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首页> 外文期刊>Leukemia Research Reports >Molecular responses in e19a2 BCR-ABL1 chronic myeloid leukemia
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Molecular responses in e19a2 BCR-ABL1 chronic myeloid leukemia

机译:E19A2中的分子反应 BCR-Abl1 慢性髓性白血病

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The vast majority of chronic myeloid leukemia (CML) patients ex-press either the e13a2 or e14a2 BCR-ABL1 oncogene fusion transcriptwith a recent international study showing that approximately 2% ofpatients express rare BCR-ABL1 fusion transcripts, usually as a result ofalternative BCR or ABL1 exon splicing [1]. The most commonly re-ported BCR-ABL1 variant in CML is the e1a2 fusion with both a geno-type-phenotype association and relatively poor responses to tyrosinekinase inhibitors (TKI) recognised [2]. The next most common variantBCR-ABL1 is the e19a2 fusion (encoding a p230 kDa oncoprotein) yetthe overall TKI response of CML patients expressing this transcript isdifficult to ascertain due to possible publication bias: most patientshave been reported as single cases or small series presenting with aty-pical or novel aspects of morphology, cytogenetics or ABL1 kinase do-main mutation status and have been treated with a variety of TKIs ei-ther as first- or second-line therapy. Furthermore, given the currentpossibility of treatment-free remission (TFR) in CML patients in longterm deep molecular responses, there remains a lack of information onthe feasibility of such an option in CML patients expressing e19a2 BCR-ABL1 transcripts.
机译:绝大多数慢性骨髓白血病(CML)患者Ex-Press E13A2或E14A2 BCR-ABCR1癌基因融合转录转录,最近的国际研究表明,大约2%的患者表达罕见的BCR-ABL1融合转录物,通常是BCR的结果或ABL1外显子拼接[1]。 CML中最常见的BCR-ABL1变体是E1A2融合,具有基因型表型关联和对酪氨酸肽抑制剂(TKI)的相对较差的反应认可[2]。下一个最常见的VariantBCR-ABL1是E19A2融合(编码P230 KDA癌蛋白),CML患者表达该转录患者的总体TKI响应是由于可能的出版物偏差,所以大多数患者被报告为单一的病例或小型系列呈现出来 - 形态学,细胞遗传学或ABL1激酶DO-MAIN突变状态的实体或新颖的方面,并已被各种TKIS EI-THE作为第一或二线疗法治疗。此外,鉴于LongTerm深度分子反应中CML患者的无治疗缓解(TFR)的受影响性,仍然缺乏关于表达E19A2 BCR-ABL1转录物的CML患者这种选择的可行性的信息。

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