HIGHLIGHTS
SUMMARY
The IGF1R is vital for cell survival, as illustrated by the lethal phenotype of mice in which the IGF1R gene was disrupted by homologous recombination. Whereas normal cells exhibit tightly regulated growth signals, transformed cells display a largely deregulated signaling capacity. In most cases, this unrestricted behavior results from the ability of cancer cells to synthesize a variety of growth factor ligands and/or their cognate cell-surface receptors. Using transient transfection assays the authors have demonstrated that E2F1 is a potent inducer of IGF1R gene_expression in prostate cancer cells. Deletion analysis indicated that . . .
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