Stage Ⅳb Pulmonary Sarcomatoid Carcinoma with EGFR L861Q KRAS Co-mutation and High PD-L1 Expression Neoadjuvant Immunochemotherapy Combined with Surgery Achieves Near MPR

Background Pulmonary sarcomatoid carcinoma (PSC) is a rare, highly aggressive non-small cell lung cancer (NSCLC) subtype (0.1%–4% of lung malignancies) ^[3] . Clinically, it mainly affects smokers, with half diagnosed at advanced stages; pathologically, it is defined by cytokeratin-vimentin co-expression. Molecularly, classical EGFR-sensitive mutations are rare (28%, mostly rare variants like L861Q), while KRAS (22%–34.4%), MET (16%–19%), and TP53 (73.6%–81%) mutations are common ^[13–17] . Traditional treatments are ineffective (chemotherapy ORR < 10%; surgical 5-year survival 12.6%–16.3%), but immunotherapy (mono/combined with chemotherapy) shows promise (73%–77% with PD-L1 ≥ 50%; ORR 37%–43%) ^{[2, 7, 18–21]} . No guidelines exist for PSC with driver mutations (e.g., EGFR/KRAS co-mutation) plus high PD-L1. Methods We retrospectively analyzed clinical, imaging, pathological, and therapeutic data of one PSC patient with informed consent. Results A 62-year-old with stage Ⅳb right upper lung PSC (EGFR L861Q/KRAS co-mutation; PD-L1 TPS 90%) received neoadjuvant "Paclitaxel + Carboplatin + Serplulimab + Denosumab," followed by thoracoscopic lobectomy and postoperative "Furmonertinib + Denosumab." Postoperatively, tumor bed viable cells accounted for 15% (meeting pPR, near MPR [residual < 10%]), with EGFR mutation loss, suggesting treatment-induced clonal evolution. Conclusion Neoadjuvant immunochemotherapy is feasible for PSC with "driver mutation + high PD-L1," providing a clinical reference. It highlights the importance of MDT collaboration and dynamic molecular monitoring in advanced PSC, addressing guideline gaps.