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1
ETV1 is a lineage survival factor that cooperates with KIT in gastrointestinal stromal tumours.ETV1 是一种谱系存活因子，与 KIT 在胃肠道间质肿瘤中协同作用。
Nature. 2010 Oct 14;467(7317):849-53. doi: 10.1038/nature09409. Epub 2010 Oct 3.
2
Phase II trial of imatinib maintenance therapy after irinotecan and cisplatin in patients with c-Kit-positive, extensive-stage small-cell lung cancer.伊立替康和顺铂治疗后 c-Kit 阳性广泛期小细胞肺癌患者的伊马替尼维持治疗的 II 期临床试验。
Clin Lung Cancer. 2010 Jul 1;11(4):223-7. doi: 10.3816/CLC.2010.n.028.
3
Clinical implications of c-Kit mutations in acute myelogenous leukemia.c-Kit 基因突变在急性髓系白血病中的临床意义。
Curr Hematol Malig Rep. 2009 Apr;4(2):77-82. doi: 10.1007/s11899-009-0011-8.
4
Effect of platelet-derived growth factor receptor-beta inhibition with STI571 on radioimmunotherapy.STI571抑制血小板衍生生长因子受体-β对放射免疫治疗的影响。
Cancer Res. 2005 Sep 1;65(17):7824-31. doi: 10.1158/0008-5472.CAN-04-3991.
5
Genetic alterations and protein expression of KIT and PDGFRA in serous ovarian carcinoma.浆液性卵巢癌中KIT和PDGFRA的基因改变与蛋白表达
Br J Cancer. 2004 Dec 13;91(12):2048-55. doi: 10.1038/sj.bjc.6602252.
6
Expression of platelet-derived growth factor and activated receptor in clinical specimens of epithelial ovarian cancer and ovarian carcinoma cell lines.血小板衍生生长因子及其活化受体在上皮性卵巢癌临床标本及卵巢癌细胞系中的表达
Gynecol Oncol. 2004 Apr;93(1):78-86. doi: 10.1016/j.ygyno.2003.12.041.
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Imatinib mesylate (Gleevec) inhibits ovarian cancer cell growth through a mechanism dependent on platelet-derived growth factor receptor alpha and Akt inactivation.甲磺酸伊马替尼（格列卫）通过一种依赖于血小板衍生生长因子受体α和Akt失活的机制抑制卵巢癌细胞生长。
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Cancer. 2003 Aug 15;98(4):758-64. doi: 10.1002/cncr.11561.
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KIT in ovarian carcinoma: disillusion about a potential therapeutic target.
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10
Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors.用激酶抑制剂靶向肿瘤脉管系统中的周细胞和内皮细胞的益处。
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c-Kit和血小板衍生生长因子受体α（PDGFRα）在上皮性卵巢肿瘤及肿瘤间质中的表达。

Expression of c-Kit and PDGFRα in epithelial ovarian tumors and tumor stroma.

作者信息

Yi Cunjian, Li Li, Chen Keming, Lin Shengrong, Liu Xiangqiong

机构信息

Department of Obstetrics and Gynecology, First Affiliated Hospital, Yangtze University, Jingzhou, Hubei 434000, P.R. China.

出版信息

Oncol Lett. 2012 Feb;3(2):369-372. doi: 10.3892/ol.2011.481. Epub 2011 Nov 15.

DOI:10.3892/ol.2011.481
PMID:22740913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3362653/
Abstract

The purpose of this study was to investigate the expression of c-Kit and platelet-derived growth factor receptor α (PDGFRα) in epithelial ovarian tumor cells and tumor stroma. The expression of c-Kit and PDGFRα in 71 malignant or benign epithelial ovarian tumor tissues and 20 normal ovarian tissues was evaluated by immunohistochemical staining. The expression of c-Kit and PDGFRα in 71 malignant epithelial ovarian tumors and tumor stroma tissue samples was analyzed. A significant increase (P<0.01) of c-Kit expression was observed in malignant ovarian tumors (50.7%) when compared to normal ovarian tissues (10.0%) or benign ovarian tumors (20.0%). The PDGFRα expression rate in malignant ovarian tumors (63.4%) was also significantly higher (P<0.01) than that in normal ovarian tissues (15.0%) or benign ovarian tumors (25.0%). c-Kit was expressed in only 4.2% of the tumor stroma samples, which was significantly lower than the expression of malignant ovarian tumors (P<0.01), whereas the PDGFRα expression in tumor stroma (87.3%) was significantly higher than that of the malignant ovarian tumors (P<0.01). The expression levels of c-Kit and PDGFRα are higher in the malignant ovarian tumors than in the benign ovarian tumors or normal tissues. In the malignant ovarian tumor stroma, c-Kit expression is low and PDGFRα expression is high, and the differential changes of c-kit and PDGFRα suggest distinct roles in ovarian cancer.

摘要

本研究的目的是调查c-Kit和血小板衍生生长因子受体α（PDGFRα）在上皮性卵巢肿瘤细胞和肿瘤基质中的表达情况。采用免疫组织化学染色法评估71例恶性或良性上皮性卵巢肿瘤组织及20例正常卵巢组织中c-Kit和PDGFRα的表达。分析71例恶性上皮性卵巢肿瘤及肿瘤基质组织样本中c-Kit和PDGFRα的表达。与正常卵巢组织（10.0%）或良性卵巢肿瘤（20.0%）相比，恶性卵巢肿瘤中c-Kit表达显著增加（P<0.01）（50.7%）。恶性卵巢肿瘤中PDGFRα表达率（63.4%）也显著高于正常卵巢组织（15.0%）或良性卵巢肿瘤（25.0%）（P<0.01）。c-Kit仅在4.2%的肿瘤基质样本中表达，显著低于恶性卵巢肿瘤的表达（P<0.01），而肿瘤基质中PDGFRα表达（87.3%）显著高于恶性卵巢肿瘤（P<0.01）。恶性卵巢肿瘤中c-Kit和PDGFRα的表达水平高于良性卵巢肿瘤或正常组织。在恶性卵巢肿瘤基质中，c-Kit表达低而PDGFRα表达高，c-kit和PDGFRα的差异变化提示它们在卵巢癌中发挥不同作用。