Multiple pathway-based genetic variations associated with tobacco related multiple primary neoplasms

PLoS One. 2012;7(1):e30013. doi: 10.1371/journal.pone.0030013. Epub 2012 Jan 11.

Abstract

Background: In order to elucidate a combination of genetic alterations that drive tobacco carcinogenesis we have explored a unique model system and analytical method for an unbiased qualitative and quantitative assessment of gene-gene and gene-environment interactions. The objective of this case control study was to assess genetic predisposition in a biologically enriched clinical model system of tobacco related cancers (TRC), occurring as Multiple Primary Neoplasms (MPN).

Methods: Genotyping of 21 candidate Single Nucleotide Polymorphisms (SNP) from major metabolic pathways was performed in a cohort of 151 MPN cases and 210 cancer-free controls. Statistical analysis using logistic regression and Multifactor Dimensionality Reduction (MDR) analysis was performed for studying higher order interactions among various SNPs and tobacco habit.

Results: Increased risk association was observed for patients with at least one TRC in the upper aero digestive tract (UADT) for variations in SULT1A1 Arg²¹³His, mEH Tyr¹¹³His, hOGG1 Ser³²⁶Cys, XRCC1 Arg²⁸⁰His and BRCA2 Asn³⁷²His. Gene-environment interactions were assessed using MDR analysis. The overall best model by MDR was tobacco habit/p53(Arg/Arg)/XRCC1(Arg³⁹⁹His)/mEH(Tyr¹¹³His) that had highest Cross Validation Consistency (8.3) and test accuracy (0.69). This model also showed significant association using logistic regression analysis.

Conclusion: This is the first Indian study on a multipathway based approach to study genetic susceptibility to cancer in tobacco associated MPN. This approach could assist in planning additional studies for comprehensive understanding of tobacco carcinogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Cell Transformation, Neoplastic / genetics
  • Demography
  • Female
  • Genetic Predisposition to Disease*
  • Genetic Variation*
  • Humans
  • Male
  • Middle Aged
  • Models, Biological
  • Multifactor Dimensionality Reduction
  • Neoplasms, Multiple Primary / genetics*
  • Penetrance
  • Polymorphism, Single Nucleotide / genetics
  • Signal Transduction / genetics*
  • Tobacco Products