Your browser doesn't support javascript.
loading
MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis.
Musa, Julian; Aynaud, Marie-Ming; Mirabeau, Olivier; Delattre, Olivier; Grünewald, Thomas Gp.
Afiliación
  • Musa J; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute for Pathology of the LMU Munich, Munich, Germany.
  • Aynaud MM; INSERM Unit 830 'Genetics and Biology of Cancers', Institut Curie Research Center, Paris, France.
  • Mirabeau O; INSERM Unit 830 'Genetics and Biology of Cancers', Institut Curie Research Center, Paris, France.
  • Delattre O; INSERM Unit 830 'Genetics and Biology of Cancers', Institut Curie Research Center, Paris, France.
  • Grünewald TG; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute for Pathology of the LMU Munich, Munich, Germany.
Cell Death Dis ; 8(6): e2895, 2017 06 22.
Article en En | MEDLINE | ID: mdl-28640249
Limitless cell proliferation, evasion from apoptosis, dedifferentiation, metastatic spread and therapy resistance: all these properties of a cancer cell contribute to its malignant phenotype and affect patient outcome. MYBL2 (alias B-Myb) is a transcription factor of the MYB transcription factor family and a physiological regulator of cell cycle progression, cell survival and cell differentiation. When deregulated in cancer cells, MYBL2 mediates the deregulation of these properties. In fact, MYBL2 is overexpressed and associated with poor patient outcome in numerous cancer entities. MYBL2 and players of its downstream transcriptional network can be used as prognostic and/or predictive biomarkers as well as potential therapeutic targets to offer less toxic and more specific anti-cancer therapies in future. In this review, we summarize current knowledge on the physiological roles of MYBL2 and highlight the impact of its deregulation on cancer initiation and progression.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Diferenciación Celular / Transactivadores / Carcinogénesis Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cell Death Dis Año: 2017 Tipo del documento: Article País de afiliación: Alemania

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Diferenciación Celular / Transactivadores / Carcinogénesis Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cell Death Dis Año: 2017 Tipo del documento: Article País de afiliación: Alemania