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Case report reveals systemic AL amyloidosis after neoadjuvant therapy in lung adenocarcinoma, suggesting need for proteomic subtyping.
Systemic AL amyloidosis is rarely reported in temporal association with immune checkpoint inhibitor use. We report a 69‐year‐old man with resectable stage IIB right upper lobe lung adenocarcinoma who received neoadjuvant pembrolizumab, carboplatin, and pemetrexed followed by robotic‐assisted lobectomy. Pathology showed a 4.6‐cm treated tumour bed with residual invasive adenocarcinoma (50% viable), negative margins, and no nodal metastasis (0/9). Tumour profiling demonstrated a PD‐L1 tumour proportion score of 100%, a high tumour mutational burden (18 mut/Mb), microsatellite stability, and variants in BRAF, TP53 and PTPRT . In addition to the treatment effect, widespread Congo red–positive deposits were identified in lung parenchyma and multiple nodal stations. Laser microdissection with LC–MS/MS confirmed AL (λ) amyloid. Subsequent workup revealed a λ‐restricted plasma cell clone (6.4%) with t (11;14), establishing systemic AL amyloidosis. He received adjuvant pembrolizumab and daratumumab‐CyBorD with partial hematologic response. This case highlighted that amyloid can unexpectedly be a second diagnosis after post‐neoadjuvant lung resections and that proteomic subtyping is essential for prompt haematologic staging and treatment.
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Ma et al. (2026) studied this question.
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