Myeloid malignancies: mutations, models and management

BMC Cancer

Review

Anne Murati¹  Mandy Brecqueville¹  Marie-Joelle Mozziconacci¹  Daniel Birnbaum¹  Véronique Gelsi-Boyer¹  Raynier Devillier¹ 

[1] Centre de Recherche en Cancérologie de Marseille, laboratoire d’Oncologie Moléculaire; UMR1068 Inserm, Institut Paoli-Calmettes, BP 30059, 27 Bd. Leï Roure, 13273, Marseille, France;

关键词: Acute Myeloid Leukemia;    Chronic Myeloid Leukemia;    Polycythemia Vera;    Essential Thrombocythemia;    Myeloid Malignancy;   

DOI  :  10.1186/1471-2407-12-304

 received in 2011-10-05, accepted in 2012-06-30,  发布年份 2012

来源: Springer

【 摘 要 】

Myeloid malignant diseases comprise chronic (including myelodysplastic syndromes, myeloproliferative neoplasms and chronic myelomonocytic leukemia) and acute (acute myeloid leukemia) stages. They are clonal diseases arising in hematopoietic stem or progenitor cells. Mutations responsible for these diseases occur in several genes whose encoded proteins belong principally to five classes: signaling pathways proteins (e.g. CBL, FLT3, JAK2, RAS), transcription factors (e.g. CEBPA, ETV6, RUNX1), epigenetic regulators (e.g. ASXL1, DNMT3A, EZH2, IDH1, IDH2, SUZ12, TET2, UTX), tumor suppressors (e.g. TP53), and components of the spliceosome (e.g. SF3B1, SRSF2). Large-scale sequencing efforts will soon lead to the establishment of a comprehensive repertoire of these mutations, allowing for a better definition and classification of myeloid malignancies, the identification of new prognostic markers and therapeutic targets, and the development of novel therapies. Given the importance of epigenetic deregulation in myeloid diseases, the use of drugs targeting epigenetic regulators appears as a most promising therapeutic approach.

【 授权许可】

Unknown   
© Murati et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.