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http://purl.uniprot.org/citations/22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22393362http://www.w3.org/2000/01/rdf-schema#comment"Myc plays an important role in tumor development, including acute myeloid leukemia (AML). However, MYC is also a powerful inducer of apoptosis, which is one of the major failsafe programs to prevent cancer development. To clarify the relative importance of the extrinsic (death receptor-mediated) versus the intrinsic (mitochondrial) pathway of apoptosis in MYC-driven AML, we coexpressed MYC together with anti-apoptotic proteins of relevance for AML; BCL-X(L)/BCL-2 (inhibiting the intrinsic pathway) or FLIP(L) (inhibiting the extrinsic pathway), in hematopoietic stems cells (HSCs). Transplantation of HSCs expressing MYC into syngeneic recipient mice resulted in development of AML and T-cell lymphomas within 7-9 weeks as expected. Importantly, coexpression of MYC together with BCL-X(L)/BCL-2 resulted in strongly accelerated kinetics and favored tumor development towards aggressive AML. In contrast, coexpression of MYC and FLIP(L) did neither accelerate tumorigenesis nor change the ratio of AML versus T-cell lymphoma. However, a change in distribution of immature CD4(+)CD8(+) versus mature CD4(+) T-cell lymphoma was observed in MYC/FLIP(L) mice, possibly as a result of increased survival of the CD4+ population, but this did not significantly affect the outcome of the disease. In conclusion, our findings provide direct evidence that BCL-X(L) and BCL-2 but not FLIP(L) acts in synergy with MYC to drive AML development."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0031366"xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/author"Sander B."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/author"Grandien A."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/author"Rozell B."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/author"Larsson L.G."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/author"Hogstrand K."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/author"Hejll E."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/pages"e31366"xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/title"Inhibition of the intrinsic but not the extrinsic apoptosis pathway accelerates and drives MYC-driven tumorigenesis towards acute myeloid leukemia."xsd:string
http://purl.uniprot.org/citations/22393362http://purl.uniprot.org/core/volume"7"xsd:string
http://purl.uniprot.org/citations/22393362http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22393362
http://purl.uniprot.org/citations/22393362http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22393362
http://purl.uniprot.org/uniprot/#_A0A0B4J1R1-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_A0A024R3Y4-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_A0A1L4AQQ4-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_E9PAP3-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_P10415-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_P10417-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_Q07817-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_A0A0S2Z3C5-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362
http://purl.uniprot.org/uniprot/#_A0A0S2Z3D2-mappedCitation-22393362http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22393362