Model of Chromosomal Instability in Oral Carcinogenesis and Progression

摘要: Epidemiologic and experimental evidence indicate that oral cancer originates progresses with the contribution of carcinogen exposure, mainly from tobacco smoking (IARC, 1986, 2004). This is thought to contribute DNA damage within mucosa and, in particular, subsequent gene mutations, chromosomal instability aneuploidy, resulting an increased risk developing cancer. Accumulation genetic/genomic aberrations over time leads a multi-step process carcinogenesis which functions genes control cell cycle (proliferation apoptosis), chromosome stability, angiogenesis, invasion metastasis, become aberrant (Califano et al., 1996; Hanahan & Weinberg 2011; Martorell-Calatayud 2009). Chromosomal are located, at 9p21, 17p13, 3q26, 11q13, 3p21, 14q32 (Forastiere 2001; Gollin, 2001) corresponding several putative tumor suppressor oncogenes including p16 9p21 TP53 17p13.