Open AccessProteomic Profiling of Signaling Networks Modulated by G-CSF/Plerixafor/Busulfan-Fludarabine Conditioning in Acute Myeloid Leukemia Patients in Remission or with Active Disease prior to Allogeneic Stem Cell Transplantation
Author(s) -
Zhihong Zeng,
Wenbin Liu,
Christopher B. Benton,
Sergej Konoplev,
Hongbo Lu,
Rui Yu Wang,
Julianne Chen,
Elizabeth J. Shpall,
Keith A. Baggerly,
Richard E. Champlin,
Marina Konopleva
Publication year - 2019
Publication title -
acta haematologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.574
H-Index - 56
eISSN - 1421-9662
pISSN - 0001-5792
DOI - 10.1159/000495456
Subject(s) - plerixafor , fludarabine , myeloid leukemia , cxcr4 , medicine , busulfan , granulocyte colony stimulating factor , cancer research , myeloid , chemotherapy , transplantation , immunology , oncology , hematopoietic stem cell transplantation , cyclophosphamide , receptor , chemokine
To characterize intracellular signaling in peripheral blood (PB) cells of acute myeloid leukemia (AML) patients undergoing pretransplant conditioning with CXCR4 inhibitor plerixafor, granulocyte colony-stimulating factor (G-CSF), and busulfan plus fludarabine (Bu+Flu) chemotherapy, we profiled 153 proteins in 33 functional groups using reverse phase protein array. CXCR4 inhibition mobilized AML progenitors and clonal AML cells, and this was associated with molecular markers of cell cycle progression. G-CSF/plerixafor and G-CSF/plerixafor/Bu+Flu modulated distinct signaling networks in AML blasts of patients undergoing conditioning with active disease compared to nonleukemic PB cells of patients in remission. We identified AML-specific proteins that remained aberrantly expressed after chemotherapy, representing putative chemoresistance markers in AML.