Mycoplasma hyorhinis infection promotes tyrosine kinase inhibitor (TKI) resistance in lung adenocarcinoma patients

被引:0
作者
Yueyu Dai
Fangyuan Zhong
Wenbin Liu
Qibin Song
Weiguo Hu
机构
[1] Renmin Hospital of Wuhan University,Cancer Center
[2] Wuhan Polytechnic University,College of Health Sciences and Nursing
来源
Journal of Cancer Research and Clinical Oncology | 2021年 / 147卷
关键词
Lung adenocarcinoma; Mycoplasma hyorhinis; Epidermal growth factor receptor; Progression-free survival; Tyrosine kinase inhibitor;
D O I
暂无
中图分类号
学科分类号
摘要
引用
收藏
页码:1379 / 1388
页数:9
相关论文
共 87 条
[1]  
Baselga J(2009)Novel anticancer targets: revisiting ERBB2 and discovering ERBB3 Nat Rev Cancer 9 463-475
[2]  
Swain SM(2018)Mycoplasma hyorhinis reduces sensitivity of human lung carcinoma cells to Nutlin-3 and promotes their malignant phenotype J Cancer Res Clin Oncol 144 1289-1300
[3]  
Boyarskikh UA(2014)Mycoplasma hyorhinis infection promotes NF-kappaB-dependent migration of gastric cancer cells Can Res 74 5782-5794
[4]  
Duan H(2014)Activation of EGFR-PI3K-AKT signaling is required for Mycoplasma hyorhinis-promoted gastric cancer cell migration Cancer cell Int 14 135-454
[5]  
Duan H(2014)Mycoplasma hyorhinis induces epithelial-mesenchymal transition in gastric cancer cell MGC803 via TLR4-NF-kappaB signaling Cancer Lett 354 447-8267
[6]  
Qu L(2014)Discovery of a potent and selective EGFR inhibitor (AZD9291) of both sensitizing and T790M resistance mutations that spares the wild type form of the receptor J Med Chem 57 8249-1160
[7]  
Shou C(2017)Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine Science 357 1156-3974
[8]  
Duan H(2018)Intratumoral bacteria may elicit chemoresistance by metabolizing anticancer agents Mol Cell Oncol 5 e1405139-537
[9]  
Qu L(1988)Evidence for high affinity binding-protein dependent transport systems in gram-positive bacteria and in Mycoplasma EMBO J 7 3971-704
[10]  
Shou C(2008)p37 from Mycoplasma hyorhinis promotes cancer cell invasiveness and metastasis through activation of MMP-2 and followed by phosphorylation of EGFR Mol Cancer Ther 7 530-401