Clinical implications of epigenetic regulation in oral cancer

Molecular markers associated with development and progression of potentially premalignant oral epithelial lesions: Current knowledge and future implications

“…12 Mounting evidence indicates that the transition from normal epithelium to PPOELs to invasive OSCC is the result of an accumulation of genetic and epigenetic alterations, the latter referring to a multitude of aberrations, including chromosomal rearrangements, mutations, methylation, and others, which affect the expression and function of oncogenes and tumor suppressor genes (reviewed elsewhere). 12,[14][15][16] In other words, the clinical appearance (e.g., OL) and microscopic changes (e.g., epithelial dysplasia) that indicate the presence of PPOELs are driven by specific molecular alterations that accumulate over time, eventually culminating in MT. Because, by definition, PPOELs and/or dysplasia are viewed as early events, it follows that elucidation of molecular alterations crucial to the progression to malignancy would predict premalignancy with greater specificity and sensitivity when coupled with clinical annotation and histopathology.…”

The association between fecal hemoglobin concentration and oral potentially malignant disorders

“…One of interesting themes, as both colorectal cancer screening with FIT and oral cancer screening with dental visual inspection have been conducted in the contemporaneous period in Taiwan, is related to oral cancer that are often caused by two risk factors, tobacco and betel quid, in addition to evidence on a series of possible genetic variants (Dai et al, ; Williams, ) and epigenetic markers (D'Souza & Saranath, ; Gasche & Goel, ; Tsai et al, ). The underlying pathways partially shared by two habits and oral cancer may be through chronic inflammation because betel quid has been associated with inflammatory markers such as C‐reactive protein (Chang et al, ; Shafique et al, ) and metabolic syndrome (Chung et al, ; Javed, Al‐Hezaimi, & Warnakulasuriya, ), and also, the association between chronic inflammation and oral potentially malignant disorders (OPMD) was noted (Mignogna, Fedele, Lo Russo, Lo Muzio, & Bucci, ; Piva et al, ; Tilakaratne, Ekanayaka, & Warnakulasuriya, ).…”

Single Nucleotide Polymorphisms and Risk of Oral Cancer: Indian Case-Control Study

“…The differential frequency of the allelotypes and genotypes in a cancer casecontrol cohort indicates association of the SNPs with the cancer. DNA methylation is an epigenetic regulation resulting in transcriptional silencing of genes and plays an important role in early and advanced stages of oral cancer [11]. The relationship between SNPs and DNA methylation have been studied in several noncommunicable diseases including obesity [12], bipolar disorder [13], alcohol dependence [14], as well as cancers of breast, colon, lung, liver, kidney, prostate, etc [15].…”