论文摘要
目的 通过检测非Hodgekin淋巴瘤(NHL)演进过程中IgH与TCR基因重排变化,探讨恶性淋巴瘤发生过程中的演进和异质化及其对分类和指导治疗的意义。 方法 运用多聚酶链反应(PCR)技术检测了84例NHL,包括10例间变性大细胞性淋巴瘤(ALCL),石蜡包埋组织中IgH及TCR基因重排情况和ALCL的经典t(2;5)(p23;q35)染色体易位;采用免疫组织化学PV9000法染色技术检测NHL与ALCL免疫表型表达。 结果 74例NHL标本中,27例TCR基因克隆性重排阳性,49例IgH基因重排阳性,其中包括8例IgH与TCR基因双重排阳性;10例ALCL均为TCR基因重排阳性,其中4例为IgH和TCR基因双重排阳性;1例ALCL呈t(2;5)(p23;q35)染色体易位。74例NHL中22例免疫表型为CD45RO阳性,48例CD20阳性,1例CD20与CD45RO均未着色,3例CD20和CD45RO双着色;10例ALCL均呈CD30阳性,5例CD45RO阳性,1例CD20阳性,1例CD20与CD45RO均未着色,2例CD20与CD45RO双着色。两组中CD20与CD45RO双着色的标本都出现了IgH与TCR克隆性基因双重排。 结论 1.NHL演进异质化必然会影响恶性淋巴瘤的克隆性基因重排改变,同样必然影响免疫表型表达。克隆性基因双重排发生的机制,我们认为与NHL演进和异质化过程密切相关,克隆性基因双重排是在单克隆陸增生发生的NHL的基础上,在其不断演进过程中发生的一种异质化表现之一。原始幼稚淋巴细胞甚至有一定定向分化淋巴细胞,在恶性转化演进进程中可以出现克隆性IgH或TCR基因重排,而表现为B或T细胞性免疫表型的可能;同时亦可能演进为同时具备克隆性IgH和TCR基因双重排,呈T和B细胞免疫表型双表达可能,其分子生物学基础为克隆性IgH和TCR基因双重排。部分NHL为干细胞型,完全有可能同时具备克隆性IgH和TCR基因双重排现象,以此为基础发育同时表达T和B细胞免疫表型,或单表达,或者均不表达。2.克隆性基因双重排的NHL临床经过和预后反而较单克隆重排表现的NHL略好,这说明基因重排与免疫表型不同层次的改变应当作为分类的考虑因素,恶性淋巴瘤的分类不是一成不变的,须根据双重排、免疫组化染色及预后综合考虑分类,以利于临床治疗。3.ALCL可能为一类介于高度恶性NHL和HL之间的淋巴瘤,起源于多能干细胞向淋巴细胞分化的早期阶段,是恶性淋巴瘤中一个较为特殊的类型,是明显异质化的淋巴瘤,是原始淋巴细胞恶性转化演进过程中出现异质化的典型表现。在演进的过程中大部分向T细胞方向分化,少部分向B细胞方向分化,近半数有IgH与YCR双重排,表现为高度异质化。4.设计长片段产物引物等进行常规PCR
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标签：非淋巴瘤论文; 间变性大细胞性淋巴瘤论文; 聚合酶链反应论文; 基因重排论文;