Quantitative assessment of the association between GSTM1 null genotype and laryngeal cancer risk

Abstract

Previous studies investigating the association between glutathione S-transferase M1 (GSTM1) null genotype and laryngeal cancer risk reported controversial results. Thus, a meta-analysis was performed to clarify the effect of GSTM1 null genotype on laryngeal cancer risk. A literature search was performed for all possible studies. We estimated summary odd ratio (OR) with its 95 % confidence interval (95 % CI) to assess the association. Subgroup analyses were performed by ethnicity or the sample size. 24 individual case-control studies involving a total of 2,809 laryngeal cancer cases and 4,478 controls were finally included into this meta-analysis. Meta-analyses of total 24 studies showed the GSTM1 null genotype was significantly associated with increased laryngeal cancer risk (random-effects OR = 1.44, 95 % CI 1.19-1.73, P < 0.001). Subgroup analyses by ethnicity showed that the GSTM1 null genotype was associated with increased laryngeal cancer risk in both Caucasians (fixed-effects OR = 1.17, 95 % CI 1.04-1.33, P = 0.012) and Asians (random-effects OR = 1.89, 95 % CI 1.28-2.77, P = 0.001). Also, subgroup analyses by sample size also further identified this association above. The cumulative meta-analyses showed a trend of more obvious association between GSTM1 null genotype and increased risk of laryngeal cancer as information accumulated by year. Meta-analysis of available data suggests that GSTM1 null genotype contributes to increased laryngeal cancer risk in both Caucasians and East Asians.

Epidemiological Evaluation of Laryngeal Cancer Incidence in Kazakhstan for The Years 1999-2009

“…Sequence variants in DNA repair and cell cycle genes are significant (Hall et al, 2007), an impaired nucleotide excision repair pathway is a risk (Sliwinski et al, 2011), the GSTM1 null genotype contributes to increased laryngeal cancer risk in both Caucasians and East Asians (Xiao et al, 2013) and GSTM1 gene polymorphisms demonstrate associations, particularly in Caucasians (Kumar et al, 2011;Ying et al, 2012). Combination of polymorphisms in COX-2 or EPHX1 with high activity polymorphisms in UGT1A1, UGT1A6, or UGT1A7 showed a risk-modulating effect in head and neck carcinogenesis, especially among heavy smokers and patients with laryngeal cancer (Lacko et al, 2013).…”