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p53 and beta-catenin expression in gallbladder tissues and correlation with tumor progression in gallbladder cancer

机译:胆囊癌组织中p53和β-catenin的表达及其与肿瘤进展的关系

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Background/Aim: The inactivation of the tumor suppressor gene and activation of the proto-oncogene are key steps in the development of human cancer. p53 and beta-catenin are examples of such genes, respectively. In the present study, our aim was to determine the role of these genes in the carcinogenesis of the gallbladder by immunohistochemistry. Patients and Methods: Sections from paraffin-embedded blocks of surgically resected specimens of gallbladder cancer (GBC) (80 cases), chronic cholecystitis (60 cases), and control gallbladders (10 cases) were stained with the monoclonal antibody p53, and polyclonal antibody beta-catenin. Results were scored semiquantitatively and statistical analysis performed. p53 expression was scored as percentage of the nuclei stained. Beta-catenin expression was scored as type of expression-membranous, cytoplasmic, and nuclear staining. Beta-catenin expression was correlated with tumor invasiveness, differentiation, and stage. Results: Over-expression of p53 was seen in 56.25% of GBC cases and was not seen in chronic cholecystitis or in control gallbladders. p53 expression in gallbladder cancer was significantly higher than in inflammatory or control gallbladders (P < 0.0001). p53 expression increased with increasing tumor grade (P = 0.039). Beta-catenin nuclear expression was seen in 75% cases of gallbladder cancer and in no case of chronic cholecystitis and control gallbladder. Beta-catenin nuclear expression increased with tumor depth invasiveness, and grade (P = 0.028 and P = 0.0152, respectively). Conclusion: p53 and beta-catenin nuclear expression is significantly higher in GBC. p53 expression correlates with increasing tumor grade while beta-catenin nuclear expression correlates with tumor grade and depth of invasion, thus suggesting a role for these genes in tumor progression of GBC.
机译:背景/目的:抑癌基因的失活和原癌基因的激活是人类癌症发展的关键步骤。 p53和β-连环蛋白分别是此类基因的实例。在本研究中,我们的目的是通过免疫组织化学确定这些基因在胆囊癌变中的作用。患者和方法:将手术切除的胆囊癌(GBC)标本(80例),慢性胆囊炎(60例)和对照胆囊(10例)的石蜡包埋块切片用单克隆抗体p53和多克隆抗体染色β-连环蛋白。对结果进行半定量评分并进行统计分析。将p53表达记为染色的细胞核的百分比。 β-catenin表达被评定为表达类型-膜,细胞质和核染色。 β-catenin表达与肿瘤的侵袭性,分化和阶段相关。结果:在GBC病例中,有56.25%的患者可见p53的过度表达,而在慢性胆囊炎或对照胆囊中则未见。胆囊癌中p53的表达明显高于炎症性胆囊癌或对照性胆囊癌(P <0.0001)。随着肿瘤等级的增加,p53表达增加(P = 0.039)。在75%的胆囊癌病例中未见β-catenin核表达,而在慢性胆囊炎和对照胆囊病例中均未见。 β-catenin核表达随肿瘤浸润深度和等级的增加而增加(分别为P = 0.028和P = 0.0152)。结论:GBC中p53和β-catenin的核表达显着较高。 p53表达与肿瘤分级增加相关,而β-catenin核表达与肿瘤分级和浸润深度相关,因此暗示这些基因在GBC肿瘤进展中的作用。

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