Inactivation patterns of p16/INK4A in oral squamous cell carcinomas

Methylation-Mediated Molecular Dysregulation in Clinical Oral Malignancy

“…Aberrant methylation of this locus in noncancer controls has not been detected [23–25]. A panel of cell lines was investigated for homozygous deletion, hypermethylation, and point mutations at p16 , with results indicating that the first two alteration types were the more common modes of p16 disruption in OSCC [26]. …”

p16INK4A genetic and epigenetic profiles differ in relation to age and site in head and neck squamous cell carcinomas

“…The formation of the newly generated RNA molecules can therefore be determined in real time by continuous monitoring of fluorescence in a Lambda Fluoro 320 reader (MWG Biotech, AG, Ebersberg, Germany). The PreTect HPV-Proofer Kit includes specific primer and molecular beacon probe sets for detection and simultaneous typing of 2 of the high-risk HPV types [14,16]. The PreTect HPV Proofer Kit also contains a primer and probe set for U1A, which is used as an extraction control.…”

“…Alterations of the p16 tumor suppressor gene have been consistently reported in HNSCC, with the prevalence of p16 alterations ranging from 25% to 83% [8][9][10][11][12]. Previous studies have noted that these alterations are predominantly in the form of deletions and methylationinduced epigenetic silencing, and also, that mutation of p16 is a less common mechanism of inactivation in head and neck cancer [13][14][15]. Previous work by this group has specifically noted that p16 deletions in HNSCC occurred in patients older than 40 years [10].…”

Hypermethylation of the RUNX3 gene in hepatocellular carcinoma

“…For DNA methylation analysis, sodium bisulfite modification of genomic DNA was performed, as described previously (Grunau et al, 2001;Lehmann et al, 2001;Lee et al, 2004). In brief, 1 µg DNA was denatured with 0.2 M NaOH in a total vol of 50 µl.…”