Abstract
Summary Background: Genetic studies of salivary gland neoplasms were mainly focused on chromosomal changes, and some specific patterns of chromosome translocations have been described. However, molecular alterations, in particular the role of HER-2/H-ras/c-myc signalling cascade in pleomor- phic adenoma pathogenesis (PA), are less well characterized. In addition, data on single nucleotide polymorphisms (SNPs) as potential susceptibility factors for PA development are also quite scarce. Methods: Mutational analyses were performed by means of real-time PCR (HER-2 and c-myc amplification analysis), PCR-SSCP and sequencing (H-ras point mutation detec- tion). Polymorphisms analysis was performed by PCR-RFLP (survivin and MMP-9 genes). Results: Amplification of HER-2 and c-myc has been found in 13% and 9% of PA cases respectively. Point mutations in H-ras codons 12/13 have been detected in 17% of PAs. No correlation could be established between these alterations and clinical characteristics of PAs, whereas they might play a role in a subset of malignant salivary gland tumours. As for survivin -31 G/C polymorphism, C allele carriers had a 4-fold decrease of the risk of developing PA (p=0.05). Carriers of the variant allele T of the -1562C/T SNP in MMP-9 gene had a 4-fold increase of the risk of developing PA (p<0.001). Conclusions: A longer follow-up of PA patients harbouring mutations could uncover a prognostic role of HER-2 and c- myc amplification as predictors of adenoma transformation into carcinoma. Both survivin and MMP-9 promoter poly- morphisms represent susceptibility factors for the develop- ment of PAs in the Serbian population.
Highlights
Salivary gland (SG) tumours are a highly heterogeneous group of tumours and include more than 35 histological subtypes, from benign adenomas to highgrade carcinomas.Pleomorphic adenoma (PA) is the most common salivary gland tumour representing about a half of all salivary gland neoplasms and 65% of parotid gland tumours [1,2,3]
A longer follow-up of PA patients harbouring mutations could uncover a prognostic role of HER-2 and cmyc amplification as predictors of adenoma transformation into carcinoma
The vast majority of pleomorphic adenomas occur in the parotid glands, but they can be found in the submandibular glands, sublingual glands, or small salivary glands
Summary
Salivary gland (SG) tumours are a highly heterogeneous group of tumours and include more than 35 histological subtypes, from benign adenomas to highgrade carcinomas.Pleomorphic adenoma (PA) is the most common salivary gland tumour representing about a half of all salivary gland neoplasms and 65% of parotid gland tumours [1,2,3]. Salivary gland (SG) tumours are a highly heterogeneous group of tumours and include more than 35 histological subtypes, from benign adenomas to highgrade carcinomas. Pleomorphic adenoma (PA) is a benign mixed salivary gland tumour, associated with abnormal karyotypes in up to 70% of cases, with nonrandom involvement of 8q12, the locus of the pleomorphic adenoma (PLAG1) gene. The vast majority of pleomorphic adenomas occur in the parotid glands, but they can be found in the submandibular glands, sublingual glands, or small salivary glands. They mostly arise between the ages of 30 and 60 years and are more commonly found in females than in males [4]. Some 2 to 17% of all pleomorphic adenomas tend to the undergo a malignant transformation, giving rise to the so-called »carcinoma ex pleomorphic adenoma« (CXPA) [3,4,5]
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