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Genetics and Molecular Mechanisms in Oral Cancer Progression

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Abstract

Exposure to tobacco in smoke or chewable form, in isolation or in association with other risk factors (i.e., alcohol or areca nut), disturbs the balanced expression of numerous genes and leads to loss of coordination of their downstream signaling pathways, finally leading to oral cancer. Initially changes like mild dysplasia and benign hyperplasia are reversible, but continuous exposure to carcinogens leads to accumulation of mutations in multiple genes involved in cell proliferation, differentiation, apoptosis, telomere maintenance, invasion, and angiogenesis, resulting in abnormal cell behavior and cell immortalization. Gains and losses occur on many chromosomal arms, and a well-characterized mutational landscape is associated with oral cancer. This chapter discusses the wide spectrum of genetic and epigenetic events that take place in oncogenes and tumor suppressor genes with special reference to oncogenic miRs (miR-21, miR-31, miR-146a, miR-134, miR-184, miR-7, miR-127, miR-518c-5p), tumor suppressor miRs (miR-200 family, miR-101, miR-26a/b, miR-29a, miR-27b, miR-137, miR-125a, miR-29a, miR-491-5p, miR-124, miR-125, miR-218, miR-99a, miR-375), and long noncoding RNA (HOTAIR, FOXCUT, MALAT1, UCA1, TUG1, CCAT2, FTH1P3, H19, HIFCAR/MIRHG) that influence oncogenic signaling pathways and enable acquisition of cancer hallmarks.

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Panta, P., Manavathi, B., Nagini, S. (2019). Genetics and Molecular Mechanisms in Oral Cancer Progression. In: Panta, P. (eds) Oral Cancer Detection. Springer, Cham. https://doi.org/10.1007/978-3-319-61255-3_2

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