ArticleCancer2009
Targeting the urokinase plasminogen activator receptor with a monoclonal antibody impairs the growth of human colorectal cancer in the liver.
Article in Cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- Therapeutic strategies targeting uPAR potentiate anti-PD-1 efficacy in diffuse-type gastric cancer.Science advances · 2022Article
- Urokinase-type plasminogen activator receptor (uPAR) as a therapeutic target in cancer.Journal of translational medicine · 2022Review
- Fibrinolytic System and Cancer: Diagnostic and Therapeutic Applications.International journal of molecular sciences · 2021Review
- Further Understanding of Urokinase Plasminogen Activator Overexpression in Urothelial Bladder Cancer Progression, Clinical Outcomes and Potential Therapeutic Targets.OncoTargets and therapy · 2021Review
- uPAR antibody (huATN-658) and Zometa reduce breast cancer growth and skeletal lesions.Bone research · 2020Article
- Multifaceted Role of the Urokinase-Type Plasminogen Activator (uPA) and Its Receptor (uPAR): Diagnostic, Prognostic, and Therapeutic Applications.Frontiers in oncology · 2018Review
- uPAR-targeted multimodal tracer for pre- and intraoperative imaging in cancer surgery.Oncotarget · 2015Article
- Prostate cancer relevant antigens and enzymes for targeted drug delivery.Journal of controlled release : official journal of the Controlled Release Society · 2014Review
- Expression of uPAR in tumor-associated stromal cells is associated with colorectal cancer patient prognosis: a TMA study.BMC cancer · 2014Article
- Article
- The many spaces of uPAR: delivery of theranostic agents and nanobins to multiple tumor compartments through a single target.Theranostics · 2013Review
- A novel animal model for in vivo study of liver cancer metastasis.World journal of gastroenterology · 2012Article
- Regulation of u-PAR gene expression by H2A.Z is modulated by the MEK-ERK/AP-1 pathway.Nucleic acids research · 2012Article
- Evaluating the value of uPAR of serum and tissue on patients with cervical cancer.Journal of clinical laboratory analysis · 2012Article
- Identification of cancer stem cells in human gastrointestinal carcinoid and neuroendocrine tumors.Gastroenterology · 2011Article
- Mechanism of p27 upregulation induced by downregulation of cathepsin B and uPAR in glioma.Molecular oncology · 2011Article
- Targeting the urokinase plasminogen activator receptor inhibits ovarian cancer metastasis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Development of novel therapeutics targeting the urokinase plasminogen activator receptor (uPAR) and their translation toward the clinic.Current pharmaceutical design · 2011Article
- An anti-urokinase plasminogen activator receptor antibody (ATN-658) blocks prostate cancer invasion, migration, growth, and experimental skeletal metastasis in vitro and in vivo.Neoplasia (New York, N.Y.) · 2010Article
- Co-depletion of cathepsin B and uPAR induces G0/G1 arrest in glioma via FOXO3a mediated p27 upregulation.PloS one · 2010Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundUrokinase plasminogen activator receptor (uPAR) expression has been shown to correlate with poor prognosis in colorectal cancer (CRC). The authors hypothesized that targeting uPAR, a receptor involved in cell proliferation, migration, invasion, adhesion, and angiogenesis, would impair the growth of CRC in the liver, the most common site of metastasis.
methodsHuman CRC cell lines were examined for uPAR expression by Western blot analysis. The in vitro effects of the uPAR monoclonal antibody (MoAb) (ATN-658) were tested in proliferation and migration assays. For in vivo studies, human HCT116 CRC cells were injected directly into the livers of mice in 2 separate studies, the first to determine the effect of therapy with ATN-658 on small-volume disease (therapy begun on Day 4), and a second study to determine the effect of therapy on established disease (therapy begun on Day 12). Mice were randomized to receive either nonspecific immunoglobulin G MoAb (control) or ATN-658, and were sacrificed 1 month after tumor implantation.
resultsuPAR was expressed by all CRC cell lines studied. In vitro, ATN-658 had minimal effect on CRC proliferation in monolayers, but significantly decreased CRC cell migration. In vivo, ATN-658 lead to significant reductions in tumor growth versus control when initiated either 4 or 12 days after tumor implantation (-65% vs control [P < or = .05] and -85% vs control [P < or = .05]). ATN-658 significantly inhibited in vivo tumor cell proliferation in both studies.
conclusionsuPAR MoAb therapy impaired CRC tumor growth in the liver in both small-volume and large-volume disease models.
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Registered trials
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.