ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
Specific targeting of tumor vasculature by diphtheria toxin-vascular endothelial growth factor fusion protein reduces angiogenesis and growth of pancreatic cancer.
Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- A Cancer and Leukemia Group B phase II study of sunitinib malate in patients with previously treated metastatic pancreatic adenocarcinoma (CALGB 80603).The oncologist · 2010Trial
- In Vitro and In Vivo Studies of a Heminecrolysin Toxin-VEGF Fusion Protein as a Novel Therapeutic for Solid Tumor Targeting.Molecular biotechnology · 2023Article
- Advances on Delivery of Cytotoxic Enzymes as Anticancer Agents.Molecules (Basel, Switzerland) · 2022Review
- Endothelial loss of Fzd5 stimulates PKC/Ets1-mediated transcription of Angpt2 and Flt1.Angiogenesis · 2018Article
- Targeting of Tumor Neovasculature with GrB/VEGFBiomedicines · 2017Review
- Overview of pre-clinical and clinical studies targeting angiogenesis in pancreatic ductal adenocarcinoma.Cancer letters · 2016Review
- The pancreatic niche inhibits the effectiveness of sunitinib treatment of pancreatic cancer.Oncotarget · 2016Article
- TCGA data and patient-derived orthotopic xenografts highlight pancreatic cancer-associated angiogenesis.Oncotarget · 2015Article
- The functionalized human serine protease granzyme B/VEGF₁₂₁ targets tumor vasculature and ablates tumor growth.Molecular cancer therapeutics · 2013Article
- A novel antiangiogenic approach for adjuvant therapy of pancreatic carcinoma.Langenbeck's archives of surgery · 2011Article
- Specific targeting of tumor endothelial cells by a shiga-like toxin-vascular endothelial growth factor fusion protein as a novel treatment strategy for pancreatic cancer.Neoplasia (New York, N.Y.) · 2010Article
- The vascular-ablative agent VEGF(121)/rGel inhibits pulmonary metastases of MDA-MB-231 breast tumors.Neoplasia (New York, N.Y.) · 2005Article
- Evaluation of vascular endothelial growth factor blockade and matrix metalloproteinase inhibition as a combination therapy for experimental human pancreatic cancer.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2003Article
- Influence of hypoxia and neoangiogenesis on the growth of pancreatic cancer.Molecular cancer · 2003Review
- Pathways for aberrant angiogenesis in pancreatic cancer.Molecular cancer · 2003Review
- Evaluation of novel antimouse VEGFR2 antibodies as potential antiangiogenic or vascular targeting agents for tumor therapy.Neoplasia (New York, N.Y.)Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor vessels abundantly express receptors for vascular endothelial growth factor (VEGF), a mediator of neoangiogenesis. The aim of this study was to specifically target and damage the vasculature of pancreatic cancer (PaCa) by fusing VEGF to diphtheria toxin (DT), which inhibits protein synthesis of target cells. DT-VEGF fusion protein was produced in vector pGEX-KG and expressed in E. coli SG12036. Human PaCa cell lines (HPAF-2 and AsPC-1) and human endothelial cells (HUVEC) were exposed to DT-VEGF (10 ng/ml - 10,000 ng/ml). Proliferation was assessed after 3 days. One mm(3) fragments of subcutaneous PaCa donor tumors were implanted into the pancreas of nude mice that received either DT-VEGF (200 microg/kg, every other day) or phosphate-buffered saline intraperitoneally for 14 weeks. Tumor volume, metastatic spread, and animal weight were determined at autopsy. Microvessel density was analyzed in CD31-stained tumor sections. Proliferation of PaCa cells was inhibited at high concentrations of DT-VEGF (>1000 ng/ml). DT-VEGF decreased the growth of HUVEC at 10 ng/ml. In vivo, DT-VEGF reduced tumor volume (HPAF-2, 76%; AsPC-1, 53%), microvessel density (HPAF-2, 54%; AsPC-1, 62%), and tumor spread (HPAF-2, 89%; AsPC-1, 50%). Survival was increased (HPAF-2, 7/8 vs. 4/8 animals; AsPC-1, 6/8 vs. 1/8 animals). Weight was not influenced by DT-VEGF. The DT-VEGF effect is due to its toxic action on the tumor vasculature rather than to direct inhibition of PaCa cell growth. DT-VEGF therapy was not associated with systemic side effects.
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