Genetic and molecular alterations associated with oral squamous cell cancer (Review)

Abstract

Abstract. The development of oral squamous cell cancer (OSCC) is a multistep process involving the accumulation of multiple genetic alterations modulated by genetic predisposition and environmental influences such as tobacco and alcohol use, chronic inflammation, and viral infections. All of these factors can lead to a wide range of genetic and molecular alterations that can be detected using a range of molecular studies. The alterations mostly affect two large groups of genes: oncogenes and tumor suppressor genes, which can be either inactivated or overexpressed through mutations, loss of heterozygosity, deletions, or epigenetic modifications such as methylation. Other molecules that are closely associated with tumor pathogenesis and prognosis also exist and warrant further study. Important advances in molecular biology are helping to shed light on oral cancer and thus aiding in the early diagnosis and development of new personalized treatment approaches. The purpose of the review is to explore the genetic and molecular alterations associated with OSCC.

Quantitative determination of c-myc facilitates the assessment of prognosis of OSCC patients

“…An oral squamous cell carcinoma (OSCC) is a tumor characterized by multiple multistep genetic alterations, that lead to genomic instability and disordered cell growth due to oncogene overexpression, subexpression of tumor-suppressor genes and other genetic, epigenetic and microRNA alterations (1)(2)(3)(4)(5). The two most studied oncogenes (dominant) in human solid tumors are HER-2/neu and c-myc; while p53 is a tumor-suppressor gene involved in almost all human malignancies (6).…”

Let-7d functions as novel regulator of epithelial-mesenchymal transition and chemoresistant property in oral cancer

“…The prognosis of OSCC remains dismal as more than 50% of the patients die of this disease or complications within 5 years under current therapies (2). To increase patient survival rate, investigations elucidating the mechanisms of tumorigenesis in OSCC are urgently needed (2).…”

“…The prognosis of OSCC remains dismal as more than 50% of the patients die of this disease or complications within 5 years under current therapies (2). To increase patient survival rate, investigations elucidating the mechanisms of tumorigenesis in OSCC are urgently needed (2). Some studies have suggested that subsets of cancer stem cells (CSC) or tumor initiating cells (TICs) are responsible for tumor progression as well as recurrence after conventional chemotherapy (3).…”

“…Head and neck squamous cell carcinoma, including oral squamous cell carcinoma (OSCC), is the sixth most prevalent malignancy worldwide and accounts for approximately 8-10% of all cancers in Southeast Asia (1,2). The prognosis of OSCC remains dismal as more than 50% of the patients die of this disease or complications within 5 years under current therapies (2).…”

Contribution of LATS1 and LATS2 promoter methylation in OSCC development

“…Oncogenes and tumor suppressor genes are the two major groups of pro-tumorigenic genes which promote tumorigenesis whenever up-regulated or down-regulated, respectively (Hanahan and Weinberg 2000). The down-regulation of tumor suppressor genes is preceded through various epigenetic modifications, mutations, loss of heterozygosities and deletions (Perez-Sayans et al 2009). The epigenetic suppression of genes take place through methylation of CpG islands or histone modifications such as methylation of histone 3, lysine 27 (H3K27) (Rad et al 2016).…”