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第十三届中国医师协会神经外科医师年会

作者： Junyu Wang Danfeng Zhang Chunlin Wang Kaiwei Han Yiming Li Liang Zhao Jigang Chen Yicheng Lu Huanhai Liu Guohan Hu Department of Neurosurgery Shanghai Changzheng HospitalSecond Military Medical University Department of Neurosurgery the 105th Hospital of PLA Department of Otorhinolaryngology(Head and Neck) Shanghai Changzheng HospitalSecond Military Medical University

egfr activation is commonly observed in many types of tumor,and contributes to tumor becoming more ***,egfr inhibitor has been considered as a promising therapeutic method for tumors including glioblastoma multiform（GBM）,which has frequent amplification of ***,the reluctant response or resistance to egfr inhibitor remains to be ***,we show that FGF2/FGFR1 signaling contributes to resistance to egfr inhibitor treatment in *** FGF2/FGFR1 signaling compromises inhibition of ERK1/2 and AKT activation in response to egfr inhibitor treatment,and lead to egfr inhibitor *** inactivated TP53 in GBM promotes FGF2 expression through transcriptionally regulation of mi R-107 to activate FGF2/FGFR1 signaling,thus finally leads to resistance to egfr inhibitor *** study unveils a TP53/miR-107/FGF2/FGFR1 axis that contributes to egfr inhibitor resistance in GBM,and provides a possible strategy to overcome egfr inhibitor resistance in GBM with combination of FGFR *** also suggests that status of TP53 and FGFR signaling activity might serve as predictive factors for egfr inhibitor ***:We show that TP53 inactivation in GBM activates FGFR signaling through mi R-107 regulated FGF2 expression to crosstalk with egfr signaling,and subsequently compromise egfr inhibitor sensitivity.

关键词： TP53 FGF2 egfr inhibitor glioblastoma

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Targeting apoptosis to manage acquired resistance to third generation egfr inhibitors

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Frontiers of Medicine 2022年第5期16卷 701-713页

作者： Shi-Yong Sun Department of Hematology and Medical Oncology Emory University School of Medicine and Winship Cancer Institute of Emory UniversityAtlantaGA 30322USA

A significant clinical challenge in lung cancer treatment is management of the inevitable acquired resistance to third-generation epidermal growth factor receptor(egfr)tyrosine kinase inhibitors(egfr-TKIs),such as osimertinib,which have shown remarkable success in the treatment of advanced NSCLC with egfr activating mutations,in order to achieve maximal response duration or treatment *** is a major type of programmed cell death tightly associated with cancer development and *** of apoptosis is considered a key hallmark of cancer and acquisition of apoptosis resistance is accordingly a key mechanism of drug acquired resistance in cancer *** has been clearly shown that effective induction of apoptosis is a key mechanism for third generation egfr-TKIs,particularly osimertinib,to exert their therapeutic efficacies and the development of resistance to apoptosis is tightly associated with the emergence of acquired ***,restoration of cell sensitivity to undergo apoptosis using various means promises an effective strategy for the management of acquired resistance to third generation egfr-TKIs.

关键词： acquired resistance egfr inhibitor apoptosis lung cancer

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Discovery of Novel Tricyclic 5H-Pyridazino[4,5-b]indoles as Potent Antitumor Agents： Design, Synthesis and Biological Evaluation

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Chemical Research in Chinese Universities 2015年第3期31卷 372-380页

作者： ZHAI Xin WANG Limei SHI Jiyue GONG Ping Key Laboratory of Structure-based Drug Design and Discovery Ministry of EducationShenyang Pharmaceutical University Shenyang 110016 P.R.China

A novel series of 5H-pyridazino[4,5-b]indoles（L-01-L-32） was synthesized and characterized by means of 1H NMR, MS and elemental analysis. The cytotoxicity of the target compounds against Bel-7402 and HT-1080 cell lines were evaluated by 3-（4,5-dimethylthiazol-2-y1）-2,5-diphenyltetrazolium bromide（MTT） assay. Most of them exhibited moderate to excellent cytotoxicity, and six compounds（L-04, L-06, L-18, L-20, L-21 and L-23） possessed dramatically increased cytotoxicity superior to Gefitinib. Of these initial hits, compound L-21 displayed remarkable cytotoxicity against the tested cell lines with half maximal inhibitory concentration（IC50） values of 4.6 and 2.1 μmol/L, respectively, which was 13.9- to 25.6-fold more potent than positive control.

关键词： 1-Anilino-5H-pyridazino[4,5-b]indole egfr inhibitor Cytotoxicity

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