We report on one patient of nine studied with Barrett's esophagus who had trisomy 7 and showed increased expression of epidermal growth factor receptor.
Precursors of the gastric proteases pepsinogen A (pepsinogen I) and pepsinogen C (pepsinogen II) and slow-moving protease were demonstrated in biopsy specimens from Barrett's epithelium in 21 of 22 patients with Barrett's esophagus; in 14 of them, in variable combinations at different sites.
The aim of this study was to establish the prevalence of p53 protein overexpression in a series of resected esophageal squamous carcinomas (n = 78), adenocarcinomas developed on Barrett's esophagus (n = 20), adenocarcinomas of the cardia (n = 36), and adenocarcinomas of the antrum (n = 30), and to correlate this expression with the clinico-pathological and flow-cytometric characteristics of the tumors.
The purpose of this study therefore was to investigate the clinical value of p53 and Ki67 as markers for tumour progression in BE, and at the same time test the validity of the concept of a metaplasia-dysplasia-carcinoma sequence in BE by correlating the expression of these markers with various grades of dysplasia.
These results indicate that p53 gene alterations contribute to the development of esophageal adenocarcinoma and precede the development of invasive carcinoma in patients with Barrett's esophagus.
In conclusion, the practical utility of mucin stainings, endocrine cell count, assessment of cell proliferation and differentiation by PCNA, EGF and TGFa seems to be limited in differentiation of the dysplastic and indefinite for dysplasia BO.
Several investigators have found that p53 alteration is a frequent event in oesophageal adenocarcinomas and is associated with malignant transformation of Barrett's oesophagus. p53 appears to be a promising prognostic marker in Barrett's oesophagus and, as research progresses, possible clinical applications are emerging.
Utilizing immunohistochemistry, p53 staining was detected in 42% of Barrett's metaplasia specimens, most of which were dysplastic, and in 58% of adenocarcinomas.
APN protein was detected by utilizing immunohistochemistry in 84% of Barrett's metaplasia specimens and in 71% of adenocarcinomas, although a decrease or loss of APN protein was sometimes observed in dysplastic Barrett's metaplasia and adenocarcinomas.
These findings demonstrate that DNA ploidy as well as c-erbB-2 oncoprotein overexpression are valuable prognostic factors in patients with adenocarcinoma of Barrett's esophagus after complete tumor resection.
Our data strongly suggest that 17p allelic losses precede the development of aneuploidy during neoplastic progression in Barrett's esophagus in vivo and, therefore, support in vitro evidence for the role of p53 in genetic instability.