髓系肿瘤铁代谢与铁下垂的研究进展。

Yudi Wang, Weiying Feng, Fudi Wang, Junxia Min
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引用次数: 0

摘要

铁代谢失调存在于多种髓系肿瘤中。急性髓系白血病的预后与铁代谢分子的差异表达有关。骨髓增生异常综合征伴铁超载患者预后较差。骨髓增殖性肿瘤通常以缺铁和红细胞增多共存为特征,可通过靶向hepcidin治疗。髓系肿瘤细胞易受活性氧积累引起的氧化损伤,对铁下垂敏感。上铁对急性髓系白血病和骨髓增生异常综合征有抗肿瘤作用。靶向铁下垂可逆转慢性髓系白血病的伊马替尼耐药。上述研究结果表明,铁代谢和铁下垂影响髓系肿瘤的发生发展,可作为髓系肿瘤的治疗靶点。本文就髓系肿瘤发生发展过程中铁代谢的特点及铁凋亡的机制进行综述,以期为开发新的治疗策略提供依据。
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[Research progress of iron metabolism and ferroptosis in myeloid neoplasms].

It is reported that iron metabolism and ferroptosis can influence the occurrence and development of myeloid tumors, which can serve as therapeutic targets. Dysregulation of iron metabolism is present in a variety of myeloid neoplasms. The prognosis of acute myeloid leukemia is related to differential expression of molecules related to iron metabolism. The prognosis of myelodysplastic syndrome patients with iron overload is poor. Myeloproliferative neoplasms are often characterized by the coexistence of iron deficiency and erythrocytosis, which can be treated by targeting hepcidin. Myeloid tumor cells are susceptible to oxidative damage caused by the accumulation of reactive oxygen species and are sensitive to ferroptosis. Ferroptosis has anti-tumor effect in acute myeloid leukemia and myelodysplastic syndrome. Targeting ferroptosis can reverse imatinib resistance in chronic myeloid leukemia. This article reviews the characteristics of iron metabolism in the development and progression of myeloid neoplasms, as well as the mechanism of ferroptosis, to provide a basis for the development of new therapeutic strategies.

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67
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