title: Identification of TIM-3 as a Leukemic Stem Cell Surface Molecule in Primary Acute Myeloid Leukemia.
abstract: Acute myeloid leukemia (AML) originates from self-renewing leukemic stem cells (LSCs), an ultimate therapeutic target in AML. Eradication of LSCs should be a critical and efficient therapeutic approach for the cure of AML. T-cell immunoglobulin mucin-3 (TIM-3) is expressed in most types of AML LSCs, but not in normal hematopoietic stem cells (HSCs); therefore, TIM-3 would be one of the promising therapeutic targets to specifically kill AML LSCs, sparing normal HSCs. In xenograft models reconstituted with human AML LSCs or human normal HSCs, an anti-human TIM-3 mouse antibody with cytotoxic activities exerts a potent anti-leukemic effect by targeting AML LSCs but does not affect normal human hematopoiesis in vivo. Here, we would like to introduce the recent studies on TIM-3 in normal and malignant hematopoiesis.
authors.affiliation: Department of Medicine and Biosystemic Sciences, Kyushu University Graduate School of Medicine, Fukuoka, Japan.
authors.forename: Yoshikane
authors.initials: Y
authors.lastname: Kikushige
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Miyamoto
mesh_terms: D000818:Animals; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects; D006410:Hematopoiesis; D006412:Hematopoietic Stem Cells / Q000187:drug effects*; D000072597:Hepatitis A Virus Cellular Receptor 2; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy*; D008565:Membrane Proteins / Q000187:drug effects*; D051379:Mice; D014411:Neoplastic Stem Cells / Q000187:drug effects*; D011991:Receptors, Virus / Q000187:drug effects; D023041:Xenograft Model Antitumor Assays
chemical_list: C448908:HAVCR2 protein, human; C442241:Havcr2 protein, mouse; D000072597:Hepatitis A Virus Cellular Receptor 2; D008565:Membrane Proteins; D011991:Receptors, Virus