Frequent mutation of p16CDKN2A exon 1 during rat tongue carcinogenesis induced by 4-nitroquinoline-1-oxide

✍ Scribed by Yun Hong; Linglan Yang; Chunyang Li; Hongbin Xia; Nelson L. Rhodus; Bin Cheng

• Book ID: 102502746
• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 365 KB
• Volume: 46
• Category: Article
• ISSN: 0899-1987
• DOI: 10.1002/mc.20197

✦ Synopsis

Abstract

In this study we explored the mutation types of p16^CDKN2A^ exon 1 and the corresponding frequencies in experimental rat tongue carcinogenesis. Twenty barrier Sprague–Dawley (SD) rats were divided into the control (n = 5) and experimental group (n = 15), to which 4‐nitroquinoline‐1‐oxide (4‐NQO) in drinking water was administered. Two samples of normal, three samples of moderate/severe dysplasia and four samples of invasive squamous cell carcinoma lesions were selected following strict histopathological examination in double‐blind manner. The PCR products of p16^CDKN2A^ exon 1 amplified from these tissues were sequenced. Point mutations of p16^CDKN2A^ exon 1 were found in all of the precancerous and cancerous lesions. Half of the mutations were detected on guanine (G). Twenty mutations, including a missense mutation of the start codon resulting in alternative reading frame of p16^CDKN2A^ exon 1, were also identified. These preliminary results suggested that mutation of p16^CDKN2A^ exon 1 might be an early molecular event of rat tongue carcinogenesis induced by 4NQO and G was the mutation hotspot. © 2006 Wiley‐Liss, Inc.