Purposes)By blocking the conversion of 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) toPurposes)By blocking the conversion of 3-Hydroxy-3-methylglutaryl-coenzyme A

Purposes)By blocking the conversion of 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) to
Purposes)By blocking the conversion of 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) to mevalonate, HMG-CoA reductase inhibitors (i.e. fluvastatin and lovstatin) inhibit the synthesis of other products derived from this metabolite. EGF induced a dose-dependent increase of PANC-1 cell invasion in vitro. Treatment of PANC-1 cells with fluvastatin markedly attenuated EGF-induced translocation of RhoA from the cytosol to the membrane fraction and actin stress fiber assembly, whereas it did not inhibit the tyrosine phosphorylation of EGF receptor and c-erbB-2 [52].Vascular Endothelial Growth Factor In pancreatic cancer, VEGF expression and the degree of MVD, which are closely correlated, are reliable markers of early tumour recurrence after resection. The soluble form of flt-1 VEGF receptor inhibits VEGF activity. PANC-1 andMolecular Cancer 2003,http://www.molecular-cancer.com/content/2/1/activity, it could possibly be a potent therapeutical approach for pancreatic cancer as well.Hepatocyte Growth Factor Hepatocyte growth factor (HGF) enhances tumour invasion and metastasis through tumour-stromal interactions. NK4 is a four-kringle fragment of HGF and acts as an HGF-antagonist and an angiogenesis inhibitor. NK4 blocked the conversion of orthotopic pancreatic tumours from in situ carcinoma to invading cancers during days 3?14, when administration of NK4 was started from the third day after orthotopic injection of SUIT-2 human pancreatic cancer cells into nude mice. NK4 therapy, started on day 10 when cancer cells were already invading surrounding tissues, suppressed tumour growth, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26778282 peritoneal dissemination, and ascites accumulation resulting in the improvement of survival rates. The antitumour effects of NK4 correlated with the reduction of MVD [60].
Molecular CancerResearchBioMed CentralOpen AccessEffects of STI571 (gleevec) on pancreatic cancer cell growthJunsheng Li, J g Kleeff, Junchao Guo, Lars Fischer, Nathalia Giese, Markus W B hler and Helmut Friess*Address: Department of General Surgery, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany Email: Junsheng Li – [email protected]; J g Leupeptin (hemisulfate) web Kleeff – [email protected]; Junchao Guo – [email protected]; Lars Fischer – [email protected]; Nathalia Giese – [email protected]; Markus W B hler – [email protected]; Helmut Friess* – [email protected] * Corresponding authorPublished: 17 September 2003 Molecular Cancer 2003, 2:Received: 05 September 2003 Accepted: 17 SeptemberThis article is available from: http://www.molecular-cancer.com/content/2/1/32 ?2003 Li et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article’s original URL.STI571pancreatic cancerchemotherapytyrosine kinasegrowth factorAbstractBackground: Pancreatic cancer is an aggressive malignancy characterized by low responsiveness to chemotherapy and radiotherapy. This resistance is partly due to the overexpression of several tyrosine kinase receptors and their ligands. STI571 has specific activity in inhibiting c-kit, PDGF and Abl receptor tyrosine kinases and has proven successful in the treatment of CML and GIST patients. Here, we investigated the potential role of STI571 in pancreatic cancer. Results: The GI50 of STI571 as well as the effects of STI571 on growth factor actions in pancr.