ArticleGenes & development2014
Lineage of origin in rhabdomyosarcoma informs pharmacological response.
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Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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73 citing papers in PubMed, 104 citations in OpenAlex.
- Dual inhibition of KDM4B and KDM5A disassembles the PAX3-FOXO1 transcriptional program in fusion-positive rhabdomyosarcoma.Biology direct · 2026Article
- A Pax7::Foxo1 conditional mouse strain.Skeletal muscle · 2026Article
- Review
- Genetic and chromosomal dysregulations of progenitor cells in the etiology and pathogenesis of pediatric cancers.American journal of stem cells · 2026Review
- From bench to bedside: combining HDAC inhibitors with standard therapies in rhabdomyosarcoma treatment.Frontiers in cell and developmental biology · 2026Review
- Somatic gene delivery faithfully recapitulates a molecular spectrum of high-risk sarcomas.Nature communications · 2025Article
- Ephrin-A5 or EphA7 stimulation is anti-proliferative for human rhabdomyosarcoma in vitro.Skeletal muscle · 2025Article
- DNA methylation patterns are influenced by Pax3::Foxo1 expression and developmental lineage in rhabdomyosarcoma tumours forming in genetically engineered mouse models.The Journal of pathology · 2025Article
- Fusion oncogenes in rhabdomyosarcoma: model systems, mechanisms of tumorigenesis, and therapeutic implications.Frontiers in oncology · 2025Review
- Developmental and therapeutic implications of IL4ra expression for rhabdomyosarcoma.Transgenic research · 2024Article
- Biological and therapeutic insights from animal modeling of fusion-driven pediatric soft tissue sarcomas.Disease models & mechanisms · 2024Review
- Review
- PAX3-FOXO1 dictates myogenic reprogramming and rhabdomyosarcoma identity in endothelial progenitors.Nature communications · 2023Article
- PROTAC-Based Protein Degradation as a Promising Strategy for Targeted Therapy in Sarcomas.International journal of molecular sciences · 2023Review
- A dysfunctional miR-1-TRPS1-MYOG axis drives ERMS by suppressing terminal myogenic differentiation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Myo-differentiation reporter screen reveals NF-Y as an activator of PAX3-FOXO1 in rhabdomyosarcoma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- HDAC3 is critical in tumor development and therapeutic resistance inScience advances · 2023Article
- A review of the therapeutic potential of histone deacetylase inhibitors in rhabdomyosarcoma.Frontiers in oncology · 2023Review
- CD203c is expressed by human fetal hepatoblasts and distinguishes subsets of hepatoblastoma.Frontiers in oncology · 2023Article
- PROX1 transcription factor controls rhabdomyosarcoma growth, stemness, myogenic properties and therapeutic targets.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
32 authors at 13 institutions in 2 countries.
Jinu AbrahamPediatric Cancer Biology Program, Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239, USA;
Yaiza Nuñez-ÁlvarezInstitute of Predictive and Personalized Medicine of Cancer (IMPPC), Germans Trias i Pujol Health Sciences Research Institute (IGTP), 08916 Badalona, Barcelona, Spain;
Simone HettmerHoward Hughes Medical Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Harvard Stem Cell Institute, Joslin Diabetes Center, Cambridge, Massachusetts 02138, USA; Department of Pediatric Oncology, Dana Farber Cancer Institute, Division of Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA;
Elvira CarrióInstitute of Predictive and Personalized Medicine of Cancer (IMPPC), Germans Trias i Pujol Health Sciences Research Institute (IGTP), 08916 Badalona, Barcelona, Spain;
Hung-I Harry ChenGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Koichi NishijoGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Elaine T HuangPediatric Cancer Biology Program, Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239, USA;
Suresh I PrajapatiGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Robert L WalkerOncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland 20877, USA;
Sean DavisOncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland 20877, USA;
Jennifer RebelesGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Hunter WiebushGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Amanda T McCleishGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Sheila T HamptonGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Christopher R R BjornsonDepartment of Neurology, Department of Neurological Sciences, Glenn Laboratories for the Biology of Aging, Stanford University, Palo Alto, California 94304, USA;
Andrew S BrackDepartment of Neurology, Department of Neurological Sciences, Glenn Laboratories for the Biology of Aging, Stanford University, Palo Alto, California 94304, USA;
Amy J WagersHoward Hughes Medical Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Harvard Stem Cell Institute, Joslin Diabetes Center, Cambridge, Massachusetts 02138, USA;
Thomas A RandoDepartment of Neurology, Department of Neurological Sciences, Glenn Laboratories for the Biology of Aging, Stanford University, Palo Alto, California 94304, USA;
Mario R CapecchiDepartment of Human Genetics, University of Utah, Salt Lake City, Utah 84112, USA;
Frank C MariniInstitute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina 27157, USA;
Benjamin R EhlerDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Lee Ann ZarzabalDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Martin W GorosDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Joel E MichalekDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Paul S MeltzerOncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland 20877, USA;
David M LangenauDepartment of Pathology, Center for Cancer Research, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA;
Robin D LeGalloDepartment of Pathology, University of Virginia, Charlottesville, Virginia 22903, USA;
Atiya MansoorDepartment of Pathology, Oregon Health and Science University, Portland, Oregon 97239, USA;
Yidong ChenGreehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
Mònica SuelvesInstitute of Predictive and Personalized Medicine of Cancer (IMPPC), Germans Trias i Pujol Health Sciences Research Institute (IGTP), 08916 Badalona, Barcelona, Spain;
Brian P RubinDepartment of Anatomic Pathology, Department of Molecular Genetics, Taussig Cancer Center, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Charles KellerPediatric Cancer Biology Program, Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239, USA;
The University of Texas Health Science Center at San Antonio · USOregon Health & Science University · USChildren's Cancer Center · USInstitute of Predictive and Personalized Medicine of Cancer · ESNational Cancer Institute · USStanford University · USCleveland Clinic · USHoward Hughes Medical Institute · USJoslin Diabetes Center · USMassachusetts General Hospital · USUniversity of Utah · USUniversity of Virginia · USWake Forest University · US
Funding
Wnt signaling in muscle stem cell agingP01AG036695 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI THOMAS A. RANDO · 2011 to 2026
$29.3MFunctional Genomics of SarcomaZIABC010759 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MELTZER, PAUL S. · 2009 to 2025
$22.3MUTSA RISE Research Training ProgramR25GM060655 · NIGMS · UNIVERSITY OF TEXAS SAN ANTONIO · PI BAREA-RODRIGUEZ, EDWIN J · 2000 to 2022
$21.6MUTSA Maximizing Access to Research Careers Research Training Program - Admin SupplementT34GM007717 · NIGMS · UNIVERSITY OF TEXAS SAN ANTONIO · PI BAREA-RODRIGUEZ, EDWIN J · 1985 to 2021
$9.5MGenetics of RhabdomyosarcomaR01CA154923 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LANGENAU, DAVID MICHAEL · 2011 to 2021
$3.8MTherapeutic Targets in Alveolar RhabdomyosarcomaR01CA133229 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KELLER, CHARLES · 2008 to 2012
$1.9MQuiescence of Muscle Stem Cells During Growth and RepairR01AR061002 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRACK, ANDREW S · 2012 to 2016
$1.7MThe Function and Regulation of Pax3 in Muscle Stem CellsR01AR062185 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI RANDO, THOMAS A. · 2011 to 2015
$1.5MRegulation of Muscle Fibrosis in Response to Injury and AgingI01BX002324 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI RANDO, THOMAS A. · 2014 to 2021
–BLRD VA I01 BX002324Howard Hughes Medical InstituteNCI NIH HHS 1R01CA154923NCI NIH HHS 5R01CA133229NCI NIH HHS R01 CA133229NCI NIH HHS R01 CA154923NIAMS NIH HHS R01 AR061002NIAMS NIH HHS R01 AR062185NIA NIH HHS P01 AG036695NIGMS NIH HHS R25 GM060655NIGMS NIH HHS T34 GM007717PHS HHS NIGMS MBRS-RISE GM 60655
Abstract
Lineage or cell of origin of cancers is often unknown and thus is not a consideration in therapeutic approaches. Alveolar rhabdomyosarcoma (aRMS) is an aggressive childhood cancer for which the cell of origin remains debated. We used conditional genetic mouse models of aRMS to activate the pathognomonic Pax3:Foxo1 fusion oncogene and inactivate p53 in several stages of prenatal and postnatal muscle development. We reveal that lineage of origin significantly influences tumor histomorphology and sensitivity to targeted therapeutics. Furthermore, we uncovered differential transcriptional regulation of the Pax3:Foxo1 locus by tumor lineage of origin, which led us to identify the histone deacetylase inhibitor entinostat as a pharmacological agent for the potential conversion of Pax3:Foxo1-positive aRMS to a state akin to fusion-negative RMS through direct transcriptional suppression of Pax3:Foxo1.
Indexed as
AnimalsAntineoplastic AgentsBenzamidesCell LineageCell Line, TumorDisease Models, AnimalEpigenesis, GeneticForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansMicePaired Box Transcription FactorsPAX3 Transcription FactorPyridinesRhabdomyosarcoma, AlveolarAntineoplastic AgentsBenzamidesentinostatForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mousePaired Box Transcription FactorsPax3 protein, mousePAX3 Transcription FactorPyridinesTumor Suppressor Protein p53alveolar rhabdomyosarcomahistonemyoblastPax3:Foxo1sarcomasatellite cell
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