SOS1 inhibitor combinations overcome KRAS inhibitor resistance
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Publisher
Springer Science and Business Media LLC
Link
https://www.nature.com/articles/s43018-024-00801-5.pdf
Reference5 articles.
1. Hofmann, M. H., Gerlach, D., Misale, S., Petronczki, M. & Kraut, N. Expanding the reach of precision oncology by drugging all KRAS mutants. Cancer Discov. 12, 24–937 (2022). This review article presents an overview of patient populations with KRAS-mutant cancer and summarizes mutant-selective and pan-RAS inhibitor approaches.
2. Awad, M. M. et al. Acquired resistance to KRASG12C inhibition in cancer. N. Engl. J. Med. 384, 2382–2393 (2021). This paper reports the diverse genomic and histologic changes clinically observed after the development of resistance to the KRASG12C inhibitor adagrasib.
3. Zhao, Y. et al. Diverse alterations associated with resistance to KRAS(G12C) inhibition. Nature 599, 679–683 (2021). This paper reports genetic alterations associated with preclinical and clinical resistance to the KRASG12C inhibitor sotorasib.
4. Hofmann, M. H. et al. BI-3406, a potent and selective SOS1-KRAS interaction inhibitor, is effective in KRAS-driven cancers through combined MEK inhibition. Cancer Discov. 11, 142–157 (2021). This paper describes the potency and selectivity of the SOS1 inhibitor tool BI-3406.
5. Rodriguez-Viciana, P., Oses-Prieto, J., Burlingame, A., Fried, M. & McCormick, F. A phosphatase holoenzyme comprised of Shoc2/Sur8 and the catalytic subunit of PP1 functions as an M-Ras effector to modulate Raf activity. Mol. Cell 22, 217–230 (2006). This paper identifies Shoc2-PP1c as a specific MRAS effector.
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