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CA Cancer J Clin. 2024 May-Jun;74(3):229-263. doi: 10.3322/caac.21834. Epub 2024 Apr 4.
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Pleural mesothelioma (PMe): The evolving molecular knowledge of a rare and aggressive cancer.胸膜间皮瘤(PMe):一种罕见且侵袭性癌症的不断发展的分子知识。
Mol Oncol. 2024 Apr;18(4):797-814. doi: 10.1002/1878-0261.13591. Epub 2024 Mar 8.
4
POLD1 Is Required for Cell Cycle Progression by Overcoming DNA Damage in Malignant Pleural Mesothelioma.POLD1 通过克服恶性胸膜间皮瘤中的 DNA 损伤来促进细胞周期进程。
Cancer Genomics Proteomics. 2024 Mar-Apr;21(2):158-165. doi: 10.21873/cgp.20437.
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Pleural Mesothelioma: Advances in Blood and Pleural Biomarkers.胸膜间皮瘤:血液和胸膜生物标志物的进展
J Clin Med. 2023 Nov 9;12(22):7006. doi: 10.3390/jcm12227006.
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Expert Opin Ther Targets. 2023 Jul-Dec;27(12):1177-1188. doi: 10.1080/14728222.2023.2288277. Epub 2023 Dec 30.
7
Preventive and therapeutic opportunities: targeting BAP1 and/or HMGB1 pathways to diminish the burden of mesothelioma.防治机会:针对 BAP1 和/或 HMGB1 途径减少间皮瘤负担。
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A Novel Irreversible TEAD Inhibitor, SWTX-143, Blocks Hippo Pathway Transcriptional Output and Causes Tumor Regression in Preclinical Mesothelioma Models.一种新型不可逆 TEAD 抑制剂 SWTX-143 可阻断 Hippo 通路转录输出并在间皮瘤临床前模型中引起肿瘤消退。
Mol Cancer Ther. 2024 Jan 3;23(1):3-13. doi: 10.1158/1535-7163.MCT-22-0681.
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The emerging roles of lysine-specific demethylase 4A in cancer: Implications in tumorigenesis and therapeutic opportunities.赖氨酸特异性去甲基化酶4A在癌症中的新作用:对肿瘤发生的影响及治疗机会
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[恶性胸膜间皮瘤的靶向治疗进展]

[Advances in Targeted Therapy for Malignant Pleural Mesothelioma].

作者信息

Fu Fen, Zhang Yang, Shen Hong

机构信息

Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, 
Nanjing 210011, China.

出版信息

Zhongguo Fei Ai Za Zhi. 2024 May 20;27(5):391-398. doi: 10.3779/j.issn.1009-3419.2024.102.18.

DOI:10.3779/j.issn.1009-3419.2024.102.18
PMID:38880927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11183316/
Abstract

Malignant pleural mesothelioma (MPM) is a rare cancer with high malignancy and aggressiveness on the pleural, caused by the following risk factors including asbestos inhalation, genetic factors, and genetic mutation. The present chemotherapy, antiangiogenic therapy, and immunotherapy methods are ineffective and the survival time of patients is very short. There is an urgent need to find potential therapeutic targets for MPM. At present, it has been found the following types of targets: gene mutation targets such as BRCA associated protein 1 (BAP1) and cyclin-dependent kinase 2A (CDKN2A); epigenetic targets such as lysine (K)-specific demethylase 4A (KDM4A) and lysine-specific demethylase 1 (LSD1), and signal protein targets such as glucose-regulated protein 78 (GRP78) and signal transducer and activator of transcription 3 (STAT3). So far, available clinical trials include phase II clinical trials of histone methyltransferase inhibitor Tazemetostat, poly (ADP-ribose) polymerase (PARP) inhibitor Rucaparib and cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitor Abemaciclib, as well as phase I clinical trials of mesothelin-targeting chimeric antigen receptor T-cell immunotherapy (CAR-T) cell injection in the thoracic cavity and TEA domain family member (TEAD) inhibitor VT3989 and IK-930, and the results of these trials have showed certain clinical efficacy.
.

摘要

恶性胸膜间皮瘤(MPM)是一种罕见的癌症,对胸膜具有高度恶性和侵袭性,由以下风险因素引起,包括吸入石棉、遗传因素和基因突变。目前的化疗、抗血管生成治疗和免疫治疗方法均无效,患者的生存时间很短。迫切需要找到MPM的潜在治疗靶点。目前,已发现以下几种类型的靶点:基因突变靶点,如BRCA相关蛋白1(BAP1)和细胞周期蛋白依赖性激酶2A(CDKN2A);表观遗传靶点,如赖氨酸(K)特异性去甲基化酶4A(KDM4A)和赖氨酸特异性去甲基化酶1(LSD1),以及信号蛋白靶点,如葡萄糖调节蛋白78(GRP78)和信号转导及转录激活因子3(STAT3)。到目前为止,可用的临床试验包括组蛋白甲基转移酶抑制剂他泽司他、聚(ADP-核糖)聚合酶(PARP)抑制剂鲁卡帕尼和细胞周期蛋白依赖性激酶4和6(CDK4/6)抑制剂阿贝西利的II期临床试验,以及间皮素靶向嵌合抗原受体T细胞免疫疗法(CAR-T)胸腔注射和TEA结构域家族成员(TEAD)抑制剂VT3989和IK-930的I期临床试验,这些试验结果已显示出一定的临床疗效。