ERBB-2 ( HER2/ neu) gene copy number, p185 HER-2 overexpression, and intratumor heterogeneity in human breast cancer. Mutagenesis in mammalian cells induced by triple helix formation and transcription-coupled repair. Site-directed recombination via bifunctional PNA–DNA conjugates.
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Triplex structures induce DNA double strand breaks via replication fork collapse in NER deficient cells. XPD-dependent activation of apoptosis in response to triplex-induced DNA damage. Triplex formation inhibits HER-2/ neu transcription in vitro. A web-based search engine for triplex-forming oligonucleotide target sequences. Targeted genome modification via triple helix formation. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. Gefitinib and EGFR gene copy number aberrations in esophageal cancer. Potential of overcoming resistance to HER2-targeted therapies through the PI3K/Akt/mTOR pathway. Pertuzumab, trastuzumab, and docetaxel in HER2-positive metastatic breast cancer. Mechanism of action of trastuzumab and scientific update. Studies of the HER-2/ neu proto-oncogene in human breast and ovarian cancer. The evolving landscape of HER2 targeting in breast cancer.
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Integrated analysis of gene expression and copy number identified potential cancer driver genes with amplification-dependent overexpression in 1,454 solid tumors. A census of amplified and overexpressed human cancer genes. Santarius, T., Shipley, J., Brewer, D., Stratton, M. Gene amplification: mechanisms and involvement in cancer. Matsui, A., Ihara, T., Suda, H., Mikami, H. Identification of druggable cancer driver genes amplified across TCGA datasets. These findings offer a general strategy for targeting tumors with amplified genomic loci.Ĭhen, Y. This strategy has demonstrated in vivo efficacy comparable to that of current precision medicines and provided a feasible alternative to combat drug resistance in HER2-positive breast and ovarian cancer models.
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Focusing on cancers driven by HER2 amplification, we find that TFOs targeting HER2 induce copy number-dependent DNA double-strand breaks (DSBs) and activate p53-independent apoptosis in HER2-positive cancer cells and human tumor xenografts via a mechanism that is independent of HER2 cellular function. Here, we introduce a therapeutic strategy for targeting cancer-associated gene amplifications by activating the DNA damage response with triplex-forming oligonucleotides (TFOs), which drive the induction of apoptosis in tumors, whereas cells without amplifications process lower levels of DNA damage. A number of drugs have been developed to inhibit the protein products of amplified driver genes, but their clinical efficacy is often hampered by drug resistance. Gene amplification drives oncogenesis in a broad spectrum of cancers.