The Expression of p53, p16, Cyclin D1 in Esophageal Squamous Cell Carcinoma and Esophageal Dysplasia.
- Author:
Sang Gyune KIM
1
;
Su Jin HONG
;
Kye Won KWON
;
Sung Won JUNG
;
Whan Yeol KIM
;
In Seop JUNG
;
Bong Min KO
;
Chang Beom RYU
;
Young Seok KIM
;
Jong Ho MOON
;
Jin Oh KIM
;
Joo Young CHO
;
Joon Seong LEE
;
Moon Sung LEE
;
Chan Sup SHIM
;
Boo Sung KIM
Author Information
1. Institute for Digestive Research, Departments of Internal Medicine, Soon Chun Hyang University College of Medicine, Bucheon and Seoul, Korea.
- Publication Type:Original Article ; Comparative Study ; English Abstract
- Keywords:
Squamous cell carcinoma;
esophagus;
p53;
p16;
Cyclin D1
- MeSH:
Aged;
Carcinoma, Neuroendocrine/*diagnosis/pathology;
Chromogranin A/analysis/immunology;
Drainage;
Female;
Humans;
Immunohistochemistry;
Liver Abscess/*radiography/surgery;
Liver Neoplasms/*diagnosis/pathology;
Radiography, Abdominal;
Synaptophysin/analysis/immunology;
Tomography, X-Ray Computed
- From:The Korean Journal of Gastroenterology
2006;48(4):269-276
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: p53 is known to play a central role in sensing and signaling for the growth arrest and apoptosis in cells with DNA damage. Mutation of p53 is a frequent event in esophageal squamous cell carcinoma (ESCC). p16 protein binds to cyclin dependent kinase 4 (CDK4) inhibiting the ability of CDK4 to interact with cyclin D1, and stimulates the passage through the G1 phase of cell cycle. We observed the expression patterns and frequencies of p53, p16, and cyclin D1 in esophageal dysplasia and in esophageal squamous cell carcinomas. METHODS: In 15 patients of ESCC, 5 patients of esophageal dysplasia and 5 volunteers with normal esophagus, tissue specimens were taken from esophageal lesions during the operation or endoscopic examination. We used specific monoclonal antibodies for p53 protein, p16INK4 protein and cyclin D1. Immunoreactivity was scored. RESULTS: Mean age of all groups was 66 years old (range 47-93) and men to women ratio was 19:1. p53 mutation was observed in 87% (13/15) of ESCC, in 80% (4/5) of esophageal dysplasia, in 0% (0/5) of normal mucosa (p=0.001). p16 expression was seen in 40% (2/5) of esophageal dysplasia, 27% (4/15) of ESCC and 100% (5/5) of normal mucosa (p=0.016). Cyclin D1 expression was not significantly different among 20% (1/5) of esophageal dysplasia, 53% (8/15) of ESCC and 20% (1/5) of normal mucosa. Either the expression of p53 mutation or the loss of p16 occurred in 80% (4/5) of esophageal dysplasia and in 93% (14/15) of ESCC. CONCLUSIONS: The expression of p53 mutation and the loss of p16 might play a central role in the pathogenesis of esophageal squamous cell carcinoma (ESCC), and contribute to the development of precancerous lesion such as dysplasia. In addition, there is a possibility that the mutations of p53 and p16 silencing would be the early events in ESCC development.
