Your browser doesn't support javascript.
loading
Combined experience of six independent laboratories attempting to create an Ewing sarcoma mouse model.
Minas, Tsion Zewdu; Surdez, Didier; Javaheri, Tahereh; Tanaka, Miwa; Howarth, Michelle; Kang, Hong-Jun; Han, Jenny; Han, Zhi-Yan; Sax, Barbara; Kream, Barbara E; Hong, Sung-Hyeok; Çelik, Haydar; Tirode, Franck; Tuckermann, Jan; Toretsky, Jeffrey A; Kenner, Lukas; Kovar, Heinrich; Lee, Sean; Sweet-Cordero, E Alejandro; Nakamura, Takuro; Moriggl, Richard; Delattre, Olivier; Üren, Aykut.
Afiliación
  • Minas TZ; Department of Oncology, Georgetown University Medical Center, Washington, DC, United States of America.
  • Surdez D; Genetics and Biology of Cancers Unit, Institut Curie Research Center, PSL Research University, Île-de-France, Paris, France.
  • Javaheri T; INSERM U830, Institut Curie Research Center, Île-de-France, Paris, France.
  • Tanaka M; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
  • Howarth M; Division of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
  • Kang HJ; Division of Hematology and Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, United States of America.
  • Han J; Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA, United States of America.
  • Han ZY; Department of Oncology, Georgetown University Medical Center, Washington, DC, United States of America.
  • Sax B; Genetics and Biology of Cancers Unit, Institut Curie Research Center, PSL Research University, Île-de-France, Paris, France.
  • Kream BE; INSERM U830, Institut Curie Research Center, Île-de-France, Paris, France.
  • Hong SH; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
  • Çelik H; Department of Medicine, and Genetics and Genome Sciences, University of Connecticut Health Science Center, Farmington, CT, United States of America.
  • Tirode F; Department of Oncology, Georgetown University Medical Center, Washington, DC, United States of America.
  • Tuckermann J; Department of Oncology, Georgetown University Medical Center, Washington, DC, United States of America.
  • Toretsky JA; Genetics and Biology of Cancers Unit, Institut Curie Research Center, PSL Research University, Île-de-France, Paris, France.
  • Kenner L; INSERM U830, Institut Curie Research Center, Île-de-France, Paris, France.
  • Kovar H; Institute of Comparative Molecular Endocrinology (CME), University of Ulm, Ulm, Germany.
  • Lee S; Department of Oncology, Georgetown University Medical Center, Washington, DC, United States of America.
  • Sweet-Cordero EA; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
  • Nakamura T; Clinical Institute of Pathology, Medical University of Vienna, Vienna, Austria.
  • Moriggl R; Department of Pathology of Laboratory Animals (UPLA), University of Veterinary Medicine, Vienna, Austria.
  • Delattre O; Department of Pediatrics, Medical University of Vienna, Vienna, Austria.
  • Üren A; Children´s Cancer Research Institute, St. Anna Kinderkrebsforschung, Vienna, Austria.
Oncotarget ; 8(21): 34141-34163, 2017 May 23.
Article en En | MEDLINE | ID: mdl-27191748
Ewing sarcoma (ES) involves a tumor-specific chromosomal translocation that produces the EWS-FLI1 protein, which is required for the growth of ES cells both in vitro and in vivo. However, an EWS-FLI1-driven transgenic mouse model is not currently available. Here, we present data from six independent laboratories seeking an alternative approach to express EWS-FLI1 in different murine tissues. We used the Runx2, Col1a2.3, Col1a3.6, Prx1, CAG, Nse, NEFL, Dermo1, P0, Sox9 and Osterix promoters to target EWS-FLI1 or Cre expression. Additional approaches included the induction of an endogenous chromosomal translocation, in utero knock-in, and the injection of Cre-expressing adenovirus to induce EWS-FLI1 expression locally in multiple lineages. Most models resulted in embryonic lethality or developmental defects. EWS-FLI1-induced apoptosis, promoter leakiness, the lack of potential cofactors, and the difficulty of expressing EWS-FLI1 in specific sites were considered the primary reasons for the failed attempts to create a transgenic mouse model of ES.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sarcoma de Ewing / Proteínas de Fusión Oncogénica / Regiones Promotoras Genéticas / Proteína EWS de Unión a ARN / Modelos Animales de Enfermedad / Proteína Proto-Oncogénica c-fli-1 Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Oncotarget Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sarcoma de Ewing / Proteínas de Fusión Oncogénica / Regiones Promotoras Genéticas / Proteína EWS de Unión a ARN / Modelos Animales de Enfermedad / Proteína Proto-Oncogénica c-fli-1 Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Oncotarget Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos