Heterogeneity of molecular markers in chronic myelomonocytic leukemia: a disease associated with several gene alterations

被引:3
作者
Bastie, Jean-Noel [1 ,2 ]
Aucagne, Romain [1 ,3 ]
Droin, Nathalie [4 ]
Solary, Eric [4 ]
Delva, Laurent [1 ]
机构
[1] Univ Bourgogne, Fac Med, INSERM, UMR 866, F-21000 Dijon, France
[2] Ctr Hosp Univ, Serv Hematol Clin, F-21000 Dijon, France
[3] Univ Montreal, Inst Rech Immunol & Cancerol, Lab Genet Mol Cellules Souches, Montreal, PQ H3C 3J7, Canada
[4] Inst Gustave Roussy, INSERM, IRCIV, UMR 1009, F-94805 Villejuif, France
关键词
Chronic myelomonocytic leukemia; Somatic mutations; Biomarkers; Heterogeneity; Mouse models; ACUTE MYELOID-LEUKEMIA; ACQUIRED UNIPARENTAL DISOMY; MYELODYSPLASTIC SYNDROMES; C-CBL; TUMOR-SUPPRESSOR; TET2; MUTATIONS; ONCOGENIC NRAS; MYELOPROLIFERATIVE NEOPLASMS; FREQUENT ALTERATIONS; NUCLEAR RECEPTORS;
D O I
10.1007/s00018-012-0956-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The relatively homogenous clinical features and poor prognosis of chronic myelomonocytic leukemia (CMML) are associated with a molecular heterogeneity, with various mutations impacting several convergent pathways. Due to the restricted understanding of the mechanism involved in leukemogenesis, CMML still appears as a diagnostic and therapeutic undertaking, and poor prognosis of leukemia. Contrary to chronic myelogenous leukemia, BCR-ABL1-positive, cytogenetic, and molecular abnormalities of CMML are not specific and not pathognomonic, confirming the different levels of heterogeneity of this disease. Various mutations can be associated with a common phenotype not distinct at the clinical level, further demonstrating that molecular probings are needed for choosing individual targeted therapies.
引用
收藏
页码:2853 / 2861
页数:9
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