Effects of iron-overload on normal hematopoiesis and disease progression of hamatological malignancies
Effects of iron-overload on normal hematopoiesis and disease progression of hamatological malignancies
批准号:
21790914
负责人:
TANAKA Hirokazu
金额:
$2.75万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2009
资助国家:
日本
项目状态:
已结题
起止时间:
2009 至 2010
中文摘要
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英文摘要
In this study, we conducted the analyses regarding how does excessive "free"iron affect the growth and differentiation of hematopoietic cells as well as the characteristic of hematopoietic stromal cells.In addition, we investigated the effects of iron overload on the proliferation of MDS clones and the pathological transformation of MDS. As a result, excessive iron impairs hematopoiesis through direct effects on hematopoietic cells and indirect effects mediated by stromal cells. Furthermore, iron overload may induce the selective proliferation of MDS clones during the deterioration of normal hematopoiesis and may be involved in the leukemic transformation. These results are significant to reveal the mechanism and treatment of various hematopoietic disorders in terms of iron-kinetics.
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骨髓肿瘤相关基因异常对 FLT3 配体介导的鼠造血干/祖细胞分化树突状细胞有不同影响
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Fujita J, Tanaka H, et al.]
通讯作者:
et al.
RUNX1 controls nucleotide excision repair (NER) system through transcriptional regulation of Gadd45a.
RUNX1 通过 Gadd45a 的转录调节来控制核苷酸切除修复 (NER) 系统。
DOI:
--
发表时间:
2009
期刊:
影响因子:
--
作者:
[Satoh S, Tanaka H, et al.]
通讯作者:
et al.
Excessive reactive iron affects both immature hematopoietic cells and stromal cells, thereby impairing total hematopoiesis.
过量的活性铁会影响未成熟的造血细胞和基质细胞,从而损害总造血功能。
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Tanaka H, et al.]
通讯作者:
et al.
Essential role of an anti-apoptotic molecule Anamorsin for both intrinsic and extrinsic regulation of murine fetal liver hematopoiesis.
抗凋亡分子阿纳莫辛对小鼠胎肝造血的内在和外在调节的重要作用。
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Tanimura A, Tanaka H, et al.]
通讯作者:
et al.
鉄代謝異常と内科系疾患
铁代谢紊乱和内科疾病
DOI:
--
发表时间:
2009
期刊:
影响因子:
--
作者:
[Miyauchi Y, Ninomiya K, Miyamoto H, Sakamoto A, Iwasaki R, Hoshi H, Miyamoto K, Hao W, Yoshida S, Morioka H, Chiba K, Kato S, Tokuhisa T, Saitou M, Toyama Y, Suda T, Miyamoto T., 田中宏和]
通讯作者:
田中宏和
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