“…The role of chromosomal instability during the genesis and progression of oral cancer has clearly been indicated by several studies but still our understanding of the molecular mechanisms is relatively poor. Analyses were performed with the use of different techniques including loss of heterozygosity (Braakhuis et al, 2004;Bremmer et al, 2008;Graveland et al, 2011;Lydiatt et al, 1998;Mithani et al, 2007;Partridge et al, 1997;Tsantoulis et al, 2007), comparative genomic hybridization and gene expression array (Bremmer et al, 2008;Cha et al, 2011;Garnis et al, 2009;Liu et al, 2006Liu et al, , 2011Smeets et al, 2009;Snijders et al, 2005;Squire et al, 2002;), in situ hybridization (Nees et al, 1993;Voravud et al, 1993), immunohistochemistry (Nees et al, 1993), multiplex ligation-dependent probe amplification (Bremmer et al, 2008;Cha et al, 2011;Liu et al, 2006), DNA image cytometry (Bremmer et al, 2008;Diwakar et al, 2005) and DNA flow cytometry (DNA FCM) (Donadini et al, 2010;Hemmer, 1990Hemmer, , 1997Pentenero et al, 2009;Saito, 1998Saito, , 1991Saito, , 1995Seoane et al, 1998). DNA FCM was often adopted as a useful technique for detecting the presence of DNA aneuploid sublines in several human predisposing and preneoplastic lesions such as Barrett's esophagus (Reid et al, 2000), ulcerative colitis (Rabinovitch et al, 1999;Risques et al, 2008), colorectal adenomas (Giaretti et al, 1994) and oral lesions …”