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Expression and Prognostic Role of FHIT, Fibronectin, and PTEN in Hepatocellular Carcinoma.
Clinical Laboratory 2016 July 2
BACKGROUND: Fragile histidine triad (FHIT), fibronectin (FN), and phosphatase and tensin homology deleted on chromosome ten (PTEN) are widely reported as having abnormal expression in malignant tumors. The role of FHIT, fibronectin, PTEN expression in patients with hepatocellular carcinoma (HCC) has not been characterized. Our study aims to investigate the expression of FHIT, fibronectin, and PTEN in human HCC and their relationship with clinicopathological features and prognosis of HCC.
METHODS: Immunohistochemistry was used to detect expression of FHIT, FN, and PTEN in tumor tissues from 138 HCC patients. The correlation between their expression and clinicopathological features and prognosis were analyzed.
RESULTS: FHIT, fibronectin, and PTEN proteins have different expressions between HCC and adjacent nontumor tissue (χ2 = 5.968, 7.380, 4.962; p < 0.05), which are expressed differently in the groups of different tumor stage, grade, tumor size, tumor number, lymph node metastasis, HBV infection, and cirrhosis in the background of nontumor sections (p < 0.05). In the FHIT and fibronectin positive expression group, the cumulative survival times were shorter than those in the negative expression groups (χ2 = 4.443, 9.867; p < 0.05), and in the PTEN positive expression group the cumulative survival times were longer than in the negative expression group (χ2 = 4.199; p < 0.05).
CONCLUSIONS: FHIT, fibronectin, and PTEN were abnormally expressed in HCC cells, which have stimulative or suppressive effects on HCC carcinogenesis and progression. FHIT and fibronectin can be used as negative makers for prognosis and PTEN as a positive one.
METHODS: Immunohistochemistry was used to detect expression of FHIT, FN, and PTEN in tumor tissues from 138 HCC patients. The correlation between their expression and clinicopathological features and prognosis were analyzed.
RESULTS: FHIT, fibronectin, and PTEN proteins have different expressions between HCC and adjacent nontumor tissue (χ2 = 5.968, 7.380, 4.962; p < 0.05), which are expressed differently in the groups of different tumor stage, grade, tumor size, tumor number, lymph node metastasis, HBV infection, and cirrhosis in the background of nontumor sections (p < 0.05). In the FHIT and fibronectin positive expression group, the cumulative survival times were shorter than those in the negative expression groups (χ2 = 4.443, 9.867; p < 0.05), and in the PTEN positive expression group the cumulative survival times were longer than in the negative expression group (χ2 = 4.199; p < 0.05).
CONCLUSIONS: FHIT, fibronectin, and PTEN were abnormally expressed in HCC cells, which have stimulative or suppressive effects on HCC carcinogenesis and progression. FHIT and fibronectin can be used as negative makers for prognosis and PTEN as a positive one.
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