Chromosomal aberrations in premalignant and malignantsquamous epithelium

Predictive Value of Dysplasia Grading and DNA Ploidy in Malignant Transformation of Oral Potentially Malignant Disorders

“…Preneoplastic oral epithelium is usually aneuploid (8)(9)(10) and DNA aneuploidy indicates risk of malignant transformation (11). These changes can be measured using karyometry, flow cytometry (12), and image analysis (13) and more subtle loss of heterozygosity by molecular methods (14).…”

Application of Host Cell Reactivation in Evaluating the Effects of Anticancer Drugs and Environmental Toxicants on Cellular DNA Repair Activity in Head and Neck Cancer

“…3.2 Alterations of DNA repair genes/activity in HNSCC and the relationship with HNSCC development, treatment, as well as patient's outcome GIN is a hallmark of most human malignancies including HNSCC that elevated microsatellite instability, aneuploidy and various genomic alterations have been found by genome-wide analyses (Bockmuhl et al, 1996;Brieger et al, 2003;Friedlander, 2001;Partridge et al, 1999;Sparano et al, 2006), suggesting that GIN may be involved in the development of HNSCC. Some studies also show that DNA repair activity is reduced in the peripheral blood cells of HNSCC patients when compared with normal individuals (Cheng et al, 1998;Paz-Elizur et al, 2006), implying that altered DNA repair genes and/or activity may play a critical role in the development of HNSCC.…”

“…Some studies also show that DNA repair activity is reduced in the peripheral blood cells of HNSCC patients when compared with normal individuals (Cheng et al, 1998;Paz-Elizur et al, 2006), implying that altered DNA repair genes and/or activity may play a critical role in the development of HNSCC. Studies using comparative genomic hybridization (CGH) have shown that gene copy numbers at chromosome 11q22-23 (ATM locus) are frequently lost in HNSCC (Bockmuhl et al, 1996;Brieger et al, 2003;van den Broek et al, 2007). Lazar et al also showed loss of heterozygosity (LOH) at 11q23 in 25% (13/52) of primary HNSCC (Lazar et al, 1998).…”

“…In contrast, studies using CGH found an overrepresentation of 17q in 9% to 47% of HNSCC (Bockmuhl et al, 1996;Brieger et al, 2003), and one array-CGH reported the gain of 17q21 in 33% (7/21) of oral cancer (Sparano et al, 2006). These controversial results by genome-wide analyses may be due to the physically close localization of ERBB2 (HER-2/neu) oncogene and the results need to be clarified by specifically looking at the BRCA1 gene locus.…”

“…Regarding the expression of BRCA1 in HNSCC, one study showed that BRCA1 immunostaining positivity was lost in 34% (26/77) of tongue cancers, which might be correlated with early-stage tumor progression (Vora et al, 2003). The results of genome-wide studies also suggest that genetic alterations at RAD51 (15q15.1) and XPC (3p25) loci may be present in HNSCC (Bockmuhl et al, 1996;Brieger et al, 2003;Partridge et al, 1999;Sparano et al, 2006;van den Broek et al, 2007). Altered RAD51 protein expression has been reported by one pilot study with twelve head and neck cancer patients (Connell et al, 2006).…”