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PPI‐G4 Glycodendrimers Upregulate TRAIL‐Induced Apoptosis in Chronic Lymphocytic Leukemia Cells
Author(s) -
FraniakPietryga Ida,
Ostrowska Kinga,
Maciejewski Henryk,
Appelhans Dietmar,
Misiewicz Małgorzata,
Ziemba Barbara,
Bednarek Michał,
Bryszewska Maria,
Borowiec Maciej
Publication year - 2017
Publication title -
macromolecular bioscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.924
H-Index - 105
eISSN - 1616-5195
pISSN - 1616-5187
DOI - 10.1002/mabi.201600169
Subject(s) - chronic lymphocytic leukemia , apoptosis , fludarabine , leukemia , cancer research , tumor necrosis factor alpha , downregulation and upregulation , chemistry , medicine , immunology , gene , biochemistry , chemotherapy , cyclophosphamide
Although chronic lymphocytic leukemia (CLL) is the most common adult leukemia in Western world, it remains incurable with conventional chemotherapeutic agents. Tumor necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) is an antitumor candidate in cancer therapy. This study examines the proapoptotic effects of poly(propylene imine) (PPI) glycodendrimers modified with the maltotriose residues (PPI‐G4‐OS‐Mal‐III and PPI‐G4‐DS‐Mal‐III) on the TNF family in CLL cells. The combination of an understanding of the signaling pathways associated with CLL and the development of a molecular profiling is a key issue for the design of personalized approaches to therapy. Gene expression is determined with two‐color microarray 8 × 60K. The findings indicate that PPI‐G4‐OS/DS‐Mal‐III affect gene expression from the TRAIL apoptotic pathway and exert a strong effect on CLL cells comparable with fludarabine. Dendrimer‐targeted technology may well prove to bridge the gap between the ineffective treatment of today and the effective personalized therapy of the future.