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The insulin-like growth factor 1 receptor (IGF-1R) is a transmembrane protein belonging to the receptor tyrosine kinase family, essential for mediating the effects of IGF-1 and IGF-2 on cell growth and survival (UniProt P08069). In the context of autologous tumor cell therapy, the target is specifically the IGF-1R messenger RNA (mRNA), which is downregulated using antisense oligonucleotides (ASOs) to inhibit the production of the receptor protein (PubMed: 33164155). This approach is notably utilized in the development of IGV-001, an autologous cell-based immunotherapy for glioblastoma multiforme, where patient-derived tumor cells are treated ex vivo with an IGF-1R ASO (Imvax). By reducing IGF-1R expression, the therapy induces apoptosis in the tumor cells and promotes the release of tumor-associated antigens, thereby stimulating a robust anti-tumor immune response when the cells are re-implanted (ClinicalTrials.gov NCT04485936). IGF-1R signaling is a major driver of oncogenesis and resistance to therapy in many cancers, making its mRNA a strategic target for precision oncology.
Antisense oligonucleotide-mediated knockdown of IGF-1R mRNA to downregulate receptor expression and induce an anti-tumor immune response.
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