Polycomb group protein Bmi1 is required for growth of RAF driven non-small-cell lung cancer

We have previously described a RAF oncogene driven transgenic mouse model for non small cell lung cancer (NSCLC). Here we examine whether tumor initiation and growth requires the stem cell self-renewal factor Bmi1. In order to evaluate Bmi1 function in NSCLC two founder lines that differ in incidenc...

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Veröffentlicht in:	PloS one 2009-01, Vol.4 (1), p.e4230
Hauptverfasser:	Becker, Matthias, Korn, Christian, Sienerth, Arnold R, Voswinckel, Robert, Luetkenhaus, Katharina, Ceteci, Fatih, Rapp, Ulf R
Format:	Artikel
Sprache:	eng
Schlagworte:	Analysis Animals Apoptosis Biotechnology Cancer Carcinoma, Non-Small-Cell Lung - metabolism Cell Biology/Cell Signaling Cell cycle Cell death Cell self-renewal Cell Transformation, Neoplastic Crosses, Genetic Cyclin-Dependent Kinase Inhibitor p16 - metabolism Gene Expression Regulation, Neoplastic Genes Genetic engineering Growth Histology INK4a protein Latency Life span Lung - metabolism Lung cancer Lung diseases Lung Neoplasms - metabolism Melanoma Mice Mice, Inbred C57BL Mice, Transgenic Microscopy Models, Genetic Mutation Non-small cell lung cancer Non-small cell lung carcinoma Nuclear Proteins - genetics Nuclear Proteins - physiology Oncology/Lung Cancer p16 Protein Polyclonal antibodies Polycomb group proteins Polycomb Repressive Complex 1 Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - physiology raf Kinases - metabolism Raf protein Repressor Proteins - genetics Repressor Proteins - physiology Respiratory Medicine/Lung Cancer Rodents Senescence Small cell lung carcinoma Stem cells Transgenic mice Tumor Suppressor Protein p14ARF - metabolism Tumorigenesis Tumors
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