Chronic myeloid leukemia stem cells and molecular target therapies for overcoming resistance and disease persistence

被引：18

作者：

Inoue, Ai ^{[1
]}

Kobayashi, Chiharu I. ^{[1
]}

Shinohara, Haruka ^{[2
]}

Miyamoto, Kenichi ^{[1
]}

Yamauchi, Nobuhiko ^{[1
]}

Yuda, Junichiro ^{[1
]}

Akao, Yukihiro ^{[2
]}

Minami, Yosuke ^{[1
]}

机构：

[1] Natl Canc Ctr Hosp East, Dept Hematol, 6-5-1 Kashiwanoha, Kashiwa, Chiba 2778577, Japan

[2] Gifu Univ, United Grad Sch Drug Discovery & Med Informat Sci, Gifu, Japan

来源：

INTERNATIONAL JOURNAL OF HEMATOLOGY | 2018年 / 108卷 / 04期

关键词：

BCR-ABL; Chronic myeloid leukemia; Leukemia stem cells; Tyrosine kinase inhibitors; CHRONIC MYELOGENOUS LEUKEMIA; RECEPTOR ACCESSORY PROTEIN; CML STEM/PROGENITOR CELLS; BCR-ABL; MAST-CELLS; PHILADELPHIA-CHROMOSOME; ISOFORM EXPRESSION; IMATINIB TREATMENT; INHIBITORS; METABOLISM;

D O I：

10.1007/s12185-018-2519-y

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Chronic myeloid leukemia (CML) is effectively treated with tyrosine kinase inhibitors (TKI) targeted against BCR-ABL. We previously reported the investigation of residual CML diseases during TKI treatment using FACS-sorting and quantitative RT-PCR of BCR-ABL among each population; total mononuclear cells, hematopoietic stem cells, and myeloid progenitors. The observations also implied that the second-generation of ABL-tyrosine kinase inhibitors (2nd TKIs), dasatinib or nilotinib therapy can be more promising approach for efficient reduction of the CML stem cells. Moreover, we need to develop the evaluation method of the residual CML diseases to establish rational therapy-cessation strategies in CML.

引用

页码：365 / 370

页数：6

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