RECEPTOR TYROSINE KINASES EXPRESSED IN METASTATIC COLON-CANCER

RECEPTOR TYROSINE KINASES EXPRESSED IN METASTATIC COLON-CANCER
复制标题

DOI:
10.1002/ijc.2910600611
复制
发表时间:
1995-03-16
影响因子:
6.4
通讯作者:
CANCE, WG
CANCE, WG
中科院分区:
医学1区
文献类型:
--
作者:
CRAVEN, RJ;XU, LH;CANCE, WG

文献摘要

被引文献

相似文献

利用基于pcr的克隆技术,我们分离了一系列编码酪氨酸激酶的DNA片段,这些片段在转移性人类结肠肿瘤中表达,并随后分析了它们在人类肿瘤蛋白水平上的表达模式。我们确定了血小板衍生生长因子受体(PDGFR)的α和β形式,axl和其他8个基因,包括3个细胞质酪氨酸激酶。为了研究它们在人类结肠癌中的表达,我们对同一患者的正常组织和癌组织进行了Western blot检测。这些结果表明,α - pdgfr在8/8正常组织中主要以200-kDa带迁移,在17/17恶性组织以及结肠息肉中以170-kDa带迁移,这表明该受体同种异构体的表达可能是结肠癌进展的标志。进一步的研究表明,Axl受体酪氨酸激酶在腹膜转移结节中的表达水平比在其他正常和恶性组织中高10倍。免疫组化显示Axl在肿瘤恶性细胞中特异过表达。这表明酪氨酸激酶受体的过度表达和可能的差异加工事件可能与结肠癌有关,并且它们是该疾病进展的潜在标记物。(C) 1995 Wiley-Liss, Inc。
Using a PCR-based cloning technique, we have isolated a series of DNA fragments coding for tyrosine kinases that are expressed in a metastatic human colon tumor, and have subsequently analyzed their expression pattern at the protein level in human tumors. We identified both the alpha and the beta forms of the platelet-derived growth factor receptor (PDGFR), axl and 8 other genes, including 3 cytoplasmic tyrosine kinases. To study their expression in human colon cancer, we performed Western blots of matched sets of normal tissues and of carcinomas from the same patient. These revealed that the alpha-PDGFR migrates predominantly as a 200-kDa band in 8/8 normal tissues, and as a 170-kDa band in 17/17 malignant tissues, as well as in colonic polyps, suggesting that expression of an isoform of this receptor may be a marker for the progression of colon cancer. Additional studies showed that the Axl receptor tyrosine kinase was expressed at 10-fold higher levels in a peritoneal metastatic nodule than in other normal and malignant tissues. Immunohistochemistry revealed Axl over-expression specifically in the malignant cells of the tumor. This indicates that over-expression and possibly a differential processing event of tyrosine kinase receptors may be involved in colon cancer, and that they are potential markers for the progression of this disease. (C) 1995 Wiley-Liss, Inc.