Literature DB >> 11584965

Association of p53, p16, and vascular endothelial growth factor protein expressions with the prognosis and metastasis of gallbladder cancer.

Z W Quan1, K Wu, J Wang, W Shi, Z Zhang, R C Merrell.   

Abstract

BACKGROUND: Tumor suppressor genes were studied in gallbladder disease including cancer for correlation. VEGF (vascular endothelial growth factor) expression was assessed against Nevin staging and metastasis of gallbladder carcinoma. The importance of p53, p16, and VEGF in gallbladder cancer was estimated. STUDY
DESIGN: Twenty-four gallbladder carcinomas, 20 gallbladder adenomas, and 18 chronic cholecystitis specimens were immunohistochemically and histopathologically investigated for the relation of p53, p16, and VEGF to Nevin staging and pathologic grading.
RESULTS: The expression rate of abnormal p53 in gallbladder carcinomas was significantly higher than that in gallbladder adenoma and chronic cholecystitis (p = 0.003, p = 0.014). The expression rate of abnormal p53 in Nevin staging S1, S2, S3 gallbladder carcinoma was significantly higher than that in S4, S5 (p = 0.01). Abnormal p16 was highest in carcinoma, next in adenoma, and lowest in chronic cholecystitis (p = 0.031, p = 0.017). Gallbladder carcinoma expressed VEGF far more often than adenoma or cholecystitis (p = 0.001); VEGF-positive rates were lower in S1, S2, S3 than S4, S5 by Nevin staging of gallbladder cancer (p = 0.044).
CONCLUSION: Mutation of p53 and p16 genes might correlate with progression of of gallbladder carcinoma. Analysis of p53 and p16 can estimate the prognosis of gallbladder cancer. VEGF expression correlates with Nevin staging in gallbladder cancer.

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Year:  2001        PMID: 11584965     DOI: 10.1016/s1072-7515(01)01012-2

Source DB:  PubMed          Journal:  J Am Coll Surg        ISSN: 1072-7515            Impact factor:   6.113


  20 in total

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8.  Expression of hypoxia-inducible factor-1 alpha (HIF-1alpha) in patients with the gallbladder carcinoma.

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9.  Suppression of breast cancer metastasis through the inhibition of VEGF-mediated tumor angiogenesis.

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