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Lineage of origin in rhabdomyosarcoma informs pharmacological response.
Abraham, Jinu; Nuñez-Álvarez, Yaiza; Hettmer, Simone; Carrió, Elvira; Chen, Hung-I Harry; Nishijo, Koichi; Huang, Elaine T; Prajapati, Suresh I; Walker, Robert L; Davis, Sean; Rebeles, Jennifer; Wiebush, Hunter; McCleish, Amanda T; Hampton, Sheila T; Bjornson, Christopher R R; Brack, Andrew S; Wagers, Amy J; Rando, Thomas A; Capecchi, Mario R; Marini, Frank C; Ehler, Benjamin R; Zarzabal, Lee Ann; Goros, Martin W; Michalek, Joel E; Meltzer, Paul S; Langenau, David M; LeGallo, Robin D; Mansoor, Atiya; Chen, Yidong; Suelves, Mònica; Rubin, Brian P; Keller, Charles.
Afiliação
  • Abraham J; Pediatric Cancer Biology Program, Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239, USA;
  • Nuñez-Álvarez Y; Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Germans Trias i Pujol Health Sciences Research Institute (IGTP), 08916 Badalona, Barcelona, Spain;
  • Hettmer S; Howard 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,
  • Carrió E; Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Germans Trias i Pujol Health Sciences Research Institute (IGTP), 08916 Badalona, Barcelona, Spain;
  • Chen HI; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Nishijo K; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Huang ET; Pediatric Cancer Biology Program, Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239, USA;
  • Prajapati SI; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Walker RL; Oncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland 20877, USA;
  • Davis S; Oncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland 20877, USA;
  • Rebeles J; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Wiebush H; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • McCleish AT; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Hampton ST; Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Bjornson CR; Department of Neurology, Department of Neurological Sciences, Glenn Laboratories for the Biology of Aging, Stanford University, Palo Alto, California 94304, USA;
  • Brack AS; Department of Neurology, Department of Neurological Sciences, Glenn Laboratories for the Biology of Aging, Stanford University, Palo Alto, California 94304, USA;
  • Wagers AJ; Howard Hughes Medical Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Harvard Stem Cell Institute, Joslin Diabetes Center, Cambridge, Massachusetts 02138, USA;
  • Rando TA; Department of Neurology, Department of Neurological Sciences, Glenn Laboratories for the Biology of Aging, Stanford University, Palo Alto, California 94304, USA;
  • Capecchi MR; Department of Human Genetics, University of Utah, Salt Lake City, Utah 84112, USA;
  • Marini FC; Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina 27157, USA;
  • Ehler BR; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Zarzabal LA; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Goros MW; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Michalek JE; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, Texas 78229, USA;
  • Meltzer PS; Oncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland 20877, USA;
  • Langenau DM; Department of Pathology, Center for Cancer Research, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA;
  • LeGallo RD; Department of Pathology, University of Virginia, Charlottesville, Virginia 22903, USA;
  • Mansoor A; Department of Pathology, Oregon Health and Science University, Portland, Oregon 97239, USA;
  • Chen Y; Greehey 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;
  • Suelves M; Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Germans Trias i Pujol Health Sciences Research Institute (IGTP), 08916 Badalona, Barcelona, Spain;
  • Rubin BP; Department of Anatomic Pathology, Department of Molecular Genetics, Taussig Cancer Center, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
  • Keller C; Pediatric Cancer Biology Program, Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97239, USA;
Genes Dev ; 28(14): 1578-91, 2014 Jul 15.
Article em En | MEDLINE | ID: mdl-25030697
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Piridinas / Benzamidas / Rabdomiossarcoma Alveolar / Antineoplásicos Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2014 Tipo de documento: Article
Texto completo
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Piridinas / Benzamidas / Rabdomiossarcoma Alveolar / Antineoplásicos Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2014 Tipo de documento: Article