Original Research
Copyright ©The Author(s) 1997. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 15, 1997; 3(2): 87-89
Published online Jun 15, 1997. doi: 10.3748/wjg.v3.i2.87
Changes in p53 and Waf1p21 expression and cell proliferation in esophageal carcinogenesis
Li-Dong Wang, Wan-Cai Yang, Qi Zhou, Ying Xing, Yun-Ying Jia, Xin Zhao
Li-Dong Wang, Wan-Cai Yang, Qi Zhou, Ying Xing, Xin Zhao, Laboratory for Cancer Research, Henan Medical University, Zhengzhou 450052, Henan Province, China
Yun-Ying Jia, Department of Gastroenterology, The People′s Hospital of Puyang City, Puyang 457000, Henan Province, China
Author contributions: All authors contributed equally to the work.
Supported by The Henan Scientific Foundation for Outstanding Young Scientists and National Natural Science Foundation of China, No.39670290, 39419711156) and U.S. NCl Grant CA 65871.
Correspondence to: Li-Dong Wang, MD, Laboratory for Cancer Research, Henan Medical University, Zhengzhou 450052, Henan Province, China
Telephone: +86-371-6970165
Received: September 28, 1996
Revised: January 31, 1997
Accepted: March 1, 1997
Published online: June 15, 1997
Abstract

AIM: To study the correlation between changes in p53 and Waf1p21 expression and cell proliferation, determined by proliferating cell nuclear antigen (PCNA), at different stages of human esophageal carcinogenesis.

METHODS: Biopsied and resected esophageal tissues from a high risk population of esophageal cancer in northern China were used in this study. All specimens were fixed in 85% alcohol and processed for routine histology. The avidin biotin peroxidase complex (ABC) method was used to detect p53, Waf1p21 and PCNA.

RESULTS: Strong nuclear staining of p53, Waf1p21 and PCNA was observed in normal esophageal epithelium and epithelia with different lesion severities. As the lesions progressed to dysplasia (DYS) and to esophageal squamous cell carcinoma (SCC), the Waf1p21 immunoreactivity percentage decreased. The number of Waf1p21-positive cells slightly increased from normal to basal cell hyperplasia (BCH), but did not further increase in DYS and SCC. The total number of Waf1p21-positive cells was lower than the number of p53-positive cells in normal and BCH esophageal epithelia and much lower in DYS and SCC. Waf1p21-positive cells were located in the third and fourth cell layers in half of the samples examined, which was 2-4 cell layers higher than the cells expressing PCNA and p53 in the same histological categories of normal, BCH and DYS.

CONCLUSION: Low Waf1p21 levels at the DYS stage may be related to a functional loss of p53. Other mechanisms may also be responsible for the decreased Waf1p21 expression in DYS and SCC.

Keywords: Esophageal neoplasms; Precancerous conditions; p53 genes; Waf1p21; Genes suppressor; Tumor