慶應義塾大学 · 医学
Sakurai教授の研究室では、血小板疾患と急性骨髄性白血病を関連する遺伝性疾患であるFPD/AMLの発症機構を、RUNX1遺伝子の機能喪失変異とその病態メカニズムに焦点を当てて解明しています。特に、ドミナントネガティブ効果を示すRUNX1変異が造血幹細幹細胞の機能に与える影響を分子細胞生物学的手法を用いて解析しています。また、臍帯血由来の造血幹細胞を用いた再生医療的応用の可能性についても探求しています。
Figures are computed from collected data and may differ slightly.
Familial platelet disorder/acute myeloid leukemia (FPD/AML) is an autosomal dominant inherited disorder characterized by thrombocytopenia and high propensity to various hematological malignancies. FPD/AML is caused by monoallelic mutations of RUNX1, which are in many cases point mutations disrupting DNA-binding or transactivating capacities of RUNX1, and these mutations are considered to act in dominant-negative manner to various degrees for residual wild-type allele. 1,2 Interestingly, some FPD
Hematopoietic stem cells (HSCs) are a rare population of cells found in the bone marrow that play a critical role in lifelong hematopoiesis and the reconstitution of the hematopoietic system after hematopoietic stem cell transplantation. Hematopoietic stem cell transplantation remains the only curative treatment for patients with refractory hematologic disorders, and umbilical cord blood (CB) serves as an alternative stem cell source due to its several advantageous characteristics, including hum
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