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首页> 外文期刊>Biomarker Research >Philadelphia chromosome positive AML arising from JAK2-positive myelofibrosis
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Philadelphia chromosome positive AML arising from JAK2-positive myelofibrosis

机译：由JAK2阳性骨髓纤维化引起的费城染色体阳性AML

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Background A feature of myeloproliferative neoplasia is transforming to more aggressive and malignant myeloid neoplasia, including acute myeloid leukemia. Different pathogenesis mechanisms participate in transformation, including transformation of existing potential preleukemic clones, since JAK2 -mutant myeloproliferative neoplasms often transform to JAK2 wild-type acute myeloid leukemia. Case presentation Here, we present an 80?year old man with a JAK2 -V617F mutant primary myelofibrosis. After 10 months the disease transform into a Philadelphia chromosome positive acute myeloid leukemia, detecting the cytogenetic aberration; t(9;22)(q34;q22) encoding the rare BCR-ABL1 fusion gene; e6a2. The patient had treatment response to tyrosine kinases, illustrating the potential benefits of such approach in treating these patients subset. Conclusion The case illustrates the potential of leukemic transformation to Philadelphia chromosome positive myeloid malignancies from potential existing preleukemic clones, and the awareness of such an evolution among patients with myeloproliferative neoplasms. Tyrosine kinases have potential effect also in patients presenting without chronic myeloid leukemia and with rare BCR-ABL1 fusion transcripts, and should probably be a part of the treatment approach.
机译：背景骨髓增生性肿瘤的特征是转变为更具侵袭性和恶性的髓样肿瘤，包括急性髓样白血病。不同的发病机制参与转化，包括现有潜在的白血病前克隆的转化，因为JAK2突变的骨髓增生性肿瘤通常转化为JAK2野生型急性髓细胞性白血病。病例介绍在这里，我们介绍了一个80岁的男子，患有JAK2-V617F突变原发性骨髓纤维化。 10个月后，该疾病转化为费城染色体阳性的急性髓性白血病，从而检测到细胞遗传学异常; t（9; 22）（q34; q22）编码罕见的BCR-ABL1融合基因; e6a2。该患者对酪氨酸激酶有治疗反应，说明了这种方法在治疗这些患者亚组中的潜在益处。结论该病例说明了从潜在的现有白血病前克隆向白血病细胞转化为费城染色体阳性髓样恶性肿瘤的可能性，以及对骨髓增生性肿瘤患者这种进化的认识。酪氨酸激酶在没有慢性粒细胞白血病和罕见的BCR-ABL1融合转录本的患者中也具有潜在的作用，可能应该是治疗方法的一部分。

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