The Epigenesis of Salivary Glands Carcinoma: From Field Cancerization to Carcinogenesis

Abstract

Salivary gland carcinomas (SGCs) are a diverse collection of malignant tumors with marked differences in biological activity, clinical presentation and microscopic appearance. Although the etiology is varied, secondary radiation, oncogenic viruses as well as chromosomal rearrangements have all been linked to the formation of SGCs. Epigenetic modifications may also contribute to the genesis and progression of SGCs. Epigenetic modifications are any heritable changes in gene expression that are not caused by changes in DNA sequence. It is now widely accepted that epigenetics plays an important role in SGCs development. A basic epigenetic process that has been linked to a variety of pathological as well as physiological conditions including cancer formation, is DNA methylation. Transcriptional repression is caused by CpG islands hypermethylation at gene promoters, whereas hypomethylation causes overexpression of a gene. Epigenetic changes in SGCs have been identified, and they have been linked to the genesis, progression as well as prognosis of these neoplasms. Thus, we conduct a thorough evaluation of the currently known evidence on the involvement of epigenetic processes in SGCs.

Keywords: DNA methylation; Salivary gland cancers; epigenetic modifications; histone modifications; noncoding RNAs.

Figure 1

Etiological factors of salivary gland carcinoma. Multiple factors are working together to drive SGC from a few aberrant cells to a tumour phenotype with the capacity to metastasis. Therefore, the optimum environment for malignant development is maintained by a complex interplay of genetic events, risk factors, and epigenetic mechanisms. All of these factors work together to promote an unstable genome and hence, promote cancer progression.

Figure 2

Salivary gland carcinomas can be affected by a number of epigenetic events that can alter the development and progression of the cancer.