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病例分享:慢性髓系白血病双费城染色体阳性同时表达P210BCR-ABL1和P195BCR-ABL1

2019-02-16 月下荷花 肿瘤资讯

费城染色体[Ph;t(9;22)(q34;q11)]和BCR-ABL1基因是慢性髓系白血病(CML)的标志,大部分CML表达P210BCR-ABL1蛋白,由e14a2或e13a2融合转录产生,5%CML表达少见异构体,包括P190(e1a2)、P195(e6a2)、P200(e8a2)、P225(e18a2)和P230(e19a2),所有异构体均有致病作用,同时也是CML的治疗靶点。Vinhas医

费城染色体[Ph;t(9;22)(q34;q11)]和BCR-ABL1基因是慢性髓系白血病(CML)的标志,大部分CML表达P210BCR-ABL1蛋白,由e14a2或e13a2融合转录产生,5%CML表达少见异构体,包括P190(e1a2)、P195(e6a2)、P200(e8a2)、P225(e18a2)和P230(e19a2),所有异构体均有致病作用,同时也是CML的治疗靶点。Vinhas医师在Haematologica杂志发文,介绍了1例CML双费城染色体阳性同时表达P210BCR-ABL1 和 P195BCR-ABL1。

病例介绍

患者男性,36岁,于1个月前出现发热盗汗,无肝、脾、淋巴结肿大,血红蛋白129g/L,白细胞58300/pL,血小板507 000/pL ,骨髓检查示1%原始细胞,BCR-ABL1荧光原位杂交(FISH)阳性率98%。对20个有丝分裂骨髓细胞进行遗传学分析:4个细胞只有1个Ph染色体,7个细胞有1个Ph染色体和三体8,9个双Ph和三体8(图1 A和B)。该患者被诊断为慢性期CML,评分Sokal 0.57,Hasford 58和EUTOS 0。

该患者开始接受伊马替尼400mg/d治疗,3个月时未达细胞遗传学反应( CyR),增量至600mg/d治疗2周,FISH阳性率为80%,再次增量至800mg/d治疗4.5个月,FISH阳性率为61% 。因未达到CyR,对BCR-ABL1基因重新分析,发现双Ph细胞存在两种基因亚型:典型的P210(e14a2)和少见的P195(e6a2)(图1C)。除了2个明确的SNPs外,2个转录本的ABL1结构域均无点突变。临床研究表明,表达e6a2的CML临床经过侵袭,对伊马替尼治疗无反应,不同个体间的临床、血液学或分子特征有显著差异。

诊断8个月后,更换二线TKI博舒替尼治疗,13个月时获得CyR,随后获得P210BCR-ABL1深度分子反应,但细胞遗传学仍为阳性(FISH阳性率为5%),最后发展为淋系急变,需要行异基因干细胞移植。

寻根溯源

有研究指出不同断裂点可能与不同预后、治疗反应和/或生存相关,如P190BCR-ABL1在急性淋巴细胞性白血病中更常见,恶性程度高于P210BCR-ABL1,P195BCR-ABL1在CML中也有报道,与侵袭性进展、不良结果相关。


图1  患者骨髓的细胞遗传学检查和分子分析(A)核型。B.FISH见4个细胞为46,XY,t(9;22)(q34.1;q11.2);7个细胞为47,XY,+8,t(9;22)(q34.1;q11.2);9个细胞为48,XY,+8,t(9;22)(q34.1;q11.2),+der(22)t(9;22)(q34.1;q11.2)。C.BCR-ABL1序列分析

表达BCR-ABL1细胞的遗传学不稳定性可能导致附加遗传学改变(ACAs),如双Ph、三体8和i(17)(q10),不足5%的CML诊断时即存在ACAs,这些改变可降低伊马替尼治疗反应,因此TKI治疗期间必需监测ACAs以发现克隆性进展。推测BCR-ABL1双嵌合基因可诱导更强的激酶活性和更活跃的原始细胞增殖。

双Ph通常与BCR-ABL1过表达相关,与侵袭性临床结果相关,认为是伊马替尼耐药的原因。由于缺少重要的调控BCR序列,较短BCR-ABL1转录本可导致侵袭性的临床表型。这可以解释本例患者的疾病进展、伊马替尼不能诱导CyR和需要三代TKI才能有效治疗。博舒替尼治疗获得P210深度分子反应和P195 CyR稳定后,对患者外周血行免疫印迹分析,结果显示蛋白质水平的BCR-ABL1表达和ABL1激酶区域磷酸化(图2)与CML的发病机制相关,博舒替尼(或伊马替尼)不能消除ABL1激酶结构域上的BCR-ABL1激活标志Tyr245磷酸化。 


图2  博舒替尼治疗获P210深度分子反应和P195 CyR稳定后,对患者外周血行免疫印迹分析

临床启示

虽然本例患者经博舒替尼治疗后P210达深度分子反应,P195 CyR稳定,但对一代TKI治疗效果不佳。该患者属于高危,治疗期间应密切监测疗效。本病例强调了明确转录本类型的重要性,特别是同时存在多个转录本时,应选择更恰当的TKI以改善治疗反应。

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    2019-10-18 tulenzi
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