ArticleOncogene2002
Dominant negative PDGF-C inhibits growth of Ewing family tumor cell lines.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 57 citations in OpenAlex.
- Pediatric cancer-pathology and microenvironment influence: a perspective into osteosarcoma and non-osteogenic mesenchymal malignant neoplasms.Discover oncology · 2024Review
- Imatinib facilitates gemcitabine sensitivity by targeting epigenetically activated PDGFC signaling in pancreatic cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Primary intracranial sarcomas: a clinicopathological investigation.Frontiers in oncology · 2023Article
- Expression and function of PDGF-C in development and stem cells.Open biology · 2021Review
- The Tumor Microenvironment of Pediatric Sarcoma: Mesenchymal Mechanisms Regulating Cell Migration and Metastasis.Current oncology reports · 2019Review
- An oncogenic activity of PDGF-C and its splice variant in human breast cancer.Growth factors (Chur, Switzerland) · 2019Article
- Article
- PDGFs and their receptors.Gene · 2017Review
- Primary intracranial soft tissue sarcomas in children, adolescents, and young adults: single institution experience and review of the literature.Journal of neuro-oncology · 2016Review
- Clinical significance of platelet derived growth factor-C and -D in gastric cancer.Oncology letters · 2015Article
- Regorafenib: Antitumor Activity upon Mono and Combination Therapy in Preclinical Pediatric Malignancy Models.PloS one · 2015Article
- Targeting the PDGF signaling pathway in tumor treatment.Cell communication and signaling : CCS · 2013Review
- Platelet-derived growth factor-C (PDGF-C) activation by serine proteases: implications for breast cancer progression.The Biochemical journal · 2012Article
- Ewing Sarcoma, an enigmatic malignancy of likely progenitor cell origin, driven by transcription factor oncogenic fusions.International journal of clinical and experimental pathology · 2010Review
- The potential for molecular therapeutic targets in Ewing's sarcoma.Current treatment options in oncology · 2005Review
- Identification of novel candidate oncogenes and tumor suppressors in malignant pleural mesothelioma using large-scale transcriptional profiling.The American journal of pathology · 2005Article
- VEGF-null cells require PDGFR alpha signaling-mediated stromal fibroblast recruitment for tumorigenesis.The EMBO journal · 2004Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nearly all cases of Ewing Family Tumors (EFT) harbor chimeric EWS/ETS transcription factors which are thought to aberrantly regulate transcriptional targets of phenotypic consequence. We have recently demonstrated that EWS/ETS proteins up-regulate platelet derived growth factor-C (PDGF-C), a novel transforming growth factor. To determine if PDGF-C signaling contributes to the malignant phenotype of EFT cell lines, we attempted to disrupt this presumed autocrine loop. AG1296, a PDGF receptor selective tyrosine kinase inhibitor, markedly inhibits anchorage-independent growth in an EFT cell line. To effect specific disruption, we have developed a dominant negative form of PDGF-C which is appropriately secreted and processed. This mutant has greatly reduced activity as a PDGF receptor agonist. When co-expressed with PDGF-C in a fibroblast transformation model, this dominant negative dramatically inhibits anchorage-independent growth. When this mutant is expressed in EFT cell lines, there is a similar reduction in anchorage-independent growth. This demonstrates that specific inhibition of PDGF-C signaling in EFT cell lines partially reverts their phenotype. These data support a significant role of PDGF-C in the biology of EFT. They also suggest that PDGF-C driven signaling may be a possible therapeutic target of more clinically relevant tyrosine kinase inhibitors.
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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.