Oral Oncology
Volume 38, Issue 8 , Pages 772-778, December 2002

Expression of β-catenin in rat oral epithelial dysplasia induced by 4-nitroquinoline 1-oxide

  • Kazumichi Sato

      Affiliations

    • Department of Oral Medicine, Tokyo Dental College, 5-11-13 Sugano, Ichikawa City, Chiba 272-8513, Japan
    • Corresponding Author InformationCorresponding author. Tel.: +81-47-322-0151; fax: +81-47-324-8577
  • ,
  • Yuichiro Okazaki

      Affiliations

    • Department of Oral Medicine, Tokyo Dental College, 5-11-13 Sugano, Ichikawa City, Chiba 272-8513, Japan
  • ,
  • Morio Tonogi

      Affiliations

    • Department of Oral Medicine, Tokyo Dental College, 5-11-13 Sugano, Ichikawa City, Chiba 272-8513, Japan
  • ,
  • Yoichi Tanaka

      Affiliations

    • Division of Surgical Pathology, Clinical Laboratory, Ichikawa General Hospital, Tokyo Dental College 5-11-13 Sugano, Ichikawa City, Chiba 272-8513, Japan
  • ,
  • Gen-yuki Yamane

      Affiliations

    • Department of Oral Medicine, Tokyo Dental College, 5-11-13 Sugano, Ichikawa City, Chiba 272-8513, Japan

Received 27 May 2002; accepted 14 June 2002.

Abstract 

The aim of this study was to evaluate whether β-catenin accumulation is useful for diagnosing the malignant potential of oral precancerous lesions. We investigated oral epithelial dysplasia adjacent to early cancer induced by 4-nitroquinoline 1-oxide in rats. Localization of β-catenin and cell proliferation were detected immunohistochemically, and exon 3 of the β-catenin gene was analyzed. Accumulation of β-catenin in the cytoplasm and nucleus was evident in 10 of 16 dysplasia lesions. Since almost all of the dysplastic lesions in these rats transformed to invasive cancer, β-catenin accumulation may contribute to the early stage of carcinogenesis. The Ki-67 labeling index was significantly higher in dysplasia and early cancer than in no change. However, there were no significant differences between the expression patterns of β-catenin protein, suggesting that other proliferation pathways are involved in the early stage of tumor development in addition to β-catenin accumulation. No mutations of exon 3 of the β-catenin gene were detected in any of the dysplasia or early cancer lesions. These findings suggested that β-catenin accumulation in the cytoplasm and nucleus without mutation of exon 3 is an early event during carcinogenesis in this tongue cancer model.

Keywords:  Dysplasia, β-Catenin, Oral carcinogenesis, 4-Nitroquinoline 1-oxide, Squamous cell carcinoma

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PII: S1368-8375(02)00044-1

doi:10.1016/S1368-8375(02)00044-1

Oral Oncology
Volume 38, Issue 8 , Pages 772-778, December 2002