2002
DOI: 10.1038/sj.onc.1206058
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In IGF-I receptor-deficient leiomyosarcoma cells autocrine IGF-II induces cell invasion and protection from apoptosis via the insulin receptor isoform A

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Cited by 151 publications
(108 citation statements)
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References 30 publications
(28 reference statements)
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“…Ratio of IGF-1R:IR in favor of IR seems to be responsible also for native resistance of some Ewing's sarcoma to anti-IGF-1R therapy and may also explain the lower level of sensitivity of other sarcomas, such as osteosarcoma and rhabdomyosarcoma. In fact, these tumors express higher levels of IR-A than IGF-1R together with IGF-2 (Sciacca et al, 2002;Avnet et al, 2009). Similarly high IR:IGF-1R ratios conveyed resistance to IMC-A12 in breast cancer cells (Ulanet et al, 2010), whereas higher levels of IGF-1R were seen in squamous cell carcinoma of patients responding to figitumumab-containing therapy as compared with non-responders (Gualberto et al, 2010).…”
Section: Discussionmentioning
confidence: 92%
“…Ratio of IGF-1R:IR in favor of IR seems to be responsible also for native resistance of some Ewing's sarcoma to anti-IGF-1R therapy and may also explain the lower level of sensitivity of other sarcomas, such as osteosarcoma and rhabdomyosarcoma. In fact, these tumors express higher levels of IR-A than IGF-1R together with IGF-2 (Sciacca et al, 2002;Avnet et al, 2009). Similarly high IR:IGF-1R ratios conveyed resistance to IMC-A12 in breast cancer cells (Ulanet et al, 2010), whereas higher levels of IGF-1R were seen in squamous cell carcinoma of patients responding to figitumumab-containing therapy as compared with non-responders (Gualberto et al, 2010).…”
Section: Discussionmentioning
confidence: 92%
“…Signaling by the IR promotes survival (Ottensmeyer et al, 2000;Sciacca et al, 2002), which, when inhibited by HNMPA-(AM 3 ), could trigger apoptosis. Accordingly, HNMPA-(AM 3 )-treated cells were assayed for apoptosis using Annexin V-FITC staining.…”
Section: Resultsmentioning
confidence: 99%
“…Although numerous studies have shown that insulin may act through IR to affect tumour progression, 42,43 we cannot rule out the possibility that IGF-1 and IGF1-R might downregulate PTEN in a similar fashion as proposed for insulin and IR. Also, IR has been shown to form hetero-receptor complexes with IGF receptor, which could be activated by other insulin-like growth factors as well.…”
Section: Discussionmentioning
confidence: 99%