Growth factor independent 1b (Gfi1b) and a new splice variant of Gfi1b are highly expressed in patients with acute and chronic leukemia
Growth factor independent 1b (Gfi1b) and a new splice variant of Gfi1b are highly expressed in patients with acute and chronic leukemia
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DOI：
10.1007/s12185-009-0286-5
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发表时间：
2009-05-01
影响因子：
2.1
通讯作者：
Moeroey, Tarik
中科院分区：
文献类型：
--
作者：
Vassen, Lothar;Khandanpour, Cyrus;Moeroey, Tarik
Gfi1b是一种转录抑制因子，对红细胞和巨核细胞至关重要，但也在造血干细胞和早期髓系祖细胞中表达。Gfi1b基因在9q34的染色体定位及其与原癌基因Gfi1的功能同源性提示Gfi1b在恶性转化和髓性白血病中的作用。我们在这里表明，与正常健康对照相比，Gfi1b在CML和AML患者中的表达强烈升高，并且广泛用于治疗CML的药物伊马替尼即使在缓解后也能进一步增强患者的Gfi1b表达。我们的数据表明，Gfi1b可能是建立或维持髓系白血病和骨髓增生性疾病的重要因素，并且Gfi1b的高表达水平可能与伊马替尼停药后或伊马替尼耐药后费城染色体阴性髓系恶性肿瘤的出现有关。
Gfi1b is a transcriptional repressor that is essential for erythroid cells and megakaryocytes, but is also expressed in hematopoietic stem cells and early myeloid progenitors. The chromosomal localization of the Gfi1b gene at 9q34 and its functional homology with the proto-oncogene Gfi1 were suggestive for a role of Gfi1b in malignant transformation and myeloid leukemia. We show here that the expression of Gfi1b is strongly elevated in CML and AML patients compared to normal healthy controls and that imatinib, a drug widely used to treat CML, further enhances Gfi1b expression in patients even after remission. Our data suggest that Gfi1b may be an important factor to establish or maintain myeloid leukemia and myeloproliferative diseases and that, high expression levels of Gfi1b might be associated with the emergence of Philadelphia chromosome negative myeloid malignancies after imatinib withdrawal or after the development of imatinib resistance.