作者: Prashanth Panta , Bramanandam Manavathi , Siddavaram Nagini
DOI: 10.1007/978-3-319-61255-3_2
关键词:
摘要: Exposure to tobacco in smoke or chewable form, isolation association with other risk factors (i.e., alcohol areca nut), disturbs the balanced expression of numerous genes and leads loss coordination their downstream signaling pathways, finally leading oral cancer. Initially changes like mild dysplasia benign hyperplasia are reversible, but continuous exposure carcinogens accumulation mutations multiple involved cell proliferation, differentiation, apoptosis, telomere maintenance, invasion, angiogenesis, resulting abnormal behavior immortalization. Gains losses occur on many chromosomal arms, a well-characterized mutational landscape is associated This chapter discusses wide spectrum genetic epigenetic events that take place oncogenes tumor suppressor special reference oncogenic miRs (miR-21, miR-31, miR-146a, miR-134, miR-184, miR-7, miR-127, miR-518c-5p), (miR-200 family, miR-101, miR-26a/b, miR-29a, miR-27b, miR-137, miR-125a, miR-491-5p, miR-124, miR-125, miR-218, miR-99a, miR-375), long noncoding RNA (HOTAIR, FOXCUT, MALAT1, UCA1, TUG1, CCAT2, FTH1P3, H19, HIFCAR/MIRHG) influence pathways enable acquisition cancer hallmarks.