biostudies-literatureRaghav KNCI NIH HHS472-478https://www.ebi.ac.uk/biostudies/studies/S-EPMC9870237biostudies-literatureUnknown41(3)<i>Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. Clinical Trial Updates provide an opportunity to disseminate additional results from studies, published in</i> JCO <i>or elsewhere, for which the primary end point has already been reported.</i>Acquired genomic alterations (Acq-GAs), specifically <i>RAS</i>, <i>BRAF</i>, and <i>EGFR</i>-ectodomain mutations and <i>ERBB2</i> and <i>MET</i> amplifications, are recognized as major mechanisms of resistance to later-line anti-EGFR-antibody therapy in metastatic colorectal cancer (mCRC). However, data regarding emergence of these Acq-GAs under the selective Journal of clinical oncology : official journal of the American Society of Clinical OncologyAcquired Genomic Alterations on First-Line Chemotherapy With Cetuximab in Advanced Colorectal Cancer: Circulating Tumor DNA Analysis of the CALGB/SWOG-80405 Trial (Alliance).PMC9870237U10 CA180882U10 CA180819U10 CA180830UG1 CA233329R01 CA184843UG1 CA180830U24 CA196171U10 CA180821U10 CA180888Kopetz SLenz HJSun RRaghav KInnocenti FOu FSVenook APfalseAcquired Genomic Alterations on First-Line Chemotherapy With Cetuximab in Advanced Colorectal Cancer: Circulating Tumor DNA Analysis of the CALGB/SWOG-80405 Trial (Alliance).<i>Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. Clinical Trial Updates provide an opportunity to disseminate additional results from studies, published in</i> JCO <i>or elsewhere, for which the primary end point has already been reported.</i>Acquired genomic alterations (Acq-GAs), specifically <i>RAS</i>, <i>BRAF</i>, and <i>EGFR</i>-ectodomain mutations and <i>ERBB2</i> and <i>MET</i> amplifications, are recognized as major mechanisms of resistance to later-line anti-EGFR-antibody therapy in metastatic colorectal cancer (mCRC). However, data regarding emergence of these Acq-GAs under the selective 2023-01-01T00:00:00Z2023 Jan2025-04-22T03:12:02.774Z2025-04-05T20:40:05.397ZS-EPMC98702373606745210.1200/JCO.22.00365