CAJ | 학술논문

目的:探讨弥漫性大B细胞淋巴瘤(DLBCL)MYC基因异常情况及其与BCL-2、BCL-6基因异常的关系.方法:应用组织芯片和FISH技术对194例DLBCL的MYC、BCL-2、BCL-6基因异常情况进行检测,并用免疫组织化学法检测CD10、BCL-6、MUM-1及Ki-67等蛋白标记物,分析其相互关系.结果:在164例MYC基因异常为38例(23.17%),其中基因易位9例(5.49%),基因扩增29例(17.68%);同时存在MYC和BCL-6基因易位有2例,未发现MYC和BCL-2同时易位或三者同时易位的病例;资料完整(同时获得三种基因FISH结果)的159例病例中,MYC基因扩增28例(17.61%)与BCL-2基因扩增38例(23.90%)呈显著正相关(r=0.2916,P=0.0004);MYC基因易位病例Ki-67高表达率(5/8,62.50%)明显高于非MYC基因易位病例(33/149,22.15%,P=0.0277),2例MYC和BCL-6同时易位的病例均为Ki-67高表达,MYC基因扩增与Ki-67高表达无显著相关性.结论:有关MYC基因在弥漫性大B细胞淋巴瘤中的异常改变除基因重排外,还有基因扩增等活化方式,目前对其作用机制尚缺乏了解,值得进行深入研究.
목적:탐토미만성대B세포림파류(DLBCL)MYC기인이상정황급기여BCL-2、BCL-6기인이상적관계.방법:응용조직심편화FISH기술대194례DLBCL적MYC、BCL-2、BCL-6기인이상정황진행검측,병용면역조직화학법검측CD10、BCL-6、MUM-1급Ki-67등단백표기물,분석기상호관계.결과:재164례MYC기인이상위38례(23.17%),기중기인역위9례(5.49%),기인확증29례(17.68%);동시존재MYC화BCL-6기인역위유2례,미발현MYC화BCL-2동시역위혹삼자동시역위적병례;자료완정(동시획득삼충기인FISH결과)적159례병례중,MYC기인확증28례(17.61%)여BCL-2기인확증38례(23.90%)정현저정상관(r=0.2916,P=0.0004);MYC기인역위병례Ki-67고표체솔(5/8,62.50%)명현고우비MYC기인역위병례(33/149,22.15%,P=0.0277),2례MYC화BCL-6동시역위적병례균위Ki-67고표체,MYC기인확증여Ki-67고표체무현저상관성.결론:유관MYC기인재미만성대B세포림파류중적이상개변제기인중배외,환유기인확증등활화방식,목전대기작용궤제상결핍료해,치득진행심입연구.
Objective:This study aims to investigate MYC gene aberration and analyze the correlation of gene aberrations among MYC, BCL-2, and BCL-6 in diffuse large B-cell lymphomas (DLBCL). Methods:Aberrations of MYC, BCL-2, and BCL-6 genes were detected using interphase fluorescence in situ hybridization (FISH), and the protein markers (CD10, BCL-6, MUM1, and Ki67) were stained using immunohistochemistry in the tissue microarrays of 194 DLBCL cases. The correlations among them were analyzed using statistical methods. Results:In 164 of the 194 cases that obtained FISH results of MYC, 38 cases revealed MYC gene aberration (38/164;23.17%). Of the 38 cases, 9 (9/164;5.49%) were MYC translocation, and the other 29 (29/164;17.68%) were MYC gene amplification. No significant difference was observed in the distribution of the aberrations between the cases with germinal central B-cell (GCB) (5/49;10.20%) and the non-GCB (24/115; 20.87%) subtypes (P=0.187). Of the 159 cases with complete FISH test data, coexistent MYC and BCL-6 gene rear-rangements were found in only two"double hit"cases. Aberrations of MYC, BCL-2, and BCL-6 genes or a coexistent rearrangement of the three was not found in the cases. A significantly positive correlation was observed between MYC (28/159, 17.61%) and BCL-2 gene amplification (38/159, 23.90%) (r=0.2916, P=0.000 4). The expression rate of Ki67 (≥90%) was apparently higher in the cases with MYC translocation (5/8, 62.50%) than those without (33/149, 22.15%) (P=0.027 7). High Ki67 expression was found in both"double hit"cases. No significant correlation was found between MYC gene amplification and high Ki67 expression. Conclusion: In addition to gene translocation, gene amplification and other activation pathways of the MYC gene were found in DLBCL. Further studies are needed to elucidate the role of MYC gene aberration in DLBCL.