Author
Listed:
- Kazuhito Naka
(Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)
- Takayuki Hoshii
(Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)
- Teruyuki Muraguchi
(Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)
- Yuko Tadokoro
(Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)
- Takako Ooshio
(Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan
Core Research for Evolution Science and Technology (CREST), Japan Science and Technology Agency (JST), Chiyoda-ku, Tokyo 102-0075, Japan)
- Yukio Kondo
(Cellular Transplantation Biology, Kanazawa University, Graduate School of Medical Science, Kanazawa, Ishikawa 920-8641, Japan)
- Shinji Nakao
(Cellular Transplantation Biology, Kanazawa University, Graduate School of Medical Science, Kanazawa, Ishikawa 920-8641, Japan)
- Noboru Motoyama
(National Institute for Longevity Sciences, National Center for Gerontology and Geriatrics, Obu, Aichi 474-8522, Japan)
- Atsushi Hirao
(Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan
Core Research for Evolution Science and Technology (CREST), Japan Science and Technology Agency (JST), Chiyoda-ku, Tokyo 102-0075, Japan)
Abstract
Leukaemia recurrence Chronic myeloid leukaemia (CML) is caused by a BCR-ABL fusion that generates a constitutively active tyrosine kinase. Although inhibition of tyrosine kinase with imatinib has been used successfully for CML therapy, it does not deplete the leukaemia-initiating cells (LICs) that drive the recurrence of CML. Naka et al. show that Foxo3a plays an essential role in the maintenance of LICs in CML, and that TGF-β is a critical regulator of Akt activation in LICs and controls Foxo3a localization. They also show that treatment of LICs in human CML with a TGF-β inhibitor impairs their colony-forming ability in vitro.
Suggested Citation
Kazuhito Naka & Takayuki Hoshii & Teruyuki Muraguchi & Yuko Tadokoro & Takako Ooshio & Yukio Kondo & Shinji Nakao & Noboru Motoyama & Atsushi Hirao, 2010.
"TGF-β–FOXO signalling maintains leukaemia-initiating cells in chronic myeloid leukaemia,"
Nature, Nature, vol. 463(7281), pages 676-680, February.
Handle:
RePEc:nat:nature:v:463:y:2010:i:7281:d:10.1038_nature08734
DOI: 10.1038/nature08734
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Cited by:
- Junho Lee & Donggu Lee & Sean Lawler & Yangjin Kim, 2021.
"Role of neutrophil extracellular traps in regulation of lung cancer invasion and metastasis: Structural insights from a computational model,"
PLOS Computational Biology, Public Library of Science, vol. 17(2), pages 1-29, February.
- Yinzhe GE & Mang XIAO, 2019.
"Chronic Myeloid Leukemia: How to Overcome the Tyrosine Kinase Inhibitors Resistance,"
Biomedical Journal of Scientific & Technical Research, Biomedical Research Network+, LLC, vol. 18(2), pages 13389-13393, May.
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