2007
DOI: 10.4161/cbt.6.11.4854
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PDGFRβ and HIF-1α inhibition with imatinib and radioimmunotherapy of experimental prostate cancer

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Cited by 16 publications
(13 citation statements)
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References 49 publications
(71 reference statements)
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“…Fibroblasts can be activated by excessive PDGF released by tumor cells [27] and proliferate in a dose dependent manner with PDGF-BB (a subtype of PDGF) stimulation [28]. Since imatinib is regarded as an inhibitor of PDGFR-beta by blocking the phosphorylation of the receptor [12,29], it is postulated that the decrease of tumor IFP by SSL-IMA is related to the inhibition of tumor fibroblasts through blocking PDGF pathway. NIH/3T3 fibroblasts expressing PDGFR-beta [30] were used to investigate the effect of SSL-IMA in vitro.…”
Section: Inhibition Of Pdgfr-beta and Fibroblast Proliferationmentioning
confidence: 99%
“…Fibroblasts can be activated by excessive PDGF released by tumor cells [27] and proliferate in a dose dependent manner with PDGF-BB (a subtype of PDGF) stimulation [28]. Since imatinib is regarded as an inhibitor of PDGFR-beta by blocking the phosphorylation of the receptor [12,29], it is postulated that the decrease of tumor IFP by SSL-IMA is related to the inhibition of tumor fibroblasts through blocking PDGF pathway. NIH/3T3 fibroblasts expressing PDGFR-beta [30] were used to investigate the effect of SSL-IMA in vitro.…”
Section: Inhibition Of Pdgfr-beta and Fibroblast Proliferationmentioning
confidence: 99%
“…It should be pointed out that the decrease of VEGF expression was identified predominantly related to the inhibition of c-Kit-induced HIF-1 activity in small cell lung cancer cells [67]. However, another study showed that imatinib inhibits HIF-1 expression in PC-3 tumors, thus improving radioimmunotherapy, and has a significant time-and dosedependent reduction in the expression of insulin-like growth factor-1 (IGF-1) but with no effect on VEGF [66]. The discrepancy in the results of imatinib on VEGF expression might be due to the use of different cell types and experimental conditions.…”
Section: Miscellaneousmentioning
confidence: 95%
“…Comparing these agents, it can be indicated that a benzoazaheterocyle, especially the quinazoline moiety, which is also the mother nuclear structrure of a class of receptor tyrosine kinase inhibitors (RTKIs), is indispensable for the antiangiogenic and anti-HIF properties of this class of compounds. And in this sense, other series of small-molecule RTKIs and monoclonal antibodies targeting VEGFR or EGFR may exhibit similar HIF-1 inhibiting activity and this is indeed the case, for example, imatinib [66], cetuximab and trastuzumab [69].…”
Section: Benzoazaheterocyclesmentioning
confidence: 99%
“…The development of improved therapy modalities should therefore be prioritized and targeted therapies based on TNPs are promising candidates to increase the therapeutic efficacy and chance for survival of this category of patients. Several studies of the therapeutic efficacy and toxicity of RIT against PCa have been performed [492,527,528,529,530,531,532,533,534,535,536,537,538,539,540,541,542,543,544]. …”
Section: The Prostate Cancer Casementioning
confidence: 99%