AI Article Synopsis
- Dysregulation of iron metabolism is linked to various myeloid neoplasms, affecting prognosis, especially in conditions like acute myeloid leukemia and myelodysplastic syndrome.
- Myeloproliferative neoplasms often show both iron deficiency and elevated red blood cell levels, which can be managed by targeting the protein hepcidin.
- Research suggests that ferroptosis, a form of cell death, could be a promising therapeutic approach to treat these neoplasms by reversing drug resistance and promoting anti-tumor effects.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736352 | PMC |
| http://dx.doi.org/10.3724/zdxbyxb-2024-0211 | DOI Listing |
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