甲磺酸伊马替尼对慢性髓系白血病有效的罕见t(9;22;16)(q34;q11;q24)易位1例报告。

Leukemia Research and Treatment Pub Date : 2011-01-01 Epub Date: 2011-07-05 DOI:10.4061/2011/592519
Masahiro Manabe, Yumi Yoshii, Satoru Mukai, Erina Sakamoto, Hiroshi Kanashima, Takeshi Inoue, Hirofumi Teshima
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引用次数: 4

摘要

约90%的慢性髓性白血病(CML)患者存在t(9;22)(q34;q11)易位。大约5-10%的CML患者有复杂的变异易位,除了第9和22号染色体外,还包括第三条染色体。在此,我们描述了一个cml慢性期男性,其复杂易位涉及染色体16,t(9;22;16)(q34;q11;q24)。首先,他接受干扰素- α和间歇性羟基脲治疗,但仅获得部分细胞遗传学反应。随后,由于另一个染色体异常,8号三体,患者接受甲磺酸伊马替尼治疗。伊马替尼治疗一年后获得了主要的分子反应,伊马替尼治疗开始后4年零3个月的随访染色体分析显示核型为46,XY正常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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A Rare t(9;22;16)(q34;q11;q24) Translocation in Chronic Myeloid Leukemia for Which Imatinib Mesylate Was Effective: A Case Report.

The t(9;22)(q34;q11) translocation is found in about 90% of chronic myeloid leukemia (CML) patients. About 5-10% of CML patients have complex variant translocations involving a third chromosome in addition to chromosomes 9 and 22. Herein, we describe a CML-chronic phase male with a complex translocation involving chromosome 16, t(9;22;16)(q34;q11;q24). First, he was treated with interferon-alpha and intermittent hydroxyurea, but only a partial cytogenetic response was attained. Subsequently, the patient was treated with imatinib mesylate because of an additional chromosome abnormality, trisomy 8. A major molecular response was obtained after one year's imatinib therapy, and the follow-up chromosomal analysis performed 4 years and 3 months after the initiation of imatinib therapy displayed a normal karyotype of 46,XY.

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