Academic Journal
Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status
| العنوان: | Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status |
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| المؤلفون: | Silva, FPG, Swagemakers, Sigrid, Erpelinck - Verschueren, Claudia, Wouters, Bas, Delwel, Ruud, Vrieling, H, van der Spek, Peter, Valk, Peter, Giphart-Gassler, M |
| المصدر: | Silva , FPG , Swagemakers , S , Erpelinck - Verschueren , C , Wouters , B , Delwel , R , Vrieling , H , van der Spek , P , Valk , P & Giphart-Gassler , M 2009 , ' Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status ' , Blood , vol. 114 , no. 14 , pp. 3001-3007 . https://doi.org/10.1182/blood-2009-03-211334 |
| سنة النشر: | 2009 |
| مصطلحات موضوعية: | /dk/atira/pure/keywords/researchprograms/AFL001000/EMCMGC020201, name=EMC MGC-02-02-01, /dk/atira/pure/keywords/researchprograms/AFL001000/EMCMM024103, name=EMC MM-02-41-03 |
| الوصف: | Minimally differentiated acute myeloid leukemia (AML-M0) is defined by immature morphology and expression of early hematologic markers. By gene expression profiling (GEP) and subsequent unsupervised analysis of 35 AML-M0 samples and 253 previously reported AML cases, we demonstrate that AML-M0 cases express a unique signature that is largely separated from other molecular subtypes. Hematologic transcription regulators such as CEBPA, CEBPD, and ETV6, and the differentiation associated gene MPO appeared strongly down-regulated, in line with the primitive state of this leukemia. AML-M0 frequently carries loss-of-function RUNX1 mutation. Unsupervised analyses revealed a subdivision between AML-M0 cases with and without RUNX1 mutations. RUNX1 mutant AML-M0 samples showed a distinct up-regulation of B cell-related genes such as members of the B-cell receptor complex, transcription regulators RUNX3, ETS2, IRF8, or PRDM1, and major histocompatibility complex class II genes. Importantly, prediction with high accuracy of the AML-M0 subtype and prediction of patients carrying RUNX1 mutation within this subtype were possible based on the expression level of only a few transcripts. We propose that RUNX1 mutations in this AML subgroup cause lineage infidelity, leading to aberrant coexpression of myeloid and B-lymphoid genes. Furthermore, our results imply that AML-M0, although originally determined by morphology, constitutes a leukemia subgroup. (Blood. 2009; 114: 3001-3007) |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | unknown |
| DOI: | 10.1182/blood-2009-03-211334 |
| الاتاحة: | https://pure.eur.nl/en/publications/6178b9bf-c3e4-41bd-a255-ef1637b89f76 https://doi.org/10.1182/blood-2009-03-211334 http://hdl.handle.net/1765/25327 |
| Rights: | info:eu-repo/semantics/closedAccess |
| رقم الانضمام: | edsbas.BC553F4B |
| قاعدة البيانات: | BASE |
| DOI: | 10.1182/blood-2009-03-211334 |
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