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- W1569642635 abstract "Growth factor receptor signals, including insulin-like growth factor (IGF)-1 receptor (IGF-1R), are required for carcinogenesis and tumour progression in many human malignancies. The concept of targeting specific tumorigenic receptors has been validated by successful clinical application of multiple new drugs, including trastuzumab and gefitinib. In this paper, we review strategies of the genetic blockade of IGF-1/IGF-1R that validate this receptor as a promising anticancer target. Adenoviruses efficiently transduce malignant epithelial cells in culture and are useful for such target validation and potentially also as clinical therapeutics. To block IGF-1R signalling, we constructed adenoviruses expressing antisense IGF-1R and two truncated IGF-1R (482 and 950 amino acids long, IGF-1R/482st and IGF-1R/950st, respectively) that function as dominant negative inhibitors (IGF-1R/dn). The truncated receptors were also cloned into tetracycline regulated expression vectors to study the effects of modulating this pathway without the use of viral vectors. Blocking for IGF-1R suppressed tumorigenicity both in vitro and in vivo and effectively blocked both IGF-1 and IGF-2-induced activation of Akt-1. IGF-1R/dn expression increased radiation- and chemotherapy-induced apoptosis and these combination therapies with chemotherapy were very effective against tumours in mice. In an intraperitoneal dissemination mouse model, blockade of IGF-1R reduced dissemination and prolonged survival times. IGF-1R/482st was more effective than IGF-1R/950st due to its bystander effect. These studies confirm the validity of IGF-1R as a therapeutic target and genetic blockade as a potential strategy for several malignancies, including lung, colon and pancreatic carcinoma." @default.
- W1569642635 created "2016-06-24" @default.
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- W1569642635 date "2004-09-17" @default.
- W1569642635 modified "2023-10-14" @default.
- W1569642635 title "Genetic Blockade of the Insulin-Like Growth Factor 1 Receptor for Human Malignancy" @default.
- W1569642635 doi "https://doi.org/10.1002/0470869976.ch11" @default.
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