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Article

Expression of a kinase-deficient IGF-I-R suppresses tumorigenicity of rhabdomyosarcoma cells constitutively expressing a wild type IGF-I-R.

International journal of cancer - 13 Apr 1998

Kalebic T, Blakesley V, Slade C, Plasschaert S, Leroith D, Helman L J

Abstract excerpt

Previous results have shown that the insulin-like growth factor type I receptor (IGF-I-R) plays a critical role in the control of rhabdomyosarcoma (RMS) growth. The purpose of this study was to investigate whether a mutated IGF-I-R, when expressed in RMS cells, may interfere with the function of the endogenous wild-type IGF-I-R. We also examined whether the expression of a mutated IGF-I-R may induce phenotypic...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Identifiers

PMID: 9537584
DOI: 10.1002/(sici)1097-0215(19980413)76:2<223::aid-ijc9>3.0.co;2-z

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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