Two-stage study of lung cancer risk modification by a functional variant in the 3 '-untranslated region of SMAD5 based on the bone morphogenetic protein pathway
AffiliationUniv Arizona, Dept Med, Div Translat & Regenerat Med
MetadataShow full item record
PublisherSPANDIDOS PUBL LTD
CitationZhang, Z., Wang, J., Zeng, X., Li, D., Ding, M., Guan, R. ... Lu, W. (2018). Two‑stage study of lung cancer risk modification by a functional variant in the 3'‑untranslated region of SMAD5 based on the bone morphogenetic protein pathway. Molecular and Clinical Oncology, 8, 38-46. https://doi.org/10.3892/mco.2017.1490
JournalMOLECULAR AND CLINICAL ONCOLOGY
Rights© Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractIncreasing evidence supports a key role for the bone morphogenetic protein (BMP) signaling pathway in lung vasculogenesis and angiogenesis. Genetic variations in BMP genes have been found to be correlated with cancer risk. In particular, the mutation in the 3'-untranslated region of BMPs may significantly affect gene function, leading to cancer susceptibility. The aim of the present study was to determine whether genetic variations in the components of the BMP family are associated with lung cancer risk. A total of 314 tag single-nucleotide polymorphisms were identified in 18 genes, which are considered to either compose or regulate BMPs, and their association with lung cancer risk was evaluated in a two-stage case-control study with 4,680 cases and controls. A consistently significant association of SMAD5 rs12719482 with elevated lung cancer risk was observed in the three types of sources of populations (adjusted additive model in the combined population: Odds ratio=1.32, 95% confidence interval: 1.16-1.51). The lung cancer risk statistically significantly increased with the increasing number of variant alleles of SMAD5 rs12719482 in a dose-dependent pattern (P for trend=4.9×10-5). Consistent evidence was identified for a significant interaction between the rs12719482 and cigarette smoking, performed as either a continuous or discrete variable. These findings indicated that SMAD5 rs12719482 may be a possible candidate marker for susceptibility to lung cancer in the Chinese population.
Note6 month embargo; published online: 6 November 2017
VersionFinal published version
SponsorsNational Natural Science Foundation of China [81520108001, 81220108001, 81170052]; 973 Key Scheme of China [2015CB553406]; National Key Research and Development Project [2016YFC0903700]; Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (2014); Guangdong Province Universities and Colleges Key Grant for Innovative Research [cxzd1142]; Guangzhou Municipal Research Project ; Guangzhou Department of Education Innovative Team [13C08]; Guangzhou Department of Education Yangcheng Scholarship [12A001S]; Guangdong Natural Science Foundation [2016A030313593]; Guangzhou Municipal University Research Projects 
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