ArticleOncogene2011
Uncommitted precursor cells might contribute to increased incidence of embryonal rhabdomyosarcoma in heterozygous Patched1-mutant mice.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Context-dependent modulation of aggressiveness of pediatric tumors by individual oncogenic RAS isoforms.Oncogene · 2021Article
- Insight into the Etiology of Undifferentiated Soft Tissue Sarcomas from a Novel Mouse Model.Molecular cancer research : MCR · 2019Article
- Wnt, Notch, and TGF-β Pathways Impinge on Hedgehog Signaling Complexity: An Open Window on Cancer.Frontiers in genetics · 2019Review
- Canonical WNT/β-Catenin Signaling Plays a Subordinate Role in Rhabdomyosarcomas.Frontiers in pediatrics · 2018Article
- Hedgehog/Patched-associated rhabdomyosarcoma formation from delta1-expressing mesodermal cells.Oncogene · 2016Article
- Article
- Hedgehog-driven myogenic tumors recapitulate skeletal muscle cellular heterogeneity.Experimental cell research · 2016Article
- Review
- Overexpression of mutant Ptch in rhabdomyosarcomas is associated with promoter hypomethylation and increased Gli1 and H3K4me3 occupancy.Oncotarget · 2015Article
- The Hedgehog pathway: role in cell differentiation, polarity and proliferation.Archives of toxicology · 2015Review
- MiR-214 and N-ras regulatory loop suppresses rhabdomyosarcoma cell growth and xenograft tumorigenesis.Oncotarget · 2014Article
- Review
- Tumor suppressor genes promote rhabdomyosarcoma progression in p53 heterozygous, HER-2/neu transgenic mice.Oncotarget · 2014Article
- Targeting hedgehog signaling in cancer: research and clinical developments.OncoTargets and therapy · 2013Review
- Patched knockout mouse models of Basal cell carcinoma.Journal of skin cancer · 2012Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Embryonal rhabdomyosarcoma (ERMS) is a tumor of the skeletal muscle in children and is frequently initiated by heterozygous germline mutations in the Hedgehog (Hh) receptor Patched1 (Ptch), both in humans and mice. Using a conditional knock-out strategy in Ptch(flox/+) mice, we demonstrate that early embryonic stages are more susceptible to ERMS development than later stages and that cells normally not committed to undergo myogenesis at this stage represent the major source of ERMS. We found that deletion of a single copy of the Ptch allele at E9.5 using the ubiquitously active Rosa26CreERT2 resulted in a tumor incidence of 88% but reached only 44% and 12% when the Ptch allele was inactivated at E11.5 and E13.5, respectively. Induction of the Ptch mutation at E9.5 did also significantly shorten ERMS-free survival and increased tumor multiplicity compared with tumor induction at E11.5 and E13.5. Interestingly, we observed a more that 10-fold reduction of ERMS incidence when the Ptch mutation was specifically introduced in Myf5-expressing cells, which is the myogenic factor expressed in all muscle cells at E9.5. We conclude that Myf5-negative cells are more susceptible to ERMS development than Myf5-positive embryonic precursors. As the propensity to undergo tumorigenic transformation declined with age, concomitant with the increase of stably committed muscle cells, it seems likely that the Ptch mutation favors tumor formation in progenitor cells, which have not yet acquired a muscle cell fate.
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