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应用免疫组化对胆囊不同病变内S-100~+树突状细胞浸润与肿瘤相关分子的表达相互关系进行对比研究.包括胆囊癌症病人切除标本30例,结石20例,慢性炎症20例.用单克隆抗p53蛋白、抗增殖细胞核抗原(PCNA)、抗癌胚抗原(CEA)及多克隆抗S-100蛋白抗体,LSAB法检查上述病变标本.结果发现癌症病人p53蛋白阳性为46.7%(14/30),PCNA为86.7%(26/30),CEA为30.0%(9/30),S-100~+DC浸润仅为40.0%(12/30);结石标本p~(53)蛋白阴性,PCNA为35.0%(7/20),CEA为15%(3/20),S-100~+DC浸润为50%(10/20);慢性炎病例p53蛋白、CEA均为阴性,PCNA为25%(5/20),而S-100~+DC浸润为 85%(17/20).S-100~+DC浸润病例数与细胞密度,在恶性肿瘤中明显低于非肿瘤良性病变(P<0.05).本研究说明:①炎性病变的上皮组织多属单纯性增生而无肿瘤相关标记分子表达,同时伴有较高的细胞免疫活性;②胆囊结石上皮存在某些不典型变化有少许肿瘤标记分子表达,并伴有机体抗肿瘤免疫反应的下降,易于癌变;③癌症病人标本突变型p53基因过度表达、PCNA明显多曾多及 S-100~+DC明显减少,可能反映了免疫监视系统受损,使肿瘤细胞逃避机体的免疫攻击以促进肿瘤发生与发展.
The relationship between S-100 ~ + dendritic cell infiltration and the expression of tumor related molecules in different lesions of gallbladder was studied by immunohistochemistry, including 30 cases of gallbladder cancer, 20 cases of stone and 20 cases of chronic inflammation. P53, anti-PCNA, CEA and polyclonal anti-S-100 antibody were detected by LSAB method.The results showed that the positive rate of p53 protein in cancer patients was 46.7% (14 / 30), PCNA was 86.7% (26/30), CEA was 30.0% (9/30), S-100 ~ + DC infiltration was only 40.0% , PCNA was 35.0% (7/20), CEA was 15% (3/20), S-100 ~ + DC infiltration was 50% (10/20) 25% (5/20), and S-100 ~ + DC infiltration was 85% (17/20) .The number of S-100 ~ + DC infiltration and cell density in malignant tumors were significantly lower than those in non-benign tumors P <0.05) .This study shows: ① inflammatory epithelial tissue mostly belong to simple hyperplasia without tumor-related marker molecules, accompanied by high cellular immune activity; ② gallstone epithelial there are some atypical changes have A few tumor marker molecules are expressed and associated The anti-tumor immune response is decreased, which is easy to be carcinogenic. (3) Mutant p53 gene overexpression, PCNA significantly increased and S-100 ~ + DC significantly decreased in cancer patients, which may reflect the damage of immune surveillance system and escape of tumor cells The body’s immune attack to promote tumorigenesis and development.