Tuesday, March 14, 2023 6:28:39 PM
From the abstract.
NRG1 gene fusions are rare, clinically actionable somatic alterations identified in 0.1% of all tumors. Previous studies have demonstrated that NRG1 fusions signal through ERBB/HER family members and that HER2 inhibition has anti-tumor activity in NRG1 fusion-driven cancers. However, NRG1 can also bind to HER4 in addition to HER3, and the contribution of individual HER family members in tumor cells with NRG1 fusions has not been fully elucidated.
Our data indicated that pan-HER tyrosine kinase inhibitors (TKIs), such as poziotinib, were more effective at blocking HER2/HER3, EGFR/HER3 and HER4 signaling in NRG1-fusion expressing cells as compared to TKIs with greater relative specificity for EGFR (erlotinib, lapatinib), HER2 (pyrotinib), EGFR/HER2 (afatinib, dacomitinib, neratinib) or HER2/HER4 (TAS0728,tucatinib).
https://www.abstractsonline.com/pp8/#!/10828/presentation/6748
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