BackgroundIn airways, a proliferative effect is played directly by cholinergic agonists through nicotinic and muscarinic receptors activation. How tumors respond to aberrantly activated cholinergic signalling is a key question in smoking-related cancer. This research was addressed to explore a possible link of cholinergic signalling changes with cancer biology.MethodsFifty-seven paired pieces of head and neck squamous cell carcinoma (HNSCC) and adjacent non-cancerous tissue (ANCT) were compared for their mRNA levels for ACh-related proteins and ACh-hydrolyzing activity.ResultsThe measurement in ANCT of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities (5.416 ± 0.501 mU/mg protein and 6.350 ± 0.599 mU/mg protein, respectively) demonstrated that upper respiratory tract is capable of controlling the availability of ACh. In HNSCC, AChE and BChE activities dropped to 3.584 ± 0.599 mU/mg protein (p = 0.002) and 3.965 ± 0.423 mU/mg protein (p < 0.001). Moreover, tumours with low AChE activity and high BChE activity were associated with shorter patient overall survival. ANCT and HNSCC differed in mRNA levels for AChE-T, α3, α5, α9 and β2 for nAChR subunits. Tobacco exposure had a great impact on the expression of both AChE-H and AChE-T mRNAs. Unaffected and cancerous pieces contained principal AChE dimers and BChE tetramers. The lack of nerve-born PRiMA-linked AChE agreed with pathological findings on nerve terminal remodelling and loss in HNSCC.ConclusionsOur results suggest that the low AChE activity in HNSCC can be used to predict survival in patients with head and neck cancer. So, the ChE activity level can be used as a reliable prognostic marker.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1402-y) contains supplementary material, which is available to authorized users.

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Background: some types of cancer have been associated with the presence of single nucleotide polymorphisms (SNPs) of some genes that encode enzymes: glutathione-S transferase (GST), whose alteration leads to loss of function and a lower capacity to eliminate toxic GSTM1 and GSTT1 null genotypes; SNPs causing loss of function of CYP1A1 or CYP1A1–2 cytochrome P450 enzymes related with a lower capacity to deactivate hydrocarbons related to smoking, which involves a higher risk of developing some smoking-dependent cancers including larynx cancer. Objective: to compare the presence of null SNPs in genes GSTM1, GSTT1, and CYP1A1 rs 4646903 T>C, and CYP1A1–2 RS1048943 A>G in patients with hypopharyngeal and larynx cancer with a healthy control group. Materials and method: The study included a total of 80 patients with hypopharyngeal and laryngeal cancer and 23 healthy subjects. Genomic DNA was obtained from saliva samples, determining genotype GSTM1 (present +, or null −), GSTT1 (present + or null −). Polymorphisms (SNP) in CYP1A1 T>C (present + CC, or absent − TC/TT), and CYP1A1–2 A>G (present + GG, or absent − AG/AA). Results: the mean age of patients with larynx cancer was 62 years and of control subjects 63 years. Of the total sample, over 95% were men, and over 90% were smokers. The presence of null genotypes for GTM1 was 50% in patients with larynx cancer (p = 0.042), while GSTT1 was 88.75% (p = 0.002). CYP1A1 rs4646903 T>C polymorphisms were detected in 100% of cases of larynx cancer and 17.39% of healthy subjects (p > 0.001). Conclusions: patients with larynx cancer present more gene GSTM1 and GSTT1 null polymorphisms, and CYP1A1 rs4646903 T>C polymorphisms.

Background DNA promoter methylation is usually an early stage in carcinogenesis process, including oral cancer. The purpose of this study was to investigate the association between T allele of specific single nucleotide polymorphism (SNP) C>T rs 16906252 and O16‐methylguanine‐DNA methyltransferase (MGMT) methylation as prospective biomarkers of malignant transformation in oral lichen planus (OLP), a chronic autoimmune mucocutaneous disease. Methods This research is an observational, analytical case–control study where a total of 85 subjects (43 control individuals and 42 OLP patients) participated. The samples (mouthwashes) from all volunteers were analyzed, and DNA extraction was carried out. The genotyping of the rs 16906252 SNP in the MGMT gene was performed by polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP). Statistical analyses of Student t test and multiple logistic regressions were used. Results C>T genotype in the control and OLP groups was detected in 2.3% and 19.0%, respectively. The presence of this genotype was associated with methylation of the MGMT gene. In fact, taking into account age and gender, subjects with C>T genotype were 10.5 (95% CI 1.03–106; P = 0.047) times more likely to methylate promoter region of the MGMT gene. Conclusions These findings indicate that C>T allele of rs 16906252, predictor of MGMT promoter methylation status, may be an important feature in the clinical prognosis of premalignant lesions of OLP, although this finding requires further clinical and laboratory investigation.