As previously reported, KRAS and NRAS mutations were mutually exclusive, and there was a strong trend for RAS mutations (N or K) to be associated with resistance to guadecitabine (CR cases were seen in 0/22 (0%) patients with RAS mutations compared to 15/100 (15%) patients without RAS mutations, p = 0.07).
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Genomic and epigenomic predictors of response to guadecitabine in relapsed/refractory acute myelogenous leukemia.
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