Autocrine activation of the MET receptor tyrosine kinase in acute myeloid leukemia

被引：0
|
作者：
Alex Kentsis
Casie Reed
Kim L Rice
Takaomi Sanda
Scott J Rodig
Eleni Tholouli
Amanda Christie
Peter J M Valk
Ruud Delwel
Vu Ngo
Jeffery L Kutok
Suzanne E Dahlberg
Lisa A Moreau
Richard J Byers
James G Christensen
George Vande Woude
Jonathan D Licht
Andrew L Kung
Louis M Staudt
A Thomas Look
机构：
[1] Dana-Farber Cancer Institute,Department of Pediatric Oncology
[2] Harvard Medical School,Division of Hematology and Oncology
[3] Children's Hospital Boston,Division of Hematology and Oncology
[4] Harvard Medical School,Department of Pathology
[5] Northwestern University Feinberg School of Medicine,Department of Haematology
[6] Brigham and Women's Hospital,Department of Hematology
[7] Harvard Medical School,Division of Hematopoietic Stem Cell and Leukemia Research
[8] Manchester Royal Infirmary,Department of Biostatistics and Computational Biology
[9] Central Manchester University Hospitals National Health Service Foundation Trust,Department of Research Pharmacology
[10] and Manchester Academic Health Science Centre,Department of Molecular Oncology
[11] Lurie Family Imaging Center,undefined
[12] Dana-Farber Cancer Institute,undefined
[13] Erasmus Medical Center,undefined
[14] City of Hope National Medical Center,undefined
[15] Dana-Farber Cancer Institute,undefined
[16] School of Cancer and Enabling Sciences,undefined
[17] Faculty of Medical and Human Sciences,undefined
[18] University of Manchester,undefined
[19] Pfizer Global Research and Development,undefined
[20] Van Andel Research Institute,undefined
[21] Center for Cancer Research,undefined
[22] National Cancer Institute,undefined
[23] National Institutes of Health,undefined
来源：
Nature Medicine | 2012年 / 18卷
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摘要：
This report identifies upregulation of HGF as an autocrine growth pathway in several subsets of AML. Ligand-dependent activation of MET represents a new oncogenic stimulus, and the dynamic regulation of HGF can overcome the effects of MET inhibition. These results suggest that combination treatments may be needed to disrupt this autocrine signaling loop and quell the growth of AML.
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页码：1118 / 1122
页数：4
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