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These include molecules that normally inhibit IGF-1R expression such as the tumor suppressor proteins BRCA1, p53, the Wilms tumor (WT1) and von Hippel-Lindau (VHL), as well as molecules that stimulate IGF-1R production such as Sp1, KLF-6 and ER [80-86]

Conclusions Few conclusive results are available from clinical trials and from the literature (Fig

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