[Diagnostic and prognostic values of repair protein hMLH1, hMSH2 and protein CD34 immunoexpression in sporadic colorectal cancer].

UNLABELLED

Colorectal carcinoma is the most common gastrointestinal malignancy in the world. The survival of patients with colorectal cancer has not varied appreciably in recent years. The knowledge that genetic factors could play a role in the etiology and prognosis of patients with sporadic colorectal cancer has opened up new lines of research. The aim of the study was to evaluate a group of patients with colorectal cancer and the possible influence on the prognosis of immunohistochemical hMLH1, hMSH2 and CD34 expression.

MATERIAL AND METHODS

37 cases of colorectal cancer were included in this study. HMLH1, hMSH2 and CD34 protein expression in tumor tissue sections was determined using immunohistochemical staining with specific monoclonal antibodies. A total of 37 tumors were analyzed for histopathology. The immunoexpression status of MMR genes was correlated with cancer stage, location, histology, gender and CD34 immunoexpression.

RESULTS

Of the 37 cases immunohistochemical analysis showed 13 (35.1%) had loss of expression of hMLH1, 5 (13.5%) had loss of expression of hMSH2, and five cases had loss of expression of both proteins. Multivariate analysis showed that right side dominance (p<0.05) poorly differentiated and male (p<0.05) were associated with loss of expression of hMLH1 or hMSH2. Loss of expression of hMLH1 or hMSH2 correlated with low CD34 expression (p>0.05). CD34 immunoexpression was higher in the left side tumor location, stage D Dukes'a (p<0.05) and G2 (p<0.05).

CONCLUSIONS

These results confirm that sporadic colorectal MMR-defective adenocarcinomas display certain specific morphological characteristics. However, these pathological features are not sufficiently predictive and immunohistochemistry is needed to identify such tumours accurately. The researches on angiogenesis of cancer cells can be used as prognostic factors for the patients with colorectal cancer.