B7-H3 and CD133 expression in non-small cell lung cancer and correlation with clinicopathologic factors and prognosis.
نویسندگان
چکیده
OBJECTIVE To detect the expression of B7-H3 and CD133 in human non-small cell lung cancer (NSCLC) specimens and lung benign lesions, and to evaluate the correlation between the 2 biomarkers and clinicopathologic features. METHODS This is a case-control study of 102 tissue specimens collected from NSCLC participants undergoing thoracic surgery in the Second Affiliated Hospital of Soochow University, Suzhou, China, between January 2006 and December 2008. From the 102 patients, 25 adjacent non-cancer samples were verified pathologically as normal tissue (positive group), and 24 benign inflammatory lesion tissues were used as control (negative group). Specimens from 126 participants were stained immunohistochemically using Image-Pro Plus software, and the cell number was measured in each section. RESULTS Of the 102 specimens, 71 expressed B7-H3, and 51 expressed CD133, higher than that in benign lesions (p<0.001) or non-cancer tissues (p<0.001). B7-H3 expression in squamous cell carcinoma (SCC) was significantly higher than those in adenocarcinoma (p=0.048), while CD133 expression in large cell lung carcinoma was higher than that in SCC (p=0.023). The mean number of tumor-infiltrating lymphocytes (TILs) in the B7-H3-positive group was lower than that in the B7-H3-negative group (p=0.026). The mean TILs in the CD133-positive group was significantly lower than that in CD133-negative group (p=0.029). We found that CD133 was related to tumor cell differentiation degree and CD133 expression was negatively correlated with B7-H3 expression. The CD133 positive or B7-H3 negative was associated with poor prognosis of NSCLC patients by Cox regression analysis. CONCLUSION Both CD133 and B7-H3 might induce apoptosis of TILs in NSCLC and tumor evading host immune surveillance. Either CD133 or B7-H3 might be an independent risk factor of NSCLC participants.
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ورودعنوان ژورنال:
- Saudi medical journal
دوره 31 9 شماره
صفحات -
تاریخ انتشار 2010