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:T52d,¹⁷⁷Lu-PSMA-617 and ¹⁷⁷Lu-PSMA I&T (collectively termed ¹⁷⁷Lu-PSMA) are currently being used for the treatment of selected metastatic castration-resistant prostate cancer (mCRPC) patients with PSMA PET-positive disease, but biomarkers for these agents remain incompletely understood. Methods: Pretreatment circulating tumor DNA (ctDNA) samples were collected from 44 mCRPC patients receiving ¹⁷⁷Lu-PSMA treatment. Prostate-specific antigen responders and nonresponders were assessed relative to the ctDNA findings at baseline. Results: The ctDNA findings indicated that nonresponders were more likely to have gene amplifications than were responders (75% vs. 39.2%, P = 0.03). In particular, amplifications in FGFR1 (25% vs. 0%, P = 0.01) and CCNE1 (31.2% vs. 0%, P = 0.001) were more likely to be present in nonresponders. CDK12 mutations were more likely to be present in nonresponders (25% vs. 3.6%, P = 0.05). Conclusion: Our analyses indicate that ctDNA assays may contain specific biomarkers predictive of response or resistance for ¹⁷⁷Lu-PSMA-treated mCRPC patients. Additional confirmatory studies are required before clinicians can use these findings to make personalized treatment decisions.

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