Journal
ENDOCRINE-RELATED CANCER
Volume 19, Issue 3, Pages 333-344Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/ERC-11-0372
Keywords
-
Categories
Funding
- American Thyroid Association Thyroid Cancer grant
- National Institutes of Health [DE019765-01]
- Cancer Center Support Grant [CA-16672]
- Halliburton Employees Fellow in Cancer Prevention funds
- National Cancer Institute, National Institutes of Health [HHSN261200800001E]
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
Ask authors/readers for more resources
Relationships are unclear between polymorphisms in genes involved in metabolism and detoxification of various chemicals and papillary thyroid cancer (PTC) risk as well as their potential modification by alcohol or tobacco intake. We evaluated associations between 1647 tagging single nucleotide polymorphisms (SNPs) in 132 candidate genes/regions involved in metabolism of exogenous and endogenous compounds (Phase I/II, oxidative stress, and metal binding pathways) and PTC risk in 344 PTC cases and 452 controls. For 15 selected regions and their respective SNPs, we also assessed interaction with alcohol and tobacco use. Logistic regression models were used to evaluate the main effect of SNPs (P-trend) and interaction with alcohol/tobacco intake. Gene- and pathway-level associations and interactions (P-gene interaction) were evaluated by combining P-trend values using the adaptive rank-truncated product method. While we found associations between PTC risk and nine SNPs (P-trend <= 0.01) and seven genes/regions (P-region<0.05), none remained significant after correction for the false discovery rate. We found a significant interaction between UGT2B7 and NAT1 genes and alcohol intake (P-gene interaction=0.01 and 0.02 respectively) and between the CYP26B1 gene and tobacco intake (P-gene interaction=0.02). Our results are suggestive of interaction between the genetic polymorphisms in several detoxification genes and alcohol or tobacco intake on risk of PTC. Larger studies with improved exposure assessment should address potential modification of PTC risk by alcohol and tobacco intake to confirm or refute our findings. Endocrine-Related Cancer (2012) 19 333-344
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available