We analyzed the alteration of the hst-1 and int-2 genes in 36 cases of esophageal squamous cell carcinoma, 42 cases of gastric adenocarcinoma, and 52 cases of colorectal adenocarcinoma.
We analyzed the alteration of the hst-1 and int-2 genes in 36 cases of esophageal squamous cell carcinoma, 42 cases of gastric adenocarcinoma, and 52 cases of colorectal adenocarcinoma.
Base substitutions at A:T pairs constitute an important fraction of ESCp53 mutations, in contrast to mutation patterns in most other types of solid tumors.
These results suggest that int-2/hst-1 coamplification is a new biological indicator of prognosis and distant organ metastasis in patients with esophageal squamous cell carcinoma.
The correlation between the clinical outcome in patients with esophageal squamous cell carcinoma and coamplification of the proto-oncogenes int-2 and hst-1, which are partially homologous to angiogenesis-inducing fibroblast growth factor, was analyzed retrospectively.
The correlation between the clinical outcome in patients with esophageal squamous cell carcinoma and coamplification of the proto-oncogenes int-2 and hst-1, which are partially homologous to angiogenesis-inducing fibroblast growth factor, was analyzed retrospectively.
Since alterations in the p53 tumor suppressor gene occur frequently in invasive esophageal squamous cell carcinoma, we examined a set of preinvasive lesions to investigate the timing of p53 mutation.
These results suggest that mutations of the p53 gene are genetic events in the pathogenesis of gastric adenocarcinoma and esophageal squamous cell carcinoma.
Furthermore, we immunohistochemically analyzed the expression of p53 protein in esophageal squamous cell carcinoma tumor tissues using a monoclonal antibody.
These results suggest that HPV-16 and -18 may play a role in the pathogenesis of esophageal SCC, particularly with regard to its striking geographical distribution; that esophageal cancers do occur in the absence of HPV infection when over-expression of p53 is present; and that the presence of HPV infection and over-expression of p53 may each be a factor indicating a relatively poor prognosis.
The expression of human glutathione S-transferase-pi (GST-pi) in esophageal squamous cell carcinoma and in corresponding morphologically normal mucosa from 17 patients was examined by Northern blots, in situ hybridization and immunohistochemistry.
The expression of human glutathione S-transferase-pi (GST-pi) in esophageal squamous cell carcinoma and in corresponding morphologically normal mucosa from 17 patients was examined by Northern blots, in situ hybridization and immunohistochemistry.
The expression of human glutathione S-transferase-pi (GST-pi) in esophageal squamous cell carcinoma and in corresponding morphologically normal mucosa from 17 patients was examined by Northern blots, in situ hybridization and immunohistochemistry.
We have previously shown that four human oesophageal squamous cell carcinoma (SCC) cell lines secrete significant quantities of transforming growth factor alpha (TGF-alpha) in vitro.
We performed an immunohistochemical analysis of the EGFR in 217 cases of human esophageal squamous cell carcinoma, 161 lymph node metastases and 23 foci of squamous dysplasias.
In this study, we analyzed immunohistochemically the localization of p53 using three different antibodies, PAb1801, DO-7, and CM-1 in 49 patients with esophageal squamous cell carcinoma.
Thus, aberration of tumor-suppressor genes was a frequent occurrence in esophageal squamous-cell carcinoma and inactivation of the p53 gene may contribute to the progression of this tumor.