CAJ | 학술논문

目的分析肿瘤抑制基因PTEN、混合系白血病(MLL)基因等在T淋巴母细胞淋巴瘤/白血病(T-LBL/ALL)的表达及意义.方法选用76例T-LBL/ALl患者淋巴结存档蜡块,应用免疫组织化学EnVision法进行 PTEN标记,用20例反应性增生淋巴结标本作正常对照.并用荧光原位杂交(FISH)技术检测MLL基因所在1 1q23染色体的断裂和扩增情况.结果 76例T-LBL/ALL中,PTEN的表达率为64.47%(49/76),低于淋巴结反应性增生的100%(20/20)(λ2=19.220,P＜0.05).PTEN表达与临床分期、Ki-67、乳酸脱氢酶(LDH)呈负相关(P＜0.05).76例T-LBL/ALL中,MLL基因发生1 1q23染色体断裂13例(17.11%),扩增18例(23.68%).MLL基因断裂组总体生存率(25.0%)低于非断裂组(43.6%)(λ2=11.357,P＜0.05).MLL基因扩增组总体生存率(17.1%)低于非扩增组(42.7%)(λ2=4.533,P＜0.05).结论抑癌基因PTEN表达降低在T-LBL/ALL的发生发展中可能具有重要作用.MLL基因发生染色体1 1q23断裂和扩增有助于对T-LBL/ALL预后的判断,发生MLL基因断裂或扩增的T-LBL/ALL预后较差,提示MLL基因断裂或扩增可能为T-LBL/ALL的一种分子亚型.
목적 분석종류억제기인PTEN、혼합계백혈병(MLL)기인등재T림파모세포림파류/백혈병(T-LBL/ALL)적표체급의의.방법 선용76례T-LBL/ALl환자림파결존당사괴,응용면역조직화학EnVision법진행 PTEN표기,용20례반응성증생림파결표본작정상대조.병용형광원위잡교(FISH)기술검측MLL기인소재1 1q23염색체적단렬화확증정황.결과 76례T-LBL/ALL중,PTEN적표체솔위64.47%(49/76),저우림파결반응성증생적100%(20/20)(λ2=19.220,P＜0.05).PTEN표체여림상분기、Ki-67、유산탈경매(LDH)정부상관(P＜0.05).76례T-LBL/ALL중,MLL기인발생1 1q23염색체단렬13례(17.11%),확증18례(23.68%).MLL기인단렬조총체생존솔(25.0%)저우비단렬조(43.6%)(λ2=11.357,P＜0.05).MLL기인확증조총체생존솔(17.1%)저우비확증조(42.7%)(λ2=4.533,P＜0.05).결론 억암기인PTEN표체강저재T-LBL/ALL적발생발전중가능구유중요작용.MLL기인발생염색체1 1q23단렬화확증유조우대T-LBL/ALL예후적판단,발생MLL기인단렬혹확증적T-LBL/ALL예후교차,제시MLL기인단렬혹확증가능위T-LBL/ALL적일충분자아형.
Objective To investigate the significance and expression of PTEN, MLL in T lymphoblastic lymphoma/leukaemia(T-LBL/ALL). Methods Seventy-six cases of T-LBL/ALL were studied by using immunohistochemical EnVision method for PTEN. Fluorescence in-situ hybridization (FISH) for MLL gene (located on chromosome 11q23) was performed to detect its breakage and amplification. Results Among the 76 cases ofT- LBL/ALL, the positive rate of PTEN was 64.47 % (49/76), lower than that in reactivated lymphoid tissue (100 %, 20/20) (λ2= 19.220, P ＜0.05). PTEN expression was reversely correlated to theclinical stage, Ki-67 index and LDH level (P ＜0.05). Among the 76 cases, MLL gene with breakage of 11q23 was detected in 13 cases (17.11%), and amplification in 18 cases (23.68 %). Survival rate ot MLL gene breakage group was lower than that of non-breakage group (25.0 %, 43.6 %). Survival rate of MLL gene amplification group was lower than that of non-amplification group too (17.1%, 42.7 %). Both of breakage and amplification were related to prognosis ( λ 2 = 11.357, λ 2 = 4.533; P ＜0.05). Conclusion Anti-oncogene PTEN down-regulation may play an important role on the development and proceeding of T-LBL/ALL. MLL gene with breakage and amplification of 11q23 are helpful to predict prognosis of T-LBL/ALL. The case with MLL gene breakage and amplification of T-LBL/ALL may have a poor prognosis. It hints this group maybe a subtype of T-LBL/ALL.