Regulation of growth, invasion and metabolism of breast ductal carcinoma through CCL2/CCR2 signaling interactions with MET receptor tyrosine kinases.

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第一作者： Diana Sofía,Acevedo

第一单位： Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Wahl Hall East 1020, Kansas City, KS 66160, USA.

作者： Diana Sofía,Acevedo ^[1] ; Wei Bin,Fang ^[1] ; Vinamratha,Rao ^[1] ; Vedha,Penmetcha ^[1] ; Hannah,Leyva ^[1] ; Gabriela,Acosta ^[1] ; Paige,Cote ^[1] ; Rebecca,Brodine ^[1] ; Russell,Swerdlow ^[2] ; Lin,Tan ^[3] ; Philip L,Lorenzi ^[3] ; Nikki,Cheng ^[4]

作者单位： Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Wahl Hall East 1020, Kansas City, KS 66160, USA. ^[1] Department of Neurology, University of Kansas Medical Center, Kansas City, KS 66160, USA. ^[2] Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. ^[3] Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Wahl Hall East 1020, Kansas City, KS 66160, USA; Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA. Electronic address: ncheng@kumc.edu. ^[4]

关键词 Breast ductal carcinoma CCL2, CCR2 GPCR LY2801653 MET receptor tyrosine kinase Metabolism