肝细胞癌NF-κB表达与CT表现的相关性
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摘要
目的探讨核因子(NF-κB)在肝细胞癌组织中的表达与CT影像特点间的关系。方法收集华西医院有完整临床资料和全肝CT扫描图像并经手术完整切除的肝癌组织标本患者80例,采用免疫组织化学方法染色定量分析癌组织中NF-κB表达情况和在不同的临床参数中表达的差异;再分别以肿瘤坏死、血供、瘤体直径和瘤周子灶的有无分四组,探讨NF-κB表达量在不同CT影像特征中有无差异。结果 CT检测80例患者中肝癌细胞核内NF-κB表达阳性有74例(92.5%)。肝细胞癌NF-κB表达与临床参数,包括性别、肝炎病史无相关性,瘤体大小与NF-κB表达无统计学差异。CT检测肿瘤血供、坏死及瘤周子灶的有无与NF-κB表达相关(P<0.05),富血供肝细胞癌NF-κB表达较乏血供者明显增高,而瘤体有坏死者较未发生坏死者低,瘤周出现子灶的病例NF-κB表达也增高,且差异有统计学意义(P<0.05)。结论肝癌血供、坏死及瘤周子灶CT影像特点与NF-κB水平密切相关。瘤体血供丰富、瘤内无坏死、瘤周伴有子灶的肝癌组织NF-κB表达水平明显增高,NF-κB表达水平量可能与肿瘤的生物学特性,疾病的转归和预后相关,CT检测可为肝癌的治疗及预防评估提供重要依据。
Objective To observe the expression of nuclear factor kappa B(NF-κB) and CT findings of hepatocellular carcinoma(HCC) for analysis of their correlation. Methods Histological samples of 80 excisional HCC were collected and examined for their NF-κB protein expression with immunohistochemical streptavidin peroxide method, CT image and clinical data of the enrolled cases were collected simultaneously. Expression of NF-κB was statistically analyzed to see difference between clinical parameters. Then, the malignant tumors were categorized with such image features as tumor necrosis, blood supply, size and daughter foci. Then combined with expression level of NF-κB to see the difference. Results The positive rate of NF-κB expression in HCC was 92.5%(74/80). While there was no difference in NF-κB level among HCC of various pathological categories. Clinical parameters and tumor size have no dependability statistically. Expression level of NF-κB was increased in those cancers with CT signs of rich blood supply and positive cellular necrosis and daughter foci, and all of them have statistical significance. Conclusion Blood supply, cellular necrosis and daughter foci of HCC have intimate correlation with NF-κB level. The tumors which were rich in blood supply and daughter foci, short of cellular necrosis have obviously high level of NF-κB expression.
Objective To observe the expression of nuclear factor kappa B(NF-κB) and CT findings of hepatocellular carcinoma(HCC) for analysis of their correlation. Methods Histological samples of 80 excisional HCC were collected and examined for their NF-κB protein expression with immunohistochemical streptavidin peroxide method, CT image and clinical data of the enrolled cases were collected simultaneously. Expression of NF-κB was statistically analyzed to see difference between clinical parameters. Then, the malignant tumors were categorized with such image features as tumor necrosis, blood supply, size and daughter foci. Then combined with expression level of NF-κB to see the difference. Results The positive rate of NF-κB expression in HCC was 92.5%(74/80). While there was no difference in NF-κB level among HCC of various pathological categories. Clinical parameters and tumor size have no dependability statistically. Expression level of NF-κB was increased in those cancers with CT signs of rich blood supply and positive cellular necrosis and daughter foci, and all of them have statistical significance. Conclusion Blood supply, cellular necrosis and daughter foci of HCC have intimate correlation with NF-κB level. The tumors which were rich in blood supply and daughter foci, short of cellular necrosis have obviously high level of NF-κB expression.
引文
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[2] Hu B,Sun M,Liu J,et al.The preventative effect of Akt knockout on liver cancer through modulating NF-κB-regulated inflammation and Bad-related apoptosis signaling pathway[J].Int J Oncol,2016,48(4):1467-1476.
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[4] Ming-Quan Wang,Qing He,Yong-Song Guan.Pulmonary carcinoma:CT manifestations and expression of nuclear factor kappa B[J].Progress in Modern Biomedicine,2008,8(4):667-673.
[5] R.Sen and D.Baltimore.Inducibility of κ immunoglobulin enhancer-binding protein Nf-κB by a posttranslational mechanism[J].Cell,1986,47 (6):921-928.
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[7] Luedde T,Schwabe RF.NF-κB in the liver—linking injury,fibrosis and hepatocellularcarcinoma[J].Nat Rev GastroenterolHepatol,2011,8(2):108-118.
[8] Viswam S.Nair,MD MS,Olivier Gevaert,et al.NF-κB protein expression associates with 18F-FDG PET tumor uptake in non-small cell lung cancer:a radiogenomics validation study to understand tumor metabolism[J].Lung Cancer,2014,83(2):189-196.
[9] Sun SC,Chang JH,Jin J.Regulation of NF-κB in Autoimmunity[J].Trends Immunol,2013,Jun;34(6):282-289.
[10] Li GJ,Gao J,Wang GL,et al.Correlation between vascular endothelial growth factor and quantitative dual-energy spectral CT in non-small-cell lung cancer[J].ClinRadiol,2016,71(4):363-368.
[11] Gao P,Gao YJ,Liang HL.Effect of NF-κ B inhibitor PDTC on VEGF and endostatin expression of mice with Lewis lung cancer[J].Asian Pac J Trop Med,2015,8(3):220-224.
[12] Hinz M,Krappmann D,Eichten A,et al.NF-κB Function in Growth Control:Regulation of Cyclin D1 Expression and G0/G1-to-S-Phase Transition[J].Mol Cell Biol,1999,19(4):2690-2698.
[13] Shuji H,Masaaki Y,Yushi U,et al.Expression of Nuclear Factor-κB,Tumor Necrosis Factor Receptor Type 1,and c-Myc in Human Astrocytomas[J].Neurologia medico-chirurgica,2001,41(4):187-195.
[14] Kou X,Jing Y,Deng W,et al.Tumor necrosis factor-α attenuates starvation-induced apoptosis through upregulation of ferritin heavy chain in hepatocellular carcinoma cells[J].BMC Cancer,2013,13:438.
[15] Haruki K,Shiba H,Fujiwara Y,et al.Inhibition of nuclear factor-κB enhances the antitumor effect of tumor necrosis factor-α gene therapy forhepatocellular carcinoma in mice[J].Surgery,2013,154(3):468-478.
[16] Balkwill F,Mantovani A.Inflammation and cancer:Back to Virchow[J].Lancet,2001,357 (9255):539-545.
[17] Neelam M,Tiffani J,Eduardo C,et al.To be an ally or an adversary in bladder cancer:the NF-κB story has not unfolded[J].Carcinogenesis,2015,36(3):299-306.
[18] Sunami Y,Ringelhan M,Kokai E,et al.Canonical NF-κB signaling in hepatocytes acts as a tumor-suppressor in hepatitis B virus surface antigen-driven hepatocellular carcinoma by controlling the unfolded protein response[J].Hepatology,2016,63(5):1592-1607.
[19] Ryan KM,Ernst MK,Rice NR.Role of NF-kB in p53-mediated programmed cell death[J].Nature,2000,404(6780):892-897.
[20] Pal S,Bhattacharjee A,Ali A,et al.Chronic inflammation and cancer:potential chemoprevention through nuclear factor kappa B and p53 mutual antagonism[J].2014,11:23.