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Infrequent Ha-ras mutations and absence of Ki-ras, N-ras, and p53 mutations in 4-nitroquinoline 1-oxide-induced rat oral lesions

✍ Scribed by Masumi Suzui; Naoki Yoshimi; Takuji Tanaka; Hideki Mori

Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
582 KB
Volume
14
Category
Article
ISSN
0899-1987

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✦ Synopsis

Abstract

The alkylating agent 4‐nitroquinoline 1‐oxide (4‐NQO) is a powerful carcinogen and induces squamous cell hyperplasia, squamous cell dysplasia, papilloma, and squamous cell carcinoma (a) in rat oral epithelia. Oral cancers induced by a single application of 4‐NQO develop through a multistage process in a way similar to the development of this cancer in humans. In this study, mutations in exons 1 and 2 of Ki‐ras, N‐ras, and Ha‐ras and exons 4–7 of p53 were examined by polymerase chain reaction (a) ‐single strand conformation polymorphism (a) analysis, followed by PCR‐direct sequencing for the confirmation of mutations. Samples for the mutation analysis were obtained from dysplasias, papillomas, and SCCs on the tongue epithelia induced in F344 rats by adding 4‐NQO (20 ppm) to their drinking water for 8 wk. The Ha‐ras mutations (^61^A→T transversions in the second position) were found in five of 29 (17%) samples (one dysplasia and four SCCs). However, no mutations were detected in either Ki‐ras, N‐ras, or p53 under two different conditions of PCR‐SSCP analysis. We suggest that some neoplasms in oral carcinogenesis induced by 4‐NQO may involve Ha‐ras mutations but not mutations in Ki‐ras, N‐ras, or p53. The 4‐NQO‐induced rat oral carcinogenesis model may provide a system for evaluation of the mechanisms of multistage oral carcinogenesis associated with Ha‐ras mutation without Ki‐ras, N‐ras, or p53 mutation. © 1995 Wiley‐ Liss, Inc.

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