Comparison of nilotinib and imatinib inhibition of FMS receptor signaling, macrophage production and osteoclastogenesis

被引：30

作者：

Brownlow, N. ^{[1
]}

Russell, A. E. ^{[1
]}

Saravanapavan, H. ^{[1
]}

Wiesmann, M. ^{[2
]}

Murray, J. M. ^{[2
]}

Manley, P. W. ^{[2
]}

Dibb, N. J. ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Inst Reprod & Dev Biol, London, England

[2] Novartis Pharma AG, Novartis Inst Biomed Res, Basel, Switzerland

来源：

LEUKEMIA | 2008年 / 22卷 / 03期

基金：

英国生物技术与生命科学研究理事会;

关键词：

D O I：

10.1038/sj.leu.2404944

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

引用

页码：649 / 652

页数：5

共 20 条

[1] Imatinib mesylate inhibits osteoclastogenesis and joint destruction in rats with collagen-induced arthritis (CIA) [J].

Ando, Wataru ;

Hashimoto, Jun ;

Nampei, Akihide ;

Tsuboi, Hideki ;

Tateishi, Kosuke ;

Ono, Takeshi ;

Nakamura, Norimasa ;

Ochi, Takahiro ;

Yoshikawa, Hideki .

JOURNAL OF BONE AND MINERAL METABOLISM, 2006, 24 (04) :274-282

[2] Altered bone and mineral metabolism in patients receiving imatinib mesylate [J].

Berman, E ;

Nicolaides, M ;

Maki, RG ;

Fleisher, M ;

Chanel, S ;

Scheu, K ;

Wilson, BA ;

Heller, G ;

Sauter, NP .

NEW ENGLAND JOURNAL OF MEDICINE, 2006, 354 (19) :2006-2013

[3] Inhibition of colony-stimulating-factor-1 signaling in vivo with the orally bioavailable cFMS kinase inhibitor GW2580 [J].

Conway, JG ;

McDonald, B ;

Parham, J ;

Keith, B ;

Rusnak, DW ;

Shaw, E ;

Jansen, M ;

Lin, PY ;

Payne, A ;

Crosby, RM ;

Johnson, JH ;

Frick, L ;

Lin, MHJ ;

Depee, S ;

Tadepalli, S ;

Votta, B ;

James, I ;

Fuller, K ;

Chambers, TJ ;

Kull, FC ;

Chamberlain, SD ;

Hutchins, JT .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (44) :16078-16083

[4] Imatinib inhibits the in vitro development of the monocyte/macrophage lineage from normal human bone marrow progenitors [J].

Dewar, AL ;

Domaschenz, RM ;

Doherty, KV ;

Hughes, TP ;

Lyons, AB .

LEUKEMIA, 2003, 17 (09) :1713-1721

[5] Imatinib as a potential antiresorptive therapy for bone disease [J].

Dewar, Andrea L. ;

Farrugia, Amanda N. ;

Condina, Mark R. ;

To, L. Bik ;

Hughes, Timothy P. ;

Vernon-Roberts, Barrie ;

Zannettino, Andrew C. W. .

BLOOD, 2006, 107 (11) :4334-4337

[6] Imatinib mesylate (Gleevec®) enhances mature osteoclast apoptosis and suppresses osteoclast bone resorbing activity [J].

Dib, Iman El Hajj ;

Gallet, Marlene ;

Mentaverri, Romuald ;

Sevenet, Nicolas ;

Brazier, Michel ;

Kamel, Said .

EUROPEAN JOURNAL OF PHARMACOLOGY, 2006, 551 (1-3) :27-33

[7] A CSF-1 receptor kinase inhibitor targets effector functions and inhibits pro-inflammatory cytokine production from murine macrophage populations [J].

Irvine, Katharine M. ;

Burns, Christopher J. ;

Wilks, Andrew F. ;

Su, Stephen ;

Hume, David A. ;

Sweet, Matthew J. .

FASEB JOURNAL, 2006, 20 (11) :1921-+

[8] Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia [J].

Manley, PW ;

Cowan-Jacob, SW ;

Mestan, J .

BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS, 2005, 1754 (1-2) :3-13

[9] Structural basis for the autoinhibition and STI-571 inhibition of c-Kit tyrosine kinase [J].

Mol, CD ;

Dougan, DR ;

Schneider, TR ;

Skene, RJ ;

Kraus, ML ;

Scheibe, DN ;

Snell, GP ;

Zou, H ;

Sang, BC ;

Wilson, KP .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (30) :31655-31663

[10] Cell specific transformation by c-fms activating loop mutations is attributable to constitutive receptor degradation [J].

Morley, GM ;

Uden, M ;

Gullick, WJ ;

Dibb, NJ .

ONCOGENE, 1999, 18 (20) :3076-3084

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