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C-kit和PDGFRβ在食管癌组织中的表达及其临床意义 被引量:8

Expression and Significance of C-kit and Platelet-derived Growth Factor Receptor-beta (PDGFRβ) in Esophageal Carcinoma
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摘要 背景与目的:有研究表明STI-571能抑制Bcr-Abl、C-kit、血小板衍生生长因子受体β(Platelet-derivedgrouthfactorreceptor-beta,PDGFR!)的酪氨酸激酶,从而抑制细胞的分化增殖和促进细胞凋亡,本研究旨在检测与STI-571相关的酪氨酸激酶受体在食管癌中的表达情况。方法:应用免疫组化的方法,检测50例食管癌组织、癌旁组织和正常组织中与STI-571相关的酪氨酸激酶受体C-kit和PDGFRβ的表达。结果:C-kit在癌组织、癌旁组织、正常组织中的强表达率较低,分别为4%、4%、12%,表达的差异无统计学意义。PDGFRβ在癌组织、癌旁组织、正常组织中的强表达率分别为68%、28%、28%,表达的差异有统计学意义。应用Logistic回归的方法,发现C-kit或PDGFRβ在癌组织、癌旁组织、正常组织中的强表达率与患者的性别、年龄、肿物的分化程度、肿物的浸润深度、肿物的部位、淋巴结转移情况和分期无相关。结论:食管癌组织中PDGFRβ的强表达率较高,且明显高于癌旁组织和正常组织。食管正常组织中C-kit的强表达率较低,癌组织和癌旁组织中C-kit的强表达率更低。 BACKGROUND & OBJECTIVE: Some researches have showed that STI-571 could inhibit tyrosine kinase of Bcr-Abl, C-kit, and platelet-derived growth factor receptor-beta (PDGFRβ), therefore, inhibit cell differentiation and proliferation and accelerate cell apoptosis. This study was to examine the expression of tyrosine kinase receptor C-kit and PDGFRβ, which is correlated to STI-571, in esophageal carcinoma. METHODS: The expression of C-kit and PDGFRβ in tumor tissue, para-tumor tissue, and normal tissue of 50 specimens of esophageal carcinoma was examined by immunohistochemistry. RESULTS: The strong expression rate of C-kit was low in tumor, para-tumor, and normal tissues (4%, 4%, and 12%, respectively), with no significant difference (P=0.220). The strong expression rate of PDGFRβ was significantly higher in tumor tissues than in para-tumor and normal tissues (68% vs. 28% and 28%, P=0.001). Logistic regression analysis revealed that the strong expression rate of C-kit and PDGFRI5 had no correlation to sex, age, differentiation degree, infiltrative depth, position, lymph node metastasis, and stage of esophageal carcinoma. CONCLUSIONS: The strong expression rate of PDGFRβ is significantly higher in tumor tissues than in para-tumor and normal tissues. The strong expression rate of C-kit in normal esophageal tissues is low, and it is lower in para-tumor and tumor tissues.
出处 《癌症》 SCIE CAS CSCD 北大核心 2006年第1期92-95,共4页 Chinese Journal of Cancer
基金 广州市科委基金(No.2002J1-C0151)~~
关键词 食管肿瘤 STI-571 C-KIT PDGFRβ 治疗应用 Esophageal neoplasms STI-571 C-kit PDGFRβ Therapeutic application
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参考文献13

  • 1GOLDMAN J M, MELO J V. Targeting the bcr-abl tyrosine kinase in chronic myeloid leukemia [J]. N Engl J Med,2001,344(14) : 1084-1086.
  • 2TRAXLER P, BOLD G, BUCHDUNGER E, et al. Tymsine kinase inhibitors: from rational design to clinical trials [J].Med Res Rev, 2001,21(6) :499-512.
  • 3WONG S, WITTE O N. Modeling Philadelphia chromosome positive leukemias [J]. Oncogene, 2001,20(40) :5644-5659.
  • 4DRUKER B J, TALPAZ M, RESTA D J, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia [J]. N Engl J Med, 2001,344(14) : 1031-1037.
  • 5NISHIDA T, YASUMASA K. Target-based therapy against gastrointestinal stromal tumors-from molecular diagnosis to molecular target therapy [J]. Gan To Kagaku Ryoho, 2003,30(8) : 1071-1078.
  • 6LIU Y C, CHEN S C, CHANG C, et al. Platelet-derived growth factor is an autocrine stimulator for the growth and survival of human esophageal carcinoma cell lines [J]. Exp Cell Res, 1996,228 (2) : 206- 211.
  • 7YOSHIDA K, KUNIYASU H, YASUI W, et al. Expression of growth factors and their receptors in human esophageal carcinomas: regulation of expression by epidermal growth factor and transforming growth factor α [J]. J Cancer Res Clin Oncol, 1993,119(7) :401-407.
  • 8HEINRICH M C, BLANKE C D, DRUKER B J, et al.Inhibition of KIT tyrosine kinase activity: a novel molecular approach to the treatment of KIT-positive malignancies [J]. J Clin Oncol, 2002,20(6) : 1692-1703.
  • 9REED J, OUBAN A, SCHICKOR F K, et al.Immunohistochemical staining for c-Kit (CD117) is a rare event in human colorectal careinoma [J]. Clin Colorectal Cancer, 2002,2(2) : 119-122.
  • 10SIMAK R, CAPODIECI P, COHEN D W, et al. Expression of c-kit and kit-ligand in benign and malignant prostatic tissues [J]. Histol Histopathol, 2000,15(2) :365-374.

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