演題詳細

一般口演 / Oral Session

一般口演 91 (Oral Session 91) :AML:細胞の特性 2

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日程
2013年10月13日(日)
時間
16:00 - 17:00
会場
第3会場 / Room No.3 (さっぽろ芸文館 3F 蓬莱)
座長・司会
矢野 道広 (Michihiro Yano):1
1:秋田大学医学部 小児科
 
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Leukemogenic function of TIM-3, a leukemia stem cell marker, in acute myelogenous leukemia

演題番号 : OS-3-100

湯田 淳一朗 (Junichiro Yuda):1、菊繁 吉謙 (Yoshikane Kikushige):1、宮本 敏浩 (Toshihiro Miyamoto):1、島 隆宏 (Takahiro Shima):1、飯野 忠史 (Tadafumi Iino):2、加藤 光次 (Koji Kato):1、牟田 毅 (Tsuyoshi Muta):1、竹中 克斗 (Katsuto Takenaka):2、岩崎 浩己 (Hiromi Iwasaki):2、赤司 浩一 (Koichi Akashi):1,2

1:Medicine and Biosystemic Science, Kyushu University Faculty of Medicine、2:Center for Cellular and Molecular Medicine, Kyushu University Hospital

 

Background: Acute myeloid leukemia (AML) originates from self-renewing leukemic stem cells (LSCs), an ultimate therapeutic target for AML. We have reported that the T-cell immunoglobulin mucin-3 (TIM-3) is expressed on LSCs in most types of AML but not on normal hematopoietic stem cells (HSCs). TIM-3+ AML cells reconstituted human AML in immunodeficient mice, whereas TIM3- AML cells did not, suggesting that the TIM-3+ population contains all functional LSCs (Kikushige et al, Cell Stem Cell, 2010). Aims: The aim of this study is to clarify the function of TIM-3 in AML. Methods: We analyzed bone marrow samples from myelodysplastic syndrome (MDS) and AML patients by multicolor FACS. Results: We found that human TIM-3 is expressed in the vast majority of CD34+CD38- LSCs of human myeloid malignancies. TIM-3 was progressively up-regulated in this population of MDS, along with disease progression into leukemia.The average percentages of TIM-3+ cells in the CD34+CD38- population was 7.8% in RCMD (n=10), 19.2% in RAEB-1 (n=10), 84.0% in RAEB-2 (n=10) and 92.2% in overt AML (n=10). Thus, TIM-3 might be useful to isolate malignant stem cells responsible for progression into AML in MDS patients. The association of TIM-3 expression with transformation into AML led us to hypothesize that TIM-3 itself has a function in AML stem cell development. Summary / Conclusion: These data suggest that TIM-3 is a surface marker useful to track malignant LSCs in progression from MDS to AML, and TIM-3 may function for maintenance of LSC through inducing survival-promoting signaling.

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