, we found 355 SNPs that caused amino acid changes. After calculating a tolerance index for each of them, we identified 103 conserved SNPs (with tolerance index <= 0.1; Table 2Citation ). After categorizing these genes by different repair pathways, we found 16 SNPs located in nucleotide excision repair genes, 26 located in base excision repair genes, 5 located in nonhomologous end-joining genes, 5 located in homologous recombination genes, 9 located in mismatch genes, 14 located in DNA polymerase genes, and 28 located in other genes involved in repair pathways.


View this table:
[in this window]
[in a new window]
  		Table 2 List of conserved single-nucleotide polymorphisms in DNA repair genes

 

   DISCUSSION
Top
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Information from interspecific alignments of homologous genes has long been recognized as an important factor for understanding contemporary deleterious genetic variation in human disease. Silent mutations are frequently observed and randomly distributed among species. In contrast, a certain fraction of amino acids in a given set of homologous genes is conserved even among distantly related species that diverged hundreds of millions of years ago. Variations that arose at such conserved positions have evidently been under strong selective constraints and eliminated from populations throughout long-term evolutionary history, suggesting critical roles for the existing invariant sequences in biological functions. In a recent study, SIFT was used to predict the damaging effects of SNPs in several human disease-related genes. The damaging effects of several SNPs in melanocyte-stimulating hormone receptor and methylenetetrahydrofolate reductase genes have been supported by evidence showing an association with human cancers (2) . Therefore, such information obtained from homologous sequence alignments may be used to predict amino acid residues in gene products that have a negative impact on protein function and are likely to cause disease if mutated in humans.

Although sequences with important functionality tend to be less variable across species because of selective pressure, to what extent evolutionary conservation is mirrored by epidemiological outcome has never been demonstrated. Results from our analyses suggest that the degree of cancer risk influenced by a particular SNP in a molecular epidemiological study was significantly associated with the conservation level of the amino acid it affected. It should be noted that some of SNP genotypes included in Table 1Citation are associated with decreased cancer risks (ORs < 1). This indicates that not all SNPs are harmful, and some of them may be beneficial. However, when the 13 studies with inverted ORs were removed from the analysis, the overall result remained unchanged. Therefore, the inversion of ORs for protective associations (e.g., 0.3 converted to 3.3) in our analysis does not seem to affect the significance of a genetic variation on cancer risk estimate. Our study provides the first evidence demonstrating a linear relationship between the detected ORs associated with cancer risk and the conservation levels of the SNP-affected amino acids. These findings confirm earlier observations that substitutions observed frequently during evolution are likely to be neutral, whereas those observed rarely are likely to be deleterious from an evolutionary perspective. A similar approach was recently used to identify potential functionally missense changes in the breast cancer susceptibility gene BRCA1 by aligning sequences from 57 eutherian mammals. It was found that most conserved residues occur in a region with the highest concentration of protein-interacting domains. In addition, a total of 38 of the 139 missense changes in the conserved region are likely to affect protein function and might be targets of further investigation in studying breast cancer susceptibility (3) . It is becoming clear that application of the molecular evolutionary approach may be a powerful tool for prioritizing SNPs to be genotyped in future molecular epidemiological studies.

This approach further allows us to identify some target SNPs in DNA repair pathways that may be worth examining in future molecular epidemiological study. DNA repair is one of the frontline defenses against human cancer, and more than 125 genes are thought to be involved in different DNA repair systems (4) . Some of these SNPs selected based on our analysis have been detected as genetic risk factors in cancer case-control studies (Table 1)Citation , whereas most of them have not been investigated before. Therefore, our analysis will provide useful information in selecting SNPs that are likely to have potential functional impact and ultimately contribute to an individual’s cancer susceptibility.

However, there are several limitations to our analysis, even though the correlation we observed is readily apparent. Because some DNA repair and metabolic genes only trigger disease in the presence of certain environmental exposures such as tobacco smoke carcinogens, the overall ORs without stratification or adjustment for important environmental factors used in the analysis may not reflect a true association between some conserved SNPs with functional impact and the diseases. Next, the accuracy with which a SNP predicts cancer risk depends on the alignment obtained. In our analysis, the amino acid sequences from different species in the alignment were restricted to those homologous sequences that were available in the protein database; therefore, the resulting alignment information varied from protein to protein. In our analysis, the number of homologous sequences used in the SIFT alignment ranged from 15 to over 100. As protein databases grow with data from sequencing whole genomes of more organisms, a larger number of homologous sequences will become available, and SIFT prediction will become more accurate. The final limitation is that our analysis did not include many SNPs that are located outside the coding regions of genes. Those SNPs located in the regulatory regions will be constrained to some extent under selective pressure and may be equally important in disease risk estimates. However, given our limited knowledge of regulatory signals in the genome, it is difficult to recognize such SNPs from the large pool of noncoding SNPs.

Nevertheless, our finding does reveal a close association between conservation levels and risk estimates, despite variations among protein families attributable to different evolutionary pressures and the heterogeneous set of sequence alignments used. Given that hundreds of thousands of SNPs are estimated to exist in the human population, the number of SNPs screened for association with disease can be greatly reduced by identifying those most likely to alter gene function. Our current analysis focuses on SNPs in the coding regions, and our findings could explain a significant fraction of the cancer risk that has been detected. This approach might also be applied to a relationship between SNP conservation levels and epidemiological studies of diseases other than cancer. More importantly, this study builds a bridge from evolutionary biology to molecular epidemiology, which may further our understanding of disease-related SNPs and ultimately facilitate SNP genotyping in future studies.


   FOOTNOTES
 
Grant support: National Cancer Institute Grants CA 74880, CA 91846, CA 85576, CA 86390 and HG 02275

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Note: Y. Zhu is currently at the Department of Epidemiology and Public Health, Yale University, New Haven, Connecticut.

Requests for reprints: Xifeng Wu, Department of Epidemiology, Unit 189, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030. Phone: (713) 745-2485; Fax: (713) 792-0807; E-mail: xwu{at}mdanderson.org

1 http://www.ncbi.nlm.nih.gov/entrez. Back

2 http://www.genome.utah.edu/genesnps and http://greengenes.llnl.gov/dpublic/secure/reseq/bin/gene_info. Back

Received 9/ 4/03. Revised 12/ 1/03. Accepted 1/13/04.


   REFERENCES
Top
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Cargill M, Altshuler D, Ireland J, et al Characterization of single-nucleotide polymorphisms in coding regions of human genes. Nat Genet, 22: 231-8, 1999.[CrossRef][Medline]
  2. Ng PC, Henikoff S. Accounting for human polymorphisms predicted to affect protein function. Genome Res, 12: 436-46, 2002.[Abstract/Free Full Text]
  3. Fleming MA, Potter JD, Ramirez CJ, Ostrander GK, Ostrander EA. Understanding missense mutations in the BRCA1 gene: an evolutionary approach. Proc Natl Acad Sci USA, 100: 1151-6, 2003.[Abstract/Free Full Text]
  4. Ronen A, Glickman BW. Human DNA repair genes. Environ Mol Mutagen, 37: 241-83, 2001.[CrossRef][Medline]
  5. Matsuo K, Hamajima N, Shinoda M, et al Gene-environment interaction between an aldehyde dehydrogenase-2 (ALDH2) polymorphism and alcohol consumption for the risk of esophageal cancer. Carcinogenesis (Lond.), 22: 913-6, 2001.[Abstract/Free Full Text]
  6. Goodman MT, McDuffie K, Kolonel LN, et al Case-control study of ovarian cancer and polymorphisms in genes involved in catecholestrogen formation and metabolism. Cancer Epidemiol Biomark Prev, 10: 209-16, 2001.[Abstract/Free Full Text]
  7. Gryfe R, Di Nicola N, Lal G, Gallinger S, Redston M. Inherited colorectal polyposis and cancer risk of the APC I1307K polymorphism. Am J Hum Genet, 64: 378-84, 1999.[CrossRef][Medline]
  8. Park JY, Muscat JE, Ren Q, et al CYP1A1 and GSTM1 polymorphisms and oral cancer risk. Cancer Epidemiol Biomark Prev, 6: 791-7, 1997.[Abstract]
  9. Takezaki T, Hamajima N, Matsuo K, et al Association of polymorphisms in the ß-2 and ß-3 adrenoceptor genes with risk of colorectal cancer in Japanese. Int J Clin Oncol, 6: 117-22, 2001.[CrossRef][Medline]
  10. Murata M, Watanabe M, Yamanaka M, et al Genetic polymorphisms in cytochrome P450 (CYP) 1A1, CYP1A2, CYP2E1, glutathione S-transferase (GST) M1 and GSTT1 and susceptibility to prostate cancer in the Japanese population. Cancer Lett, 165: 171-7, 2001.[CrossRef][Medline]
  11. Huang XE, Hamajima N, Saito T, et al Possible association of ß2- and ß3-adrenergic receptor gene polymorphisms with susceptibility to breast cancer. Breast Cancer Res, 3: 264-9, 2001.[CrossRef][Medline]
  12. London SJ, Daly AK, Fairbrother KS, et al Lung cancer risk in African-Americans in relation to a race-specific CYP1A1 polymorphism. Cancer Res, 55: 6035-7, 1995.[Abstract/Free Full Text]
  13. Aktas D, Guney I, Alikasifoglu M, et al CYP1A1 gene polymorphism and risk of epithelial ovarian neoplasm. Gynecol Oncol, 86: 124-8, 2002.[CrossRef][Medline]
  14. Miyoshi Y, Takahashi Y, Egawa C, Noguchi S. Breast cancer risk associated with CYP1A1 genetic polymorphisms in Japanese women. Breast J, 8: 209-15, 2002.[CrossRef][Medline]
  15. Ishitobi M, Miyoshi Y, Ando A, et al Association of BRCA2 polymorphism at codon 784 (Met/Val) with breast cancer risk and prognosis. Clin Cancer Res, 9: 1376-80, 2003.[Abstract/Free Full Text]
  16. Wang AH, Sun CS, Li LS, Huang JY, Chen QS. Relationship of tobacco smoking CYP1A1 GSTM1 gene polymorphism and esophageal cancer in Xi’an. World J Gastroenterol, 8: 49-53, 2002.[Medline]
  17. Auranen A, Spurdle AB, Chen X, et al BRCA2 Arg372His polymorphism and epithelial ovarian cancer risk. Int J Cancer, 103: 427-30, 2003.[CrossRef][Medline]
  18. McWilliams JE, Evans AJ, Beer TM, et al Genetic polymorphisms in head and neck cancer risk. Head Neck, 22: 609-17, 2000.[CrossRef][Medline]
  19. Spurdle AB, Hopper JL, Chen X, et al The BRCA2 372 HH genotype is associated with risk of breast cancer in Australian women under age 60 years. Cancer Epidemiol Biomark Prev, 11: 413-6, 2002.[Abstract/Free Full Text]
  20. Basham VM, Pharoah PD, Healey CS, et al Polymorphisms in CYP1A1 and smoking: no association with breast cancer risk. Carcinogenesis (Lond.), 22: 1797-800, 2001.[Abstract/Free Full Text]
  21. Esteller M, Garcia A, Martinez-Palones JM, Xercavins J, Reventos J. Germ line polymorphisms in cytochrome-P450 1A1 (C4887 CYP1A1) and methylenetetrahydrofolate reductase (MTHFR) genes and endometrial cancer susceptibility. Carcinogenesis (Lond.), 18: 2307-11, 1997.[Abstract/Free Full Text]
  22. Bergman-Jungestrom M, Wingren S. Catechol-O-methyltransferase (COMT) gene polymorphism and breast cancer risk in young women. Br J Cancer, 85: 859-62, 2001.[CrossRef][Medline]
  23. Hung RJ, Boffetta P, Brockmoller J, et al CYP1A1 and GSTM1 genetic polymorphisms and lung cancer risk in Caucasian non-smokers: a pooled analysis. Carcinogenesis (Lond.), 24: 875-82, 2003.[Abstract/Free Full Text]
  24. Hamajima N, Matsuo K, Tajima K, et al Limited association between a catechol-O-methyltransferase (COMT) polymorphism and breast cancer risk in Japan. Int J Clin Oncol, 6: 13-8, 2001.[CrossRef][Medline]
  25. De Vivo I, Hankinson SE, Li L, Colditz GA, Hunter DJ. Association of CYP1B1 polymorphisms and breast cancer risk. Cancer Epidemiol Biomark Prev, 11: 489-92, 2002.[Abstract/Free Full Text]
  26. Yim DS, Parkb SK, Yoo KY, et al Relationship between the Val158Met polymorphism of catechol O-methyl transferase and breast cancer. Pharmacogenetics, 11: 279-86, 2001.[CrossRef][Medline]
  27. Zheng W, Xie DW, Jin F, et al Genetic polymorphism of cytochrome P450–1B1 and risk of breast cancer. Cancer Epidemiol Biomark Prev, 9: 147-50, 2000.[Abstract/Free Full Text]
  28. Garner EI, Stokes EE, Berkowitz RS, Mok SC, Cramer DW. Polymorphisms of the estrogen-metabolizing genes CYP17 and catechol-O-methyltransferase and risk of epithelial ovarian cancer. Cancer Res, 62: 3058-62, 2002.[Abstract/Free Full Text]
  29. Tang YM, Green BL, Chen GF, et al Human CYP1B1 Leu432Val gene polymorphism: ethnic distribution in African-Americans, Caucasians and Chinese; oestradiol hydroxylase activity; and distribution in prostate cancer cases and controls. Pharmacogenetics, 10: 761-6, 2000.[CrossRef][Medline]
  30. Goodman JE, Lavigne JA, Hengstler JG, et al Catechol-O-methyltransferase polymorphism is not associated with ovarian cancer risk. Cancer Epidemiol Biomark Prev, 9: 1373-6, 2000.[Abstract/Free Full Text]
  31. Wedren S, Rudqvist TR, Granath F, et al Catechol-O-methyltransferase gene polymorphism and post-menopausal breast cancer risk. Carcinogenesis (Lond.), 24: 681-7, 2003.[Abstract/Free Full Text]
  32. London SJ, Daly AK, Leathart JB, Navidi WC, Idle JR. Lung cancer risk in relation to the CYP2C9*1/CYP2C9*2 genetic polymorphism among African-Americans and Caucasians in Los Angeles County, California. Pharmacogenetics, 6: 527-33, 1996.[CrossRef][Medline]
  33. Severi G, Giles GG, Southey MC, et al ELAC2/HPC2 polymorphisms, prostate-specific antigen levels, and prostate cancer. J Natl Cancer Inst (Bethesda), 95: 818-24, 2003.[Abstract/Free Full Text]
  34. Lin HJ, Lakkides KM, Keku TO, et al Prostaglandin H synthase 2 variant (Val511Ala) in African Americans may reduce the risk for colorectal neoplasia. Cancer Epidemiol Biomark Prev, 11: 1305-15, 2002.[Abstract/Free Full Text]
  35. Moysich KB, Shields PG, Freudenheim JL, et al Polychlorinated biphenyls, cytochrome P4501A1 polymorphism, and postmenopausal breast cancer risk. Cancer Epidemiol Biomark Prev, 8: 41-4, 1999.[Abstract/Free Full Text]
  36. Iughetti P, Suzuki O, Godoi PH, et al A polymorphism in endostatin, an angiogenesis inhibitor, predisposes for the development of prostatic adenocarcinoma. Cancer Res, 61: 7375-8, 2001.[Abstract/Free Full Text]
  37. Hamada GS, Sugimura H, Suzuki I, et al The heme-binding region polymorphism of cytochrome P450IA1 (CypIA1), rather than the RsaI polymorphism of IIE1 (CypIIE1), is associated with lung cancer in Rio de Janeiro. Cancer Epidemiol Biomark Prev, 4: 63-7, 1995.[Abstract]
  38. Benhamou S, Reinikainen M, Bouchardy C, Dayer P, Hirvonen A. Association between lung cancer and microsomal epoxide hydrolase genotypes. Cancer Res, 58: 5291-3, 1998.[Abstract/Free Full Text]
  39. Sugimura H, Wakai K, Genka K, et al Association of Ile462Val (exon 7) polymorphism of cytochrome P450 IA1 with lung cancer in the Asian population: further evidence from a case-control study in Okinawa. Cancer Epidemiol Biomark Prev, 7: 413-7, 1998.[Abstract]
  40. London SJ, Smart J, Daly AK. Lung cancer risk in relation to genetic polymorphisms of microsomal epoxide hydrolase among African-Americans and Caucasians in Los Angeles County. Lung Cancer, 28: 147-55, 2000.[CrossRef][Medline]
  41. Huang CS, Shen CY, Chang KJ, Hsu SM, Chern HD. Cytochrome P4501A1 polymorphism as a susceptibility factor for breast cancer in postmenopausal Chinese women in Taiwan. Br J Cancer, 80: 1838-43, 1999.[CrossRef][Medline]
  42. Spurdle AB, Purdie DM, Webb PM, et al The microsomal epoxide hydrolase Tyr113His polymorphism: association with risk of ovarian cancer. Mol Carcinog, 30: 71-8, 2001.[CrossRef][Medline]
  43. Olshan AF, Weissler MC, Watson MA, Bell DA. GSTM1, GSTT1, GSTP1, CYP1A1, and NAT1 polymorphisms, tobacco use, and the risk of head and neck cancer. Cancer Epidemiol Biomark Prev., 9: 185-91, 2000.[Abstract/Free Full Text]
  44. Lancaster JM, Brownlee HA, Bell DA, et al Microsomal epoxide hydrolase polymorphism as a risk factor for ovarian cancer. Mol Carcinog, 17: 160-2, 1996.[CrossRef][Medline]
  45. Song N, Tan W, Xing D, Lin D. CYP 1A1 polymorphism and risk of lung cancer in relation to tobacco smoking: a case-control study in China. Carcinogenesis (Lond.), 22: 11-6, 2001.[Abstract/Free Full Text]
  46. To-Figueras J, Gene M, Gomez-Catalan J, et al Lung cancer susceptibility in relation to combined polymorphisms of microsomal epoxide hydrolase and glutathione S-transferase P1. Cancer Lett, 173: 155-62, 2001.[CrossRef][Medline]
  47. London SJ, Yuan JM, Coetzee GA, et al CYP1A1 I462V genetic polymorphism and lung cancer risk in a cohort of men in Shanghai, China. Cancer Epidemiol Biomark Prev, 9: 987-91, 2000.[Abstract/Free Full Text]
  48. Harrison DJ, Hubbard AL, MacMillan J, Wyllie AH, Smith CA. Microsomal epoxide hydrolase gene polymorphism and susceptibility to colon cancer. Br J Cancer, 79: 168-71, 1999.[CrossRef][Medline]
  49. Setiawan VW, Zhang ZF, Yu GP, et al GSTP1 polymorphisms and gastric cancer in a high-risk Chinese population. Cancer Causes Control, 12: 673-81, 2001.[CrossRef][Medline]
  50. Baxter SW, Choong DY, Campbell IG. Microsomal epoxide hydrolase polymorphism and susceptibility to ovarian cancer. Cancer Lett, 177: 75-81, 2002.[CrossRef][Medline]
  51. Zhao H, Spitz MR, Gwyn KM, Wu X. Microsomal epoxide hydrolase polymorphisms and lung cancer risk in non-Hispanic whites. Mol Carcinog, 33: 99-104, 2002.[CrossRef][Medline]
  52. Drakoulis N, Cascorbi I, Brockmoller J, Gross CR, Roots I. Polymorphisms in the human CYP1A1 gene as susceptibility factors for lung cancer: exon-7 mutation (4889 A to G), and a T to C mutation in the 3'-flanking region. Clin Investig, 72: 240-8, 1994.[Medline]
  53. Ulrich CM, Bigler J, Whitton JA, Bostick R, Fosdick L, Potter JD. Epoxide hydrolase Tyr113His polymorphism is associated with elevated risk of colorectal polyps in the presence of smoking and high meat intake. Cancer Epidemiol Biomark Prev, 10: 875-82, 2001.[Abstract/Free Full Text]
  54. Tiemersma EW, Omer RE, Bunschoten A, et al Role of genetic polymorphism of glutathione-S-transferase T1 and microsomal epoxide hydrolase in aflatoxin-associated hepatocellular carcinoma. Cancer Epidemiol Biomark Prev, 10: 785-91, 2001.[Abstract/Free Full Text]
  55. Xing DY, Tan W, Song N, Lin DX. Ser326Cys polymorphism in hOGG1 gene and risk of esophageal cancer in a Chinese population. Int J Cancer, 95: 140-3, 2001.[CrossRef][Medline]
  56. Le Marchand L, Donlon T, Lum-Jones A, Seifried A, Wilkens LR. Association of the hOGG1 Ser326Cys polymorphism with lung cancer risk. Cancer Epidemiol Biomark Prev, 11: 409-12, 2002.[Abstract/Free Full Text]
  57. Sugimura H, Kohno T, Wakai K, et al hOGG1 Ser326Cys polymorphism and lung cancer susceptibility. Cancer Epidemiol Biomark Prev, 8: 669-74, 1999.[Abstract/Free Full Text]
  58. Choi JY, Hamajima N, Tajima K, et al hOGG1 Ser326Cys polymorphism and breast cancer risk among Asian women. Breast Cancer Res Treat, 79: 59-62, 2003.[CrossRef][Medline]
  59. Takezaki T, Gao CM, Wu JZ, et al hOGG1 Ser(326)Cys polymorphism and modification by environmental factors of stomach cancer risk in Chinese. Int J Cancer, 99: 624-7, 2002.[CrossRef][Medline]
  60. Xing D, Tan W, Song N, Lin D. Genetic polymorphism in hOGG1 and susceptibility to esophageal cancer[in Chinese]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 17: 377-80, 2000.[Medline]
  61. Ito H, Hamajima N, Takezaki T, et al A limited association of OGG1 Ser326Cys polymorphism for adenocarcinoma of the lung. J Epidemiol, 12: 258-65, 2002.[Medline]
  62. Hanaoka T, Sugimura H, Nagura K, et al hOGG1 exon7 polymorphism and gastric cancer in case-control studies of Japanese Brazilians and non-Japanese Brazilians. Cancer Lett, 170: 53-61, 2001.[CrossRef][Medline]
  63. Goodman MT, Wu AH, Tung KH, et al Association of galactose-1-phosphate uridyltransferase activity and N314D genotype with the risk of ovarian cancer. Am J Epidemiol, 156: 693-701, 2002.[Abstract/Free Full Text]
  64. Cozen W, Peters R, Reichardt JK, et al Galactose-1-phosphate uridyl transferase (GALT) genotype and phenotype, galactose consumption, and the risk of borderline and invasive ovarian cancer (United States). Cancer Causes Control, 13: 113-20, 2002.[CrossRef][Medline]
  65. Chang BL, Zheng SL, Hawkins GA, et al Joint effect of HSD3B1 and HSD3B2 genes is associated with hereditary and sporadic prostate cancer susceptibility. Cancer Res, 62: 1784-9, 2002.[Abstract/Free Full Text]
  66. Lewis SJ, Cherry NM, Niven RM, Barber PV, Povey AC. GSTM1, GSTT1 and GSTP1 polymorphisms and lung cancer risk. Cancer Lett, 180: 165-71, 2002.[CrossRef][Medline]
  67. Margiotti K, Kim E, Pearce CL, Spera E, Novelli G, Reichardt JK. Association of the G289S single nucleotide polymorphism in the HSD17B3 gene with prostate cancer in Italian men. Prostate, 53: 65-8, 2002.[CrossRef][Medline]
  68. Shepard TF, Platz EA, Kantoff PW, et al No association between the I105V polymorphism of the glutathione S-transferase P1 gene (GSTP1) and prostate cancer risk: a prospective study. Cancer Epidemiol Biomark Prev, 9: 1267-8, 2000.[Free Full Text]
  69. Kim JW, Roh JW, Park NH, et al Interferon, {alpha}17 (IFNA17) Ile184Arg polymorphism and cervical cancer risk. Cancer Lett, 189: 183-8, 2003.[CrossRef][Medline]
  70. Zhao M, Lewis R, Gustafson DR, et al No apparent association of GSTP1 A(313)G polymorphism with breast cancer risk among postmenopausal Iowa women. Cancer Epidemiol Biomark Prev, 10: 1301-2, 2001.[Free Full Text]
  71. Wang W, Xue S, Ingles SA, et al An association between genetic polymorphisms in the ileal sodium-dependent bile acid transporter gene and the risk of colorectal adenomas. Cancer Epidemiol Biomark Prev, 10: 931-6, 2001.[Abstract/Free Full Text]
  72. Yamamura K, Kiyohara C, Nakanishi Y, Takayama K, Hara N. Lung cancer risk and genetic polymorphism at the glutathione S-transferase P1 locus in male Japanese[in Japanese]. Fukuoka Igaku Zasshi, 91: 203-6, 2000.[Medline]
  73. Kaur TB, Travaline JM, Gaughan JP, et al Role of polymorphisms in codons 143 and 160 of the O6-alkylguanine DNA alkyltransferase gene in lung cancer risk. Cancer Epidemiol Biomark Prev, 9: 339-42, 2000.[Abstract/Free Full Text]
  74. Jeronimo C, Varzim G, Henrique R, et al I105V polymorphism and promoter methylation of the GSTP1 gene in prostate adenocarcinoma. Cancer Epidemiol Biomark Prev, 11: 445-50, 2002.[Abstract/Free Full Text]
  75. Mitrunen K, Sillanpaa P, Kataja V, et al Association between manganese superoxide dismutase (MnSOD) gene polymorphism and breast cancer risk. Carcinogenesis (Lond.), 22: 827-9, 2001.[Abstract/Free Full Text]
  76. Wang LI, Miller DP, Sai Y, et al Manganese superoxide dismutase alanine-to-valine polymorphism at codon 16 and lung cancer risk. J Natl Cancer Inst (Bethesda), 93: 1818-21, 2001.[Free Full Text]
  77. Ulrich CM, Kampman E, Bigler J, et al Lack of association between the C677T MTHFR polymorphism and colorectal hyperplastic polyps. Cancer Epidemiol Biomark Prev, 9: 427-33, 2000.[Abstract/Free Full Text]
  78. To-Figueras J, Gene M, Gomez-Catalan J, et al Genetic polymorphism of glutathione S-transferase P1 gene and lung cancer risk. Cancer Causes Control, 10: 65-70, 1999.[CrossRef][Medline]
  79. Ma J, Stampfer MJ, Giovannucci E, et al Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer. Cancer Res, 57: 1098-102, 1997.[Abstract/Free Full Text]
  80. Helzlsouer KJ, Selmin O, Huang HY, et al Association between glutathione S-transferase M1, P1, and T1 genetic polymorphisms and development of breast cancer. J Natl Cancer Inst (Bethesda), 90: 512-8, 1998.[Abstract/Free Full Text]
  81. Chen J, Giovannucci E, Kelsey K, et al A methylenetetrahydrofolate reductase polymorphism and the risk of colorectal cancer. Cancer Res, 56: 4862-4, 1996.[Abstract/Free Full Text]
  82. Campbell IG, Baxter SW, Eccles DM, Choong DY. Methylenetetrahydrofolate reductase polymorphism and susceptibility to breast cancer. Breast Cancer Res, 4: 1-4, 2002.[Medline]
  83. Wang Y, Spitz MR, Schabath MB, et al Association between glutathione S-transferase P1 polymorphisms and lung cancer risk in Caucasians: a case-control study. Lung Cancer, 40: 25-32, 2003.[CrossRef][Medline]
  84. Miao X, Xing D, Tan W, et al Susceptibility to gastric cardia adenocarcinoma and genetic polymorphisms in methylenetetrahydrofolate reductase in an at-risk Chinese population. Cancer Epidemiol Biomark Prev, 11: 1454-8, 2002.[Abstract/Free Full Text]
  85. Shen H, Xu Y, Zheng Y, et al Polymorphisms of 5,10-methylenetetrahydrofolate reductase and risk of gastric cancer in a Chinese population: a case-control study. Int J Cancer, 95: 332-6, 2001.[CrossRef][Medline]
  86. Marugame T, Tsuji E, Inoue H, et al Methylenetetrahydrofolate reductase polymorphism and risk of colorectal adenomas. Cancer Lett, 151: 181-6, 2000.[CrossRef][Medline]
  87. Xie D, Shu XO, Deng Z, et al Population-based, case-control study of HER2 genetic polymorphism and breast cancer risk. J Natl Cancer Inst (Bethesda), 92: 412-7, 2000.[Abstract/Free Full Text]
  88. Wiencke JK, Spitz MR, McMillan A, Kelsey KT. Lung cancer in Mexican-Americans and African-Americans is associated with the wild-type genotype of the NAD(P)H: quinone oxidoreductase polymorphism. Cancer Epidemiol Biomark Prev, 6: 87-92, 1997.[Abstract]
  89. Wang L, Habuchi T, Takahashi T, et al No association between HER-2 gene polymorphism at codon 655 and a risk of bladder cancer. Int J Cancer, 97: 787-90, 2002.[CrossRef][Medline]
  90. Park SJ, Zhao H, Spitz MR, Grossman HB, Wu X. An association between NQO1 genetic polymorphism and risk of bladder cancer. Mutat Res, 536: 131-7, 2003.[Medline]
  91. Keshava C, McCanlies EC, Keshava N, Wolff MS, Weston A. Distribution of HER2(V655) genotypes in breast cancer cases and controls in the United States. Cancer Lett, 173: 37-41, 2001.[CrossRef][Medline]
  92. Sjalander A, Birgander R, Hallmans G, et al p53 polymorphisms and haplotypes in breast cancer. Carcinogenesis (Lond.), 17: 1313-6, 1996.[Abstract/Free Full Text]
  93. Ratnasinghe D, Tangrea JA, Andersen MR, et al Glutathione peroxidase codon 198 polymorphism variant increases lung cancer risk. Cancer Res, 60: 6381-3, 2000.[Abstract/Free Full Text]
  94. Soulitzis N, Sourvinos G, Dokianakis DN, Spandidos DA. p53 codon 72 polymorphism and its association with bladder cancer. Cancer Lett, 179: 175-83, 2002.[CrossRef][Medline]
  95. Sjalander A, Birgander R, Rannug A, et al Association between the p21 codon 31 A1 (Arg) allele and lung cancer. Hum Hered, 46: 221-5, 1996.[Medline]
  96. Xing D, Qi J, Tan W, et al Association of genetic polymorphisms in the DNA repair gene XPD with risk of lung and esophageal cancer in a Chinese population in Beijing[in Chinese]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 20: 35-8, 2003.[Medline]
  97. Henner WD, Evans AJ, Hough KM, et al Association of codon 72 polymorphism of p53 with lower prostate cancer risk. Prostate, 49: 263-6, 2001.[CrossRef][Medline]
  98. Spitz MR, Wu X, Wang Y, et al Modulation of nucleotide excision repair capacity by XPD polymorphisms in lung cancer patients. Cancer Res, 61: 1354-7, 2001.[Abstract/Free Full Text]
  99. Fan R, Wu MT, Miller D, et al The p53 codon 72 polymorphism and lung cancer risk. Cancer Epidemiol Biomark Prev, 9: 1037-42, 2000.[Abstract/Free Full Text]
  100. David-Beabes GL, Lunn RM, London SJ. No association between the XPD (Lys751G1n) polymorphism or the XRCC3 (Thr241Met) polymorphism and lung cancer risk. Cancer Epidemiol Biomark Prev, 10: 911-2, 2001.[Free Full Text]
  101. Biros E, Kalina I, Biros I, et al Polymorphism of the p53 gene within the codon 72 in lung cancer patients. Neoplasma, 48: 407-11, 2001.[Medline]
  102. Sturgis EM, Zheng R, Li L, et al XPD/ERCC2 polymorphisms and risk of head and neck cancer: a case-control analysis. Carcinogenesis (Lond.), 21: 2219-23, 2000.[Abstract/Free Full Text]
  103. Shen H, Zheng Y, Sturgis EM, Spitz MR, Wei Q. P53 codon 72 polymorphism and risk of squamous cell carcinoma of the head and neck: a case-control study. Cancer Lett, 183: 123-30, 2002.[CrossRef][Medline]
  104. Park JY, Lee SY, Jeon HS, et al Lys751Gln polymorphism in the DNA repair gene XPD and risk of primary lung cancer. Lung Cancer, 36: 15-6, 2002.[CrossRef][Medline]
  105. Pierce LM, Sivaraman L, Chang W, et al Relationships of TP53 codon 72 and HRAS1 polymorphisms with lung cancer risk in an ethnically diverse population. Cancer Epidemiol Biomark Prev, 9: 1199-204, 2000.[Abstract/Free Full Text]
  106. Stern MC, Johnson LR, Bell DA, Taylor JA. XPD codon 751 polymorphism, metabolism genes, smoking, and bladder cancer risk. Cancer Epidemiol Biomark Prev, 11: 1004-11, 2002.[Abstract/Free Full Text]
  107. Chen S, Tang D, Xue K, et al DNA repair gene XRCC1 and XPD polymorphisms and risk of lung cancer in a Chinese population. Carcinogenesis (Lond.), 23: 1321-5, 2002.[Abstract/Free Full Text]
  108. Tenti P, Vesentini N, Rondo Spaudo M, et al p53 codon 72 polymorphism does not affect the risk of cervical cancer in patients from northern Italy. Cancer Epidemiol Biomark Prev, 9: 435-8, 2000.[Abstract/Free Full Text]
  109. Olshan AF, Watson MA, Weissler MC, Bell DA. XRCC1 polymorphisms and head and neck cancer. Cancer Lett, 178: 181-6, 2002.[CrossRef][Medline]
  110. Madeleine MM, Shera K, Schwartz SM, et al The p53 Arg72Pro polymorphism, human papillomavirus, and invasive squamous cell cervical cancer. Cancer Epidemiol Biomark Prev, 9: 225-7, 2000.[Abstract/Free Full Text]
  111. Shen H, Xu Y, Qian Y, et al Polymorphisms of the DNA repair gene XRCC1 and risk of gastric cancer in a Chinese population. Int J Cancer, 88: 601-6, 2000.[CrossRef][Medline]
  112. Marchesani M, Hakkarainen A, Tuomainen TP, et al New paraoxonase 1 polymorphism I102V and the risk of prostate cancer in Finnish men. J Natl Cancer Inst (Bethesda), 95: 812-8, 2003.[Abstract/Free Full Text]
  113. Ratnasinghe D, Yao SX, Tangrea JA, et al Polymorphisms of the DNA repair gene XRCC1 and lung cancer risk. Cancer Epidemiol Biomark Prev, 10: 119-23, 2001.[Abstract/Free Full Text]
  114. Kerridge I, Lincz L, Scorgie F, et al Association between xenobiotic gene polymorphisms and non-Hodgkin’s lymphoma risk. Br J Haematol, 118: 477-81, 2002.[CrossRef][Medline]
  115. Stern MC, Umbach DM, van Gils CH, Lunn RM, Taylor JA. DNA repair gene XRCC1 polymorphisms, smoking, and bladder cancer risk. Cancer Epidemiol Biomark Prev, 10: 125-31, 2001.[Abstract/Free Full Text]
  116. Paltoo D, Woodson K, Taylor P, et al Pro12Ala polymorphism in the peroxisome proliferator-activated receptor-{gamma} (PPAR-{gamma}) gene and risk of prostate cancer among men in a large cancer prevention study. Cancer Lett, 191: 67-74, 2003.[CrossRef][Medline]
  117. Memisoglu A, Hankinson SE, Manson JE, Colditz GA, Hunter DJ. Lack of association of the codon 12 polymorphism of the peroxisome proliferator-activated receptor {gamma} gene with breast cancer and body mass. Pharmacogenetics, 12: 597-603, 2002.[CrossRef][Medline]
  118. Abdel-Rahman SZ, Soliman AS, Bondy ML, et al Inheritance of the 194Trp and the 399Gln variant alleles of the DNA repair gene XRCC1 are associated with increased risk of early-onset colorectal carcinoma in Egypt. Cancer Lett, 159: 79-86, 2000.[CrossRef][Medline]
  119. Spurdle AB, Hopper JL, Chen X, et al The progesterone receptor exon 4 Val660Leu G/T polymorphism and risk of breast cancer in Australian women. Cancer Epidemiol Biomark Prev, 11: 439-43, 2002.[Abstract/Free Full Text]
  120. Spurdle AB, Webb PM, Purdie DM, et al No significant association between progesterone receptor exon 4 Val660Leu G/T polymorphism and risk of ovarian cancer. Carcinogenesis (Lond.), 22: 717-21, 2001.[Abstract/Free Full Text]
  121. Febbo PG, Kantoff PW, Platz EA, et al The V89L polymorphism in the 5{alpha}-reductase type 2 gene and risk of prostate cancer. Cancer Res, 59: 5878-81, 1999.[Abstract/Free Full Text]
  122. Nam RK, Toi A, Vesprini D, et al V89L polymorphism of type-2, 5-{alpha} reductase enzyme gene predicts prostate cancer presence and progression. Urology, 57: 199-204, 2001.[CrossRef][Medline]
  123. Park JY, Lee SY, Jeon HS, et al Polymorphism of the DNA repair gene XRCC1 and risk of primary lung cancer. Cancer Epidemiol Biomark Prev, 11: 23-7, 2002.[Abstract/Free Full Text]
  124. Pearce CL, Makridakis NM, Ross RK, et al Steroid 5-{alpha} reductase type II V89L substitution is not associated with risk of prostate cancer in a multiethnic population study. Cancer Epidemiol Biomark Prev, 11: 417-8, 2002.[Free Full Text]
  125. Li Z, Habuchi T, Mitsumori K, et al Association of V89L SRD5A2 polymorphism with prostate cancer development in a Japanese population. J Urol, 169: 2378-81, 2003.[CrossRef][Medline]
  126. Wang Y, Spitz MR, Tsou AM, et al Sulfotransferase (SULT) 1A1 polymorphism as a predisposition factor for lung cancer: a case-control analysis. Lung Cancer, 35: 137-42, 2002.[CrossRef][Medline]
  127. Zheng W, Xie D, Cerhan JR, et al Sulfotransferase 1A1 polymorphism, endogenous estrogen exposure, well-done meat intake, and breast cancer risk. Cancer Epidemiol Biomark Prev, 10: 89-94, 2001.[Abstract/Free Full Text]
  128. Nelson HH, Kelsey KT, Mott LA, Karagas MR. The XRCC1 Arg399Gln polymorphism, sunburn, and non-melanoma skin cancer: evidence of gene-environment interaction. Cancer Res, 62: 152-5, 2002.[Abstract/Free Full Text]
  129. Wu MT, Wang YT, Ho CK, et al SULT1A1 polymorphism and esophageal cancer in males. Int J Cancer, 103: 101-4, 2003.[CrossRef][Medline]
  130. Ziv E, Cauley J, Morin PA, Saiz R, Browner WS. Association between the T29->C polymorphism in the transforming growth factor ß1 gene and breast cancer among elderly white women: the study of osteoporotic fractures. JAMA, 285: 2859-63, 2001.[Abstract/Free Full Text]
  131. Zhou W, Liu G, Miller DP, et al Polymorphisms in the DNA repair genes XRCC1 and ERCC2, smoking, and lung cancer risk. Cancer Epidemiol Biomark Prev, 12: 359-65, 2003.[Abstract/Free Full Text]
  132. MacLeod SL, Nowell S, Plaxco J, Lang NP. An allele-specific polymerase chain reaction method for the determination of the D85Y polymorphism in the human UDP-glucuronosyltransferase 2B15 gene in a case-control study of prostate cancer. Ann Surg Oncol, 7: 777-82, 2000.[Abstract]
  133. Divine KK, Gilliland FD, Crowell RE, et al The XRCC1 399 glutamine allele is a risk factor for adenocarcinoma of the lung. Mutat Res, 461: 273-8, 2001.[Medline]
  134. Gsur A, Preyer M, Haidinger G, et al A polymorphism in the UDP-Glucuronosyltransferase 2B15 gene (D85Y) is not associated with prostate cancer risk. Cancer Epidemiol Biomark Prev, 11: 497-8, 2002.[Free Full Text]
  135. Butkiewicz D, Rusin M, Enewold L, et al Genetic polymorphisms in DNA repair genes and risk of lung cancer. Carcinogenesis (Lond.), 22: 593-7, 2001.[Abstract/Free Full Text]
  136. Stern MC, Umbach DM, Lunn RM, Taylor JA. DNA repair gene XRCC3 codon 241 polymorphism, its interaction with smoking and XRCC1 polymorphisms, and bladder cancer risk. Cancer Epidemiol Biomark Prev, 11: 939-43, 2002.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Eur Respir JHome page
K. M. Kim, S. H. Park, J. S. Kim, W. K. Lee, S. I. Cha, C. H. Kim, Y. M. Kang, T. H. Jung, I. S. Kim, and J. Y. Park
Polymorphisms in the type IV collagen {alpha}3 gene and the risk of COPD
Eur. Respir. J., July 1, 2008; 32(1): 35 - 41.
[Abstract] [Full Text] [PDF]

Home page
 Int J EpidemiolHome page
J. P. Ioannidis, P. Boffetta, J. Little, T. R O'Brien, A. G Uitterlinden, P. Vineis, D. J Balding, A. Chokkalingam, S. M Dolan, W D. Flanders, et al.
Assessment of cumulative evidence on genetic associations: interim guidelines
Int. J. Epidemiol., February 1, 2008; 37(1): 120 - 132.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
A. G. Jegga, S. Gowrisankar, J. Chen, and B. J. Aronow
PolyDoms: a whole genome database for the identification of non-synonymous coding SNPs with the potential to impact disease
Nucleic Acids Res., January 12, 2007; 35(suppl_1): D700 - D706.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
L. Wang, H. Liu, Z. Zhang, M. R. Spitz, and Q. Wei
Association of Genetic Variants of O6-Methylguanine-DNA Methyltransferase with Risk of Lung Cancer in Non-Hispanic Whites
Cancer Epidemiol. Biomarkers Prev., December 1, 2006; 15(12): 2364 - 2369.
[Abstract] [Full Text] [PDF]

Home page
 Am J EpidemiolHome page
P. Bhatti, D. M. Church, J. L. Rutter, J. P. Struewing, and A. J. Sigurdson
Candidate Single Nucleotide Polymorphism Selection using Publicly Available Tools: A Guide for Epidemiologists
Am. J. Epidemiol., October 15, 2006; 164(8): 794 - 804.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
L. E. Mechanic, R. C. Millikan, J. Player, A. R. de Cotret, S. Winkel, K. Worley, K. Heard, K. Heard, C.-K. Tse, and T. Keku
Polymorphisms in nucleotide excision repair genes, smoking and breast cancer in African Americans and whites: a population-based case-control study
Carcinogenesis, July 1, 2006; 27(7): 1377 - 1385.
[Abstract] [Full Text] [PDF]

Home page
 Int J EpidemiolHome page
J. P A Ioannidis
Commentary: Grading the credibility of molecular evidence for complex diseases
Int. J. Epidemiol., June 1, 2006; 35(3): 572 - 578.
[Full Text] [PDF]

Home page
 CarcinogenesisHome page
R. C. Millikan, A. Hummer, C. Begg, J. Player, A. R. de Cotret, S. Winkel, H. Mohrenweiser, N. Thomas, B. Armstrong, A. Kricker, et al.
Polymorphisms in nucleotide excision repair genes and risk of multiple primary melanoma: the Genes Environment and Melanoma Study
Carcinogenesis, March 1, 2006; 27(3): 610 - 618.
[Abstract] [Full Text] [PDF]

Home page
 Neuro OncolHome page
M. Wrensch, K. T. Kelsey, M. Liu, R. Miike, M. Moghadassi, J. D. Sison, K. Aldape, A. McMillan, J. Wiemels, and J. K. Wiencke
ERCC1 and ERCC2 polymorphisms and adult glioma
Neuro-oncol, October 1, 2005; 7(4): 495 - 507.
[Abstract] [PDF]