scholarly journals The insulin-like growth factor-I receptor kinase inhibitor NVP-ADW742 sensitizes medulloblastoma to the effects of chemotherapy

2011 ◽  
Author(s):  
Nu Zhang
Keyword(s):  
Growth Factor ◽  
Kinase Inhibitor ◽  
Insulin Like Growth Factor ◽  
Receptor Kinase ◽  
Factor I ◽  
Growth Factor I

scholarly journals Antitumor Activity of the Insulin-Like Growth Factor-I Receptor Kinase Inhibitor NVP-AEW541 in Musculoskeletal Tumors

2005 ◽  
Vol 65 (9) ◽  
pp. 3868-3876 ◽  
Author(s):  
Katia Scotlandi ◽  
Maria Cristina Manara ◽  
Giordano Nicoletti ◽  
Pier-Luigi Lollini ◽  
Stella Lukas ◽  
...  
Keyword(s):  
Growth Factor ◽  
Antitumor Activity ◽  
Kinase Inhibitor ◽  
Insulin Like Growth Factor ◽  
Receptor Kinase ◽  
Factor I ◽  
Musculoskeletal Tumors ◽  
Growth Factor I

Insulin-like growth factor I receptor is downregulated after alveolarization in an apoptotic fibroblast subset

2002 ◽  
Vol 282 (3) ◽  
pp. L457-L467 ◽  
Author(s):  
Suseela Srinivasan ◽  
Jennifer Strange ◽  
Feyisola Awonusonu ◽  
Margaret C. Bruce
Keyword(s):  
Growth Factor ◽  
Kinase Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Lung Fibroblasts ◽  
Normal Lung ◽  
Insulin Like Growth Factor ◽  
Lung Maturation ◽  
Factor I ◽  
Growth Factor I ◽  
Alveolar Formation

After alveolar formation, >20% of interstitial lung fibroblasts undergo apoptosis, a process that is of critical importance for normal lung maturation. The immature lung contains two morphologically distinct fibroblast populations, lipid-filled interstitial fibroblasts (LIF) and non-LIF (NLIF), which differ with respect to contractile protein content, proliferative capacity, and expression of mRNAs for fibronectin and types I and III collagen, but not tropoelastin. After alveolarization, apoptosis occurs in only one fibroblast population, the LIF. Using flow cytometry to analyze fibroblasts stained with a lipophilic, fluorescent dye, we identified a subset, designated LIF(−), that contained fewer lipid droplets. Unlike LIF that retain lipid, LIF(+), the LIF(−) do not undergo apoptosis after alveolarization. In LIF(+), apoptosis was correlated with downregulation of insulin-like growth factor I receptor (IGF-IR) mRNA and cell surface protein expression. Treatment with anti-IGF-IR decreased total lung fibroblast survival ( P = 0.05) as did treatment with the phosphatidylinositol 3-kinase inhibitor LY-294002 and the ras-raf-mitogen-activated protein kinase inhibitor PD-98059 ( P < 0.002), which block IGF-I/insulin receptor survival pathways. These observations implicate downregulation of IGF-IR expression in fibroblast apoptosis after alveolar formation.

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