Shimizu Ritsuko
Department of Molecular Hematology, Tohoku University Graduate School of Medicine.
Rinsho Ketsueki. 2024;65(9):902-910. doi: 10.11406/rinketsu.65.902.
GATA1, GATA2, and GATA3, collectively known as hematopoietic GATA factors, play a central role in the transcription factor network that governs hematopoietic homeostasis. Dysfunction of these factors leads to various hematopoietic disorders. Aberrant function of GATA1 factor, crucial in erythrocyte and megakaryocyte differentiation, not only causes anemia and thrombocytopenia, but also triggers erythroid leukemia and acute megakaryoblastic leukemia. Similarly, GATA2 factor expression is dynamic in the hematopoietic hierarchy, and dysfunction of GATA2 factor contributes not only to dysfunction of the myeloid and lymphoid lineages but also to the development of diverse hematopoietic neoplasms such as myelodysplastic syndromes, acute myeloid leukemia, and myeloproliferative neoplasms. GATA3, critical for T-lymphocyte differentiation, is relevant to lymphocytic leukemia. This review discusses hematopoietic disorders caused by aberrant GATA transcription functions, with a particular emphasis on hematopoietic malignancies.
GATA1、GATA2和GATA3统称为造血GATA因子,在调控造血稳态的转录因子网络中发挥核心作用。这些因子功能失调会导致各种造血系统疾病。GATA1因子在红细胞和巨核细胞分化中起关键作用,其功能异常不仅会导致贫血和血小板减少,还会引发红系白血病和急性巨核细胞白血病。同样,GATA2因子的表达在造血层级中呈动态变化,GATA2因子功能失调不仅会导致髓系和淋巴系功能障碍,还会引发多种造血系统肿瘤,如骨髓增生异常综合征、急性髓系白血病和骨髓增殖性肿瘤。GATA3对T淋巴细胞分化至关重要,与淋巴细胞白血病有关。本综述讨论了由GATA转录功能异常引起的造血系统疾病,尤其着重于造血系统恶性肿瘤。