Molecular underpinning of extranodal NK/T-cell lymphoma

被引:65
作者
Huang, Yenlin [1 ,2 ]
de Leval, Laurence [3 ]
Gaulard, Philippe [4 ,5 ,6 ]
机构
[1] Chang Gung Mem Hosp, Dept Anat Pathol, Tao Yuan 33305, Taiwan
[2] Chang Gung Univ, Sch Med, Tao Yuan 33305, Taiwan
[3] Univ Hosp Lausanne CHUV, Univ Inst Pathol, Lausanne, Switzerland
[4] Hop Henri Mondor, INSERM, U955, F-94000 Creteil, France
[5] Univ Paris Est, F-94000 Creteil, France
[6] Grp Henri Mondor Albert Chenevier, AP HP, Dept Pathol, Creteil, France
关键词
extranodal NK/T-cell lymphoma; natural killer; Epstein-Barr virus; gene expression profiling; tumor suppressor genes; NATURAL-KILLER-CELL; ENDOTHELIAL GROWTH-FACTOR; TUMOR-SUPPRESSOR GENE; COMPARATIVE GENOMIC HYBRIDIZATION; ASPARAGINASE-BASED REGIMEN; NASAL-TYPE; FACTOR RECEPTOR; K-RAS; C-KIT; DIFFERENTIAL EXPRESSION;
D O I
10.1016/j.beha.2013.04.006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Peripheral NK/T-cell lymphoma (PTCL) is a heterogeneous group of uncommon hematologic malignancies with aggressive clinical course and unfavorable prognosis. Extranodal NK/T-cell lymphoma, nasal type (NKTCL) is the most common extranodal entity worldwide, with heterogeneous geographic distribution, and it is characterized by its association with EBV, a nasal or less often extranasal presentation and aggressive behavior. Recent works using array-based technologies have provided novel insights into the pathogenesis and discovered new biomarkers with diagnostic and therapeutic implications in NKTCL. Gene expression profiling identified that most of the NKTCL are derived from activated natural killer cells with distinctively high expression of granzyme H compared to other PTCLs, which might serve as a new diagnostic biomarker. Frequent deletions and promoter methylations in PRDM1, ATG5, AIM1, FOXO3, HACE1 mapping to 6q21-q25, suggest their roles as potential tumor suppressors. The deregulation of oncogenic pathways (PDGF, JAK-STAT, AKT) provides a rationale for developing targeted therapies in the future. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:57 / 74
页数:18
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