1a:I[76865,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"Grid"] 1b:I[17291,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"GridCol"] 1c:I[34616,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"Avatar"] 1d:I[32972,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"default"] 1e:T4b8,ERBB2 abnormalities frequently occur and serve as rationale therapeutic targets in cancer. In this study, clinical and next-generation sequencing data from 14,956 patients across more than 20 tumor types were collected. A total of 406 (2.7%) patients were identified with ERBB2 amplifications, and 303 (2.0%) patients with pathogenic somatic ERBB2 mutations. ERBB2 amplifications fell most frequently in breast (15.9%) and stomach (8.3%) cancers. Somatic ERBB2 SNVs/indels occurred most common in bladder/urinary tract (7.3%) and intestine (6.1%) cancers. The top mutated ERBB2 SNVs/indels were p.Y772_A775dup (25.5%) and p.S310F/Y (19.9%). Significantly higher rates of ERBB2 SNV/indels were found in women compared to men (2.8% vs. 1.5%, p < 0.0001). CDK12 was the most common co-amplification gene with ERBB2 in cancers with a high frequency of ERBB2 amplifications. Patients with ERBB2 amplifications or mutations had higher TMB compared with patients with non-ERBB2 alterations. The study provided the landscape of ERBB2 alterations across a variety of solid tumors that may benefit from anti-HER2 agents.

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