期刊文献+

MRI影像组学对135例肝癌耐药蛋白PFKFB3的预测价值

Value of enhanced MRI radiomics in predicting the drug-resistant protein PFKFB3 in 135 cases of hepatocellular carcinoma
原文传递
导出
摘要 目的探讨原发性肝细胞肝癌(HCC)MRI强化特点、影像组学特征与癌组织中PFKFB3表达的相关性,建立HCC耐药相关蛋白的影像组学预测模型。方法回顾性分析2015年1月至2020年12月接受手术治疗并行术前增强MRI HCC患者135例,统计患者的临床数据(年龄、性别、吸烟史、饮酒史、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、甲胎蛋白、病理分级、乙型肝炎病毒感染)、传统影像学指标(肿瘤大小、包膜、动脉期强化特征、肿瘤坏死、门静脉侵犯、肿瘤供血类型、出血、肝内卫星灶、动脉期肿瘤-肝差异)及影像组学特征,并通过免疫组织化学法检测PFKFB3表达。二元Logistic分析筛选出独立预测因素(P<0.05),根据筛选后的训练集特征构建影像组学预测模型。利用受试者工作特征(ROC)曲线评估预测模型的准确性并在验证集中进行验证。结果HCC患者丙氨酸氨基转移酶(OR=0.36,95%CI:0.16~0.83,P=0.017)及肝内卫星灶(OR=6.89,95%CI:1.76~27.03,P=0.006)是PFKFB3阳性表达的独立预测因子,MRI影像组学模型训练集AUC值为0.99,在验证集AUC值为0.80、95%CI为0.61~1.00、灵敏度为0.78、特异度为0.75。结论增强MRI影像组学预测模型可一定程度预测原发性HCC中PFKFB3的表达,可为HCC治疗肿瘤耐药提供重要的信息。 Objective To investigate the correlation between MRI enhancement features,radiomics characteristics and PFKFB3 expression in primary hepatocellular carcinoma(HCC)tissue,and to establish a radiomics prediction model for drug-resistant related proteins of HCC.Methods Information of 135 HCC patients who received preoperative multiphase MRI and surgical resection during Jan.2015 and Dec.2020 was retrospectively analyzed.The clinical data(age,gender,history of smoking and drinking,alanine aminotransferase,aspartate transaminase,alpha-fetoprotein,pathologic stage and hepatitis B infection),conventional imaging features(tumor size,capsular,enhancement characteristics in arterial phase,necrosis,portal vein invasion,blood-supply type,hemorrhage,intrahepatic satellite foci and arterial tumor-liver differences in arterial phase),and radiomic features were recorded.The expression of PFKFB3 was detected with immunohistochemistry.The independent predictors were screened with multivariate analysis(P<0.05).The radiomics prediction model was constructed based on the features of the selected training set.The receiver operating characteristic(ROC)curve was drawn.The accuracy of the prediction model was evaluated with the area under the curve(AUC)and verified in the validation set.Results Alanine aminotransferase(OR=0.36,95%CI:0.16-0.83,P=0.017)and the presence of intrahepatic satellite foci(OR=6.89,95%CI:1.76-27.03,P=0.006)were independent predictors of positive PFKFB3 expression.The AUC of the MRI radiomics model was 0.99 in the training set and 0.80 in the validation set,with 95%CI of 0.61-1.00,sensitivity of 0.78 and specificity of 0.75.Conclusion The model of enhanced MRI radiomics can predict the expression of PFKFB3 in primary HCC,which can provide important information of tumor drug resistance in the treatment of HCC.
作者 靳新娟 左立平 邓展昊 李安宁 于德新 JIN Xinjuan;ZUO Liping;DENG Zhanhao;LI Anning;YU Dexin(Department of Radiology,Qilu Hospital of Shandong University,Jinan 250012,Shandong,China)
出处 《山东大学学报(医学版)》 CAS 北大核心 2023年第6期79-86,共8页 Journal of Shandong University:Health Sciences
关键词 肝细胞肝癌 耐药 PFKFB3 影像组学 磁共振成像 Hepatocellular carcinoma Drug resistance PFKFB3 Radiomics Magnetic resonance imaging
  • 相关文献

参考文献3

二级参考文献22

  • 1Yalcin A, Clem BF, Imbert-Fernandez Y, Ozcan SC, Peker S, O'Neal J, Klarer AC, Clem AL, Telang S, Chesney J. 6-Phosphofructo-2-kinase (PFKFB3) promotes cell cycle progression and suppresses apoptosis via Cdk1-mediated phosphorylation of p27. Cell Death Dis 2014; 5: e1337 PubMed DOI.
  • 2Roessler S, Jia HL, Budhu A, Forgues M, Ye QH, Lee JS, Thorgeirsson SS, Sun Z, Tang ZY, Qin LX, Wang XW. A unique metastasis gene signature enables prediction of tumor relapse in early-stage hepatocellular carcinoma patients. Cancer Res 2010; 70: 10202-10212 PubMed DOI.
  • 3Minchenko A, Leshchinsky I, Opentanova I, Sang N, Srinivas V, Armstead V, Caro J. Hypoxia-inducible factor-1-mediated expression of the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) gene. Its possible role in the Warburg effect. J Biol Chem 2002; 277: 6183-6187 PubMed DOI.
  • 4Obach M, Navarro-Sabaté A, Caro J, Kong X, Duran J, Gómez M, Perales JC, Ventura F, Rosa JL, Bartrons R. 6-Phosphofructo-2-kinase (pfkfb3) gene promoter contains hypoxia-inducible factor-1 binding sites necessary for transactivation in response to hypoxia. J Biol Chem 2004; 279: 53562-53570 PubMed DOI.
  • 5Yamamoto T, Takano N, Ishiwata K, Ohmura M, Nagahata Y, Matsuura T, Kamata A, Sakamoto K, Nakanishi T, Kubo A, Hishiki T, Suematsu M. Reduced methylation of PFKFB3 in cancer cells shunts glucose towards the pentose phosphate pathway. Nat Commun 2014; 5: 3480 PubMed DOI.
  • 6Seo M, Lee YH. PFKFB3 regulates oxidative stress homeostasis via its S-glutathionylation in cancer. J Mol Biol 2014; 426: 830-842 PubMed DOI.
  • 7Novellasdemunt L, Obach M, Millán-Ari?o L, Manzano A, Ventura F, Rosa JL, Jordan A, Navarro-Sabate A, Bartrons R. Progestins activate 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in breast cancer cells. Biochem J 2012; 442: 345-356 PubMed DOI.
  • 8Novellasdemunt L, Bultot L, Manzano A, Ventura F, Rosa JL, Vertommen D, Rider MH, Navarro-Sabate à, Bartrons R. PFKFB3 activation in cancer cells by the p38/MK2 pathway in response to stress stimuli. Biochem J 2013; 452: 531-543 PubMed DOI.
  • 9Imbert-Fernandez Y, Clem BF, O'Neal J, Kerr DA, Spaulding R, Lanceta L, Clem AL, Telang S, Chesney J. Estradiol stimulates glucose metabolism via 6-phosphofructo-2-kinase (PFKFB3). J Biol Chem 2014; 289: 9440-9448 PubMed DOI.
  • 10Calvo MN, Bartrons R, Casta?o E, Perales JC, Navarro-Sabaté A, Manzano A. PFKFB3 gene silencing decreases glycolysis, induces cell-cycle delay and inhibits anchorage-independent growth in HeLa cells. FEBS Lett 2006; 580: 3308-3314 PubMed DOI.

共引文献385

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部