ArticleSurgery today2009
TSU68, an antiangiogenic receptor tyrosine kinase inhibitor, induces tumor vascular normalization in a human cancer xenograft nude mouse model.
Article in Surgery today, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma.Frontiers in immunology · 2023Article
- FGFR Inhibitors: Clinical Activity and Development in the Treatment of Cholangiocarcinoma.Current oncology reports · 2021Review
- TSP-1 as a novel biological marker of tumor vasculature normalization in colon carcinoma induced by Endostar.Oncology letters · 2020Article
- Sunitinib impedes brain tumor progression and reduces tumor-induced neurodegeneration in the microenvironment.Cancer science · 2015Article
- Antitumor effects of different administration sequences of cisplatin and Endostar on Lewis lung carcinoma.Oncology letters · 2015Article
- Targeting platelet-derived growth factor (PDGF) signaling in gastrointestinal cancers: preclinical and clinical considerations.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Bevacizumab-induced alterations in vascular permeability and drug delivery: a novel approach to augment regional chemotherapy for in-transit melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Vascular normalization as a therapeutic strategy for malignant and nonmalignant disease.Cold Spring Harbor perspectives in medicine · 2012Review
- Fibroblast growth factor receptor 2: expression, roles, and potential as a novel molecular target for colorectal cancer.Pathology research international · 2012Article
- Article
- Normalization of the vasculature for treatment of cancer and other diseases.Physiological reviews · 2011Review
- HCC and angiogenesis: possible targets and future directions.Nature reviews. Clinical oncology · 2011Review
- Cystic peritoneal mesothelioma: report of a case.Surgery today · 2011Article
- Current status of and prospects for the English medical journal Surgery Today.Surgery today · 2010Article
- Recent concepts of antiangiogenic therapy.Surgery today · 2010Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeCombination therapy using antiangiogenic and cytotoxic agents is a useful strategy for advanced cancer, but the mechanism has not yet been elucidated. Moreover, there is a persistent paradox that destroying tumor vasculature with antiangiogenic agents disturbs the delivery of cytotoxic agents. It has been hypothesized that antiangiogenic agents can lead to normalization of tumor vessels that are structurally and functionally abnormal. The normalization means enhancing the deliver of cytotoxic agents. Our purpose was to investigate whether TSU68, a multiple receptor tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR), would induce the normalization of tumor vessels.
methodsTSU68 was administered for 7 days to mice with xenografted tumors. Tumors of interstitial fluid pressure (IFP) were measured before and after administration of agents. Immunofluorescence double staining for CD31 and alpha-SMA was performed, and a medical video endoscopy system with narrowband illumination (NBI) was used to visualize the vascular pattern.
resultsTSU68 treatment decreased IFP significantly. Immunofluorescence double staining showed a significant increase in the fraction of pericyte coverage in the TSU68-treated group. NBI endoscopy showed that many tumor vessels in TSU68-treated mice were pruned and the diameters of remaining vessels were reduced.
conclusionThe data supported our hypothesis of tumor vascular normalization by the antiangiogenic agent TSU68.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.