Case-only gene-environment interaction studies: When does association imply mechanistic interaction?

Genetic Epidemiology

Volumn 34, Issue 4, 2010, Pages 327-334

  VanderWeele, Tyler J ^a   Hernández Díaz, Sonia ^a   Hernán, Miguel A ^a,b  

^a HARVARD SCHOOL OF PUBLIC HEALTH   (United States)

^b HARVARD MIT DIVISION OF HEALTH SCIENCES AND TECHNOLOGY   (United States)

Author keywords

Case only; Multiplicative interaction; Sufficient cause; Synergism

Indexed keywords

ARTICLE; ENVIRONMENTAL FACTOR; GENE INTERACTION; GENETIC ANALYSIS; HEREDITY;

ALGORITHMS; ASTHMA; DATA INTERPRETATION, STATISTICAL; ENVIRONMENT; FEMALE; FOLIC ACID; GENETIC PREDISPOSITION TO DISEASE; GENOME-WIDE ASSOCIATION STUDY; HUMANS; LUNG NEOPLASMS; MALE; MODELS, GENETIC; MODELS, STATISTICAL; POLYMORPHISM, GENETIC; RESEARCH DESIGN; RISK; SMOKING;

EID: 77951543375     PISSN: 07410395     EISSN: 10982272     Source Type: Journal    
DOI: 10.1002/gepi.20484     Document Type: Article

References (28)

1. Albert PS, Ratnasinghe D, Tangrea J, Wacholder S. 2001. Limitations of the case-only design for identifying gene-environment interactions. Am J Epidemiol 154:687-693. (Pubitemid 32971488)
2. Begg CB, Zhang ZF. 1994. Statistical analysis of molecular epidemiology studies employing case-series. Cancer Epidemiol Biomark Prev 3:173-175. (Pubitemid 124000417)
3. Bennett WP, Alavanja MCR, Blomeke B, Vähäkangas KH, Castrén K, Welsh JA, Bowman ED, Khan MA, Flieder DB, Harris CC. 1999. Environmental tobacco smoke, genetic susceptibility, and risk of lung cancer in never-smoking women. J Natl Cancer Inst 91:2009-2014.
4. Chatterjee N, Carroll RJ. 2005. Semiparametric maximum likelihood estimation exploiting gene-environment independence in case-control studies. Biometrika 92:399-418. (Pubitemid 40937643)
5. Chen YH. 2007. A semi-parametric odds ratio model for measuring association. Biometrics 63:413-421.
6. Cordell HJ. 2009. Detecting gene-gene interaction that underlie human diseases. Nat Rev Genet 10:392-404.
7. Friedman N, Linial M, Nachman I, Pe'er D. 2000. Using Bayesian networks to analyze expression data. J Comp Biol 7:601-620.
8. Gatto NM, Campbell UB, Rundle AG, Ahsan H. 2004. Further development of the case-only design for assessing gene-environment interaction: evaluation of and adjustment for bias. Int J Epidemiol 33:1014-1024. (Pubitemid 39429994)
9. Hernán MA, Hernández-Diaz S, Robins JM. 2004. A structural approach to selection bias. Epidemiology 15:615-625.
10. Khoury MJ, Flanders WD. 1996. Nontraditional epidemiologic approaches in the analysis of gene-environment interaction: case-control studies with no controls! Epidemiology 144:207-213.
11. Milne E, de Klerk NH, van Bockxmeer F, Kees UR, Thompson JR, Baker D, Armstrong BK. 2006. Is there a folate-related gene-environment interaction in the etiology of childhood acute lymphoblastic leukemia? Int J Cancer 119:229-232.
12. Pearl J. 1995. Casual diagrams for empirical research (with discussion). Biometrika 82:669-710.
13. Piegorsch WW, Weinberg CR, Taylor JA. 1994. Non-hierarchical logistic models and case-only designs for assessing susceptibility in population-based case-control studies. Statist Med 13:153-162.
14. Phillips PC. 2008. Epistasis - the essential role of gene interactions in the structure and evolution of genetic systems. Nat Rev Genet 9:855-867.
15. Rothman KJ. 1976. Causes. Am J Epidemiol 104:587-592.
16. Schmidt S, Schaid DJ. 1999. Potential misinterpretation of the case-only study to assess gene-environment interaction. Am J Epidemiol 150:878-885. (Pubitemid 29482841)
17. Tchetgen Tchetgen EJ, Robins JM. 2009. The semi-parametric case-only estimator. Harvard School of Public Health Technical Report.
18. VanderWeele TJ. 2009. Sufficient cause interactions and statistical interactions. Epidemiology 20:6-13.
19. VanderWeele TJ. 2010a. Epistatic interactions. Statist App Genet Mol Biol, in press.
20. VanderWeele TJ. 2010b. Empirical tests for compositional epistasis. Nat Rev Genet, in press.
21. VanderWeele TJ. 2010c. Sufficient cause interactions for categorical and ordinal exposures. Revised for Biometrika.
22. VanderWeele TJ, Robins JM. 2007a. The identification of synergism in the sufficient-component cause framework. Epidemiology 18:329-339.
23. VanderWeele TJ, Robins JM. 2007b. Directed acyclic graphs, sufficient causes and the properties of conditioning on a common effect. Am J Epidemiol 166:1096-1104.
24. VanderWeele TJ, Robins JM. 2008. Empirical and counterfactual conditions for sufficient cause interactions. Biometrika 95:49-61.
25. VanderWeele TJ, Robins JM. 2009. Minimal sufficient causation and directed acyclic graphs. Ann Statist 37:1437-1465.
26. Vansteelandt S, VanderWeele TJ, Tchetgen Tchetgen EJ, Robins JM. 2008. Multiply robust inference for statistical interactions. J Am Statist Assoc 103:1693-1704.
27. Wu H, Romieu I, Sienra-Monge J-J, del Rio-Navarro BE, Anderson DM, Dunn EW, Steiner LL, Lara-Sanchez IC, London SJ. 2007. Parental smoking modifies the relation between genetic variation tumor necrosis factor-alpha (TNF) and childhood asthma. Environ Health Persp 115:616-622.
28. Yang Q, Khoury MJ, Fengzhu S, Flanders WD. 1999. Case-only design to measure gene-gene interaction. Epidemiology 10:167-170. (Pubitemid 29093954)