| Lung cancer is one of the most common malignity carcinoma worldwild and the rate of death is increasing in recent years, especially the city male mortality from lung cancer resulting from air pollution or cigarette smoking could be 38. 08 every one hundred of thousand people. It threatens human beings health heavily. Non - small cell lung cancer accounts for 75% - 80% of all lung tumors. The understanding of the molecular pathogenesis of this disease may help to prevent it and to provide a new and more sensitive means to diagnose and treat lung cancer patients. In 1996, the Fragile Histidine Triad ( FHTT) gene was cloned and considered as a novel tumor suppressor gene. It has been described that there is a high frequency of FHTT al-lelic deletion and abnormal mRNA transcripts in human cancers, such as lung, head and neck, esophageal, stomach and breast cancer. We investigate the expression of FHTT protein, products of this novel tumor suppressor gene, in non - small cell lung cancer and a few of precancerous lesion to access the significance of FHTT protein in diagnosis and therapy. At the same time we detect PCNA expression to learn the association of FHTT protein and cell proliferation.Materials and methodsParaffin blocks were obtained from 76 patients with primary NSCLC who underwent curative operations at the Liaoning Tumor Hospital from November 1999 to February 2000. Other 26 NSCLC specimens were obtained from patients with surgical excision at the First Hospital affiliated to China Medical University in 2002. These specimens were divided into two parts; one was frozen immediately at -70*0 and the other one was fixed with formalin and made into paraffin block. FHTT protein and PCNA were detected by immunohistochemis-try in 102 NSCLCs and 30 bronchial precamcerous lesions. Western blot was used to detected FHTT protein in 26 fresh specimens.500 tumor cells were observed in view of high magnification per slide at random. FHFT immunostaining was classified in the following three groups according to both intensity and extent; (1) Negative, no staining was present or immunostaining was present in less than 10% of all 500 cells. (2) Mild positive, immunostaining was weak or similar to that of positive control cells and such cells were more than 10% cells or strong staining cells were more than 10% cells and less than 50%. (3) Marked positive, strong staining cell were more than 50% cells. Compute PCNA index ( PI) according to this equation; PI = cells with nuclear staining 7500. PCNA expression was divided into two groups, PI <0. 5 and PI >0.5. Western blot; There were special bands between 15,000da and 20,000da marker bands, which were mensurated by Computer Image Analysis System.All the data were analyzed with SPSS For Windows 10. 0 software. Survival analysis used Kaplan - Meier and Cox model;The rela-tionship between expression of FHIT protein and clinical pathology characters was analyzed with chi - squared test. The cut - off for statistical significance was defined as P <0.05.ResultsImmunostaining location; There was cytoplasm staining of FHIT protein not only in cancer cells but also in normal bronchial epithelial cells, bronchial glands, type II alveolar cells, and macrophages. The staining of PCNA was located in nuclear of tumor cells.Expression in NSCLC and normal lung tissue; 71 (69. 6% ) Of the 102 cases of non - small cell lung cancer were negative for FHIT protein while 10(9.8% )were negative in all 102 cases of normal lung tissue, the difference was significant.Correlation of protein expression with clinicopathological features : The rate ( complete absence or decrease) of loss of FHIT expression is correlated with histological type,clinical stage and smoking history. The rate of loss of FHIT protein in squamous cell cancer was higher than that in adenocarcinoma( P = 0.01). The loss rate in early stage was higher than that in late stage ( P < 0.05 ). The loss rate in the cases with a smoking history was higher than that in cases without a smoking history. ( P =0.0...
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