Potential role and chronology of abnormal expression of the Deleted in Colon Cancer (DCC) and the p53 proteins in the development of gastric cancer

BMC Cancer. 2001:1:9. doi: 10.1186/1471-2407-1-9. Epub 2001 Aug 1.

Abstract

Background: Loss of activity of tumor suppressor genes is considered a fundamental step in a genetic model of carcinogenesis. Altered expression of the p53 and the Deleted in Colon Cancer (DCC) proteins has been described in gastric cancer and this event may have a role in the development of the disease. According to this hypothesis, we investigated the p53 and the DCC proteins expression in different stages of gastric carcinomas.

Methods: An immunohistochemical analysis for detection of p53 and DCC proteins expression was performed in tumor tissue samples of patients with UICC stage I and II gastric cancer. For the purpose of the analysis, the staining results were related to the pathologic data and compared between stage categories.

Results: Ninety-four cases of gastric cancer were analyzed. Disease stage categories were pT1N0 in 23 cases, pT2N0 in 20 cases, pT3N0 in 20 cases and pT1-3 with nodal involvement in 31 cases. Stage pT1-2N0 tumors maintained a positive DCC expression while it was abolished in pT3N0 tumors (p <.001). A significant higher proportion of patients with N2 nodal involvement showed DCC negative tumors. In muscular-invading tumors (pT2-3N0) the majority of cases showed p53 overexpression, whereas a significantly higher proportion of cases confined into the mucosa (pT1N0) showed p53 negative tumors. Also, a higher frequency of p53 overexpression was detected in cases with N1 and N2 metastatic lymph nodal involvement.

Conclusions: Altered expression of both DCC and p53 proteins is detectable in gastric carcinomas. It seems that loss of wild-type p53 gene function and consequent p53 overexpression may be involved in early stages of tumor progression while DCC abnormalities are a late event.

Publication types

  • Multicenter Study

MeSH terms

  • Aged
  • Aged, 80 and over
  • Cell Adhesion Molecules / biosynthesis*
  • Cell Adhesion Molecules / genetics*
  • Cell Adhesion Molecules / physiology
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / physiopathology
  • DCC Receptor
  • Female
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / pathology
  • Gene Expression Regulation, Neoplastic*
  • Genes, DCC / genetics
  • Genes, DCC / physiology
  • Genes, Tumor Suppressor*
  • Humans
  • Lymph Nodes / pathology
  • Male
  • Middle Aged
  • Neoplasm Invasiveness / genetics
  • Neoplasm Invasiveness / physiopathology
  • Receptors, Cell Surface
  • Stomach Neoplasms / etiology*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / physiopathology
  • Tumor Suppressor Protein p53 / biosynthesis*
  • Tumor Suppressor Protein p53 / genetics*
  • Tumor Suppressor Protein p53 / physiology
  • Tumor Suppressor Proteins / biosynthesis*
  • Tumor Suppressor Proteins / genetics*
  • Tumor Suppressor Proteins / physiology

Substances

  • Cell Adhesion Molecules
  • DCC Receptor
  • DCC protein, human
  • Receptors, Cell Surface
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins