期刊文献+

Pancreatic cancer–Outlook: targeted therapy

Pancreatic cancer–Outlook: targeted therapy
下载PDF
导出
摘要 Pancreatic cancer is a devastating disease characterized by almost identical incidence and mortality rates. Since this tumour is mostly diagnosed in an advanced stage there is usually no option for a curative surgical resection. In addition, pancreatic cancers known to be resistant to conventional treatment modalities such as chemotherapy and radiotherapy. Therefore, novel strategies for targeting these tumors are urgently needed. The increasing knowledge on the underlying pathogenetic mechanisms has led to the identification of surface receptor molecules that initiate intracellular signalling cascades upon ligand binding, thus leading to tumor progression. Targeting these receptors or their secreted ligands is therefore an attractive new approach for cancer therapy. The epidermal growth factor receptor (EGFR) and the vascular endothelial growth factor receptor (VEGFR) are transmembrane tyrosine kinase receptors which can be targeted by various compounds such as antibodies or small molecule inhibitors. In addition, various molecules targeting proteins secreted by pancreatic cancers such as matrix metalloproteinases (MMP’s) or intracellular oncogenic signalling components such as the farnesyltransferase have been proposed as potential new approaches for targeted cancer therapy. The use of these agents alone or in combination with conventional therapeutic regimens is currently being evaluated and shows first promising results for pancreatic cancer therapy.
出处 《The Chinese-German Journal of Clinical Oncology》 CAS 2007年第2期176-180,共5页 中德临床肿瘤学杂志(英文版)
关键词 pancreatic cancer targeted therapy 胰腺癌 靶向治疗 前景 EGFR VEGF MPS
  • 相关文献

参考文献43

  • 1Warshaw AL, Fernandez-del Castillo C. Pancreatic carcinoma. N Engl J Med, 1992, 326: 455--465.
  • 2Gress TM. Exocrine pancreas cancer-The European Pancreatic Cancer-Research Cooperative (EPC-RC). In: Felsenstein, Hannover, 2005, 42-59.
  • 3Yeo C J, Cameron JL. Improving results of pancreaticoduodencectomy for pancreatic cancer. World J Surg, 1999, 23: 907-912.
  • 4Parker SL, Tong T, Bolden S, et al. Cancer statistics. CA Cancer J Clin, 1996, 46: 5-27.
  • 5Vimalachandran D, Ghaneh P, Costello E, et al. Genetics and prevention of pancreatic cancer. Cancer Control, 2004, 11: 6-14.
  • 6Casey G, Yamanaka Y, Friess H, et al. p53 mutations are common in pancreatic cancer and are absent in chronic pancreatitis. Cancer Lett, 1993, 69: 151-160.
  • 7Rozenblum E, Schutte M, Goggins M, et al. Tumor-suppressive pathways in pancreatic carcinoma. Cancer Res, 1997, 57: 1731-1734.
  • 8Wilentz RE, Lacobuzio-Donahue CA, Argani P, et al. Loss of expression of Dpc4 in pancreatic intraepithelial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression. Cancer Res, 2000, 60, 2002-2006.
  • 9Hruban RH, van Mansfeld AD, Offerhaus G J, et al. K-ras oncogene activation in adenocarcinoma of the human pancreas. A study of 82 carcinomas using a combination of mutant-enriched polymerase chain reaction analysis and allele-specific oligonucleotide hybridization. Am J Pathol, 1993, 143: 545-554.
  • 10Ullrich A, Coussens L, Hayflick JS, et al. Human epidermal growth factor receptor cDNA sequence and aberrant expression of the amplified gene in A431 epidermoid carcinoma cells. Nature, 1984, 309: 418-425.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部