ArticleMolecular and cellular biology2002
Pax3-FKHR knock-in mice show developmental aberrations but do not develop tumors.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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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
43 citing papers in PubMed, 74 citations in OpenAlex.
- Loss of Nf1 and Ink4a/Arf Are Associated with Sex-Dependent Growth Differences in a Mouse Model of Embryonal Rhabdomyosarcoma.Current issues in molecular biology · 2023Article
- PAX Genes in Cardiovascular Development.International journal of molecular sciences · 2022Review
- Review
- Preclinical In Vivo Modeling of Pediatric Sarcoma-Promises and Limitations.Journal of clinical medicine · 2021Review
- A review of soft-tissue sarcomas: translation of biological advances into treatment measures.Cancer management and research · 2018Review
- Relevance of Fusion Genes in Pediatric Cancers: Toward Precision Medicine.Molecular therapy. Nucleic acids · 2017Review
- FOXO Signaling Pathways as Therapeutic Targets in Cancer.International journal of biological sciences · 2017Review
- Development and potential applications of CRISPR-Cas9 genome editing technology in sarcoma.Cancer letters · 2016Review
- FOXO transcription factors in cancer development and therapy.Cellular and molecular life sciences : CMLS · 2016Review
- Probing for a deeper understanding of rhabdomyosarcoma: insights from complementary model systems.Nature reviews. Cancer · 2015Review
- The PAX3-FOXO1 fusion protein present in rhabdomyosarcoma interferes with normal FOXO activity and the TGF-β pathway.PloS one · 2015Article
- Modeling of the human alveolar rhabdomyosarcoma Pax3-Foxo1 chromosome translocation in mouse myoblasts using CRISPR-Cas9 nuclease.PLoS genetics · 2015Article
- Deep Sequencing the microRNA profile in rhabdomyosarcoma reveals down-regulation of miR-378 family members.BMC cancer · 2014Article
- Comprehensive genomic analysis of rhabdomyosarcoma reveals a landscape of alterations affecting a common genetic axis in fusion-positive and fusion-negative tumors.Cancer discovery · 2014Article
- Alveolar rhabdomyosarcoma - The molecular drivers of PAX3/7-FOXO1-induced tumorigenesis.Skeletal muscle · 2012Article
- Animal models of extracranial pediatric solid tumors.Oncology letters · 2012Article
- Mouse models of sarcomas: critical tools in our understanding of the pathobiology.Clinical sarcoma research · 2012Article
- Childhood rhabdomyosarcoma: recent advances and prospective views.Journal of dental research · 2012Review
- Modeling sarcomagenesis using multipotent mesenchymal stem cells.Cell research · 2012Review
- Advances in pediatric rhabdomyosarcoma characterization and disease model development.Histology and histopathology · 2012Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Alveolar rhabdomyosarcoma is a pediatric disease specified by the recurrent chromosome translocations t(2;13) and t(1;13). These translocations result in the formation of the PAX3-FKHR and PAX7-FKHR fusion genes, which are thought to play a causal role in the genesis of this disease. Although PAX3-FKHR exhibits transforming activity in immortalized fibroblast cell lines, a direct role of this fusion protein in tumorigenesis in vivo has not been shown. We determined whether expression of Pax3-FKHR in the mouse germ line would render these animals prone to the development of rhabdomyosarcomas. By targeting FKHR cDNA sequences into the Pax3 locus of embryonic stem cells, we used these cells to generate mice carrying a Pax3-FKHR knock-in allele. Despite low expression of the knock-in allele, heterozygous offspring of Pax3-FKHR chimeric mice showed developmental abnormalities. These included intraventricular septum defects, tricuspid valve insufficiency, and diaphragm defects, which caused congestive heart failure leading to perinatal death. In addition, Pax3-FKHR heterozygous offspring displayed malformations of some but not all hypaxial muscles. However, neither newborn heterozygous pups nor their chimeric parents showed any signs of malignancy. We conclude that the Pax3-FKHR allele causes lethal developmental defects in knock-in mice but might be insufficient to cause muscle tumors.
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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.