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西妥昔单抗可抑制子宫内膜癌的生长、腹膜播散以及淋巴结和肺转移,并延长宿主生存期。

Cetuximab inhibits growth, peritoneal dissemination, and lymph node and lung metastasis of endometrial cancer, and prolongs host survival.

作者信息

Takahashi Kayoko, Saga Yasushi, Mizukami Hiroyuki, Takei Yuji, Machida Shizuo, Fujiwara Hiroyuki, Ozawa Keiya, Suzuki Mitsuaki

机构信息

Department of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Tochigi, Japan.

出版信息

Int J Oncol. 2009 Oct;35(4):725-9. doi: 10.3892/ijo_00000385.

DOI:10.3892/ijo_00000385
PMID:19724908
Abstract

The purpose of this study was to explore the possibility of molecular-targeted therapy with anti-epidermal growth factor receptor (EGFR) antibody (cetuximab) for endometrial cancer to develop a new treatment for advanced endometrial cancer. We analyzed EGFR protein expression and gene mutations in the human endometrial cancer cell line HEC1A, and evaluated the in vitro and in vivo effects of cetuximab on HEC1A. EGFR expression was observed in HEC1A cells, but no mutations in the EGFR gene were detected. Cetuximab inhibited HEC1A cell growth and invasion and VEGF-A production in vitro, and HECIA cell tumor growth, its peritoneal dissemination with ascites, and lymph node and lung metastasis in vivo. In addition, the antibody prolonged the survival of a mouse model of systemic metastasis. These results suggest the possibility of molecular-targeted therapy using cetuximab for endometrial cancer.

摘要

本研究的目的是探索使用抗表皮生长因子受体(EGFR)抗体(西妥昔单抗)对子宫内膜癌进行分子靶向治疗的可能性,以开发一种针对晚期子宫内膜癌的新疗法。我们分析了人子宫内膜癌细胞系HEC1A中EGFR蛋白的表达和基因突变情况,并评估了西妥昔单抗对HEC1A的体外和体内作用。在HEC1A细胞中观察到EGFR表达,但未检测到EGFR基因的突变。西妥昔单抗在体外抑制了HEC1A细胞的生长、侵袭以及VEGF-A的产生,在体内抑制了HEC1A细胞肿瘤的生长、其伴有腹水的腹膜播散以及淋巴结和肺转移。此外,该抗体延长了全身转移小鼠模型的生存期。这些结果表明使用西妥昔单抗对子宫内膜癌进行分子靶向治疗的可能性。

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Ann Transl Med. 2021 Jan;9(1):5. doi: 10.21037/atm-20-3166.
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Combined silencing of VEGF-A and angiopoietin-2, a more effective way to inhibit the Ishikawa endometrial cancer cell line.
联合沉默血管内皮生长因子-A(VEGF-A)和血管生成素-2,是抑制石川子宫内膜癌细胞系的更有效方法。
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mA mRNA methylation regulates AKT activity to promote the proliferation and tumorigenicity of endometrial cancer.mA mRNA 甲基化调节 AKT 活性,促进子宫内膜癌的增殖和致瘤性。
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