1998
DOI: 10.1007/978-1-4615-5357-1_6
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Use of the IGF-I Antisense Strategy in the Treatment of the Hepatocarcinoma

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Cited by 17 publications
(17 citation statements)
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“…[30][31][32] Furthermore, oligonucleotide antisense therapy against IGF-I mRNA has shown decreased HCC growth rates in vitro and in vivo, indicating a significant role for IGF-I in progression of HCC. 33,34 Most of the effects of IGF-I are exerted through ligand binding to a specific heterodimeric IGF-IR. 18,19 Ligand binding leads to activation of intracytoplasmic tyrosine kinases located on the receptor ␤-chain and receptor autophosphorylation.…”
mentioning
confidence: 99%
“…[30][31][32] Furthermore, oligonucleotide antisense therapy against IGF-I mRNA has shown decreased HCC growth rates in vitro and in vivo, indicating a significant role for IGF-I in progression of HCC. 33,34 Most of the effects of IGF-I are exerted through ligand binding to a specific heterodimeric IGF-IR. 18,19 Ligand binding leads to activation of intracytoplasmic tyrosine kinases located on the receptor ␤-chain and receptor autophosphorylation.…”
mentioning
confidence: 99%
“…The arrest of IGF-I expression diminishes or stops neoplastic development [7,29,30] due to the consequential apoptosis and anti-tumor immune response (MHC-I) [31][32][33] . These two phenomena, which play an important role in the mechanism of IGF-I, are barely present (if not non-existent) in other oncoprotein and growth factor mechanisms such as EGF, VEGF, or TGF-beta [34][35][36][37] .…”
Section: Igf-1 Biomarkermentioning
confidence: 99%
“…[149][150][151][152][153][154][155] Antisense against N-ras or against the fibroblast growth factor-2 mRNA inhibits the proliferation of HCC in vitro and reduces the tumorigenicity of the cells in the nude mice model. 153 The low proliferative ability and tumorigenic potential of HCC cells treated by antigens anti-IGF-1 has been demonstrated to correlate with apoptosis mechanisms and the induction of an immune response against tumor cells due to IGF-1-mediated re-expression of MHC B7 molecules at the surface of tumor cells.…”
Section: Playing With the Biological Activation Pathwaysmentioning
confidence: 99%
“…153 The low proliferative ability and tumorigenic potential of HCC cells treated by antigens anti-IGF-1 has been demonstrated to correlate with apoptosis mechanisms and the induction of an immune response against tumor cells due to IGF-1-mediated re-expression of MHC B7 molecules at the surface of tumor cells. 150,154 Most of the reported results depict experiments performed with HCC cells manipulated ex vivo to overexpress the antisense oligonucleotide inhibitor prior to be reinjected in the animal, which does not reflect the therapeutical potential of this approach.…”
Section: Playing With the Biological Activation Pathwaysmentioning
confidence: 99%