Pulmonary pleomorphic carcinoma (PPC) is a non-small-cell lung cancer, resistant to chemotherapy and no standard therapy has as yet been established. We herein report the case of a 59-year-old man with PPC who showed a longterm response with durvalumab after chemoradiotherapy. He was referred to our hospital with a mass shadow at the right upper lung. PPC clinical stage IIIB was diagnosed, and the tumor proportion score of programmed death-ligand 1 (PD-L1) was 100%. Six days after transbronchial biopsy, he had difficulty walking owing to sensory abnormalities. We found that the primary tumor had invaded the spinal cord and compressed the cord at T1-T4, resulting in the abnormalities. He underwent tumor resection and received chemotherapy involving cisplatin (CDDP) + S-1 and concurrent radiotherapy (66 Gy). Subsequently, durvalumab treatment as consolidation therapy was commenced. After one year of durvalumab treatment had been completed, he had no apparent signs of relapse or severe adverse events. This case suggests that a long-term response can be achieved with durvalumab after chemoradiotherapy for stage III inoperable PPC showing high PD-L1 expression. Key PointsSignificant findings of the report A long-term response might be achieved with durvalumab after chemoradiotherapy in patients with stage III inoperable pulmonary pleomorphic carcinoma showing high expression of programmed death-ligand 1. What this study adds It is possible to continue durvalumab treatment for one year without any severe adverse events. Although pulmonary pleomorphic carcinoma is considered to have a poor prognosis, the combination therapy of immune checkpoint inhibitors and radiotherapy may be an effective treatment option.

Multiple EGFR-mutant and ALK-mutant lung cancers are rare, and standard treatment has not been established because of the small number of cases. A 79-year-old man was found to harbor nodular shadows in right S1, right S5, and left S3. He was surgically diagnosed with stage IIB (pT3N0M0) EGFR G719X-mutant lung adenocarcinoma in left S3 and stage IA1 (pT1aN0M0) ALK-mutant lung adenocarcinoma in right S5. Owing to the relapse of the EGFR-mutant adenocarcinoma, gefitinib treatment was commenced 3 months postoperatively. The tumor shrank temporarily; however, the nodular shadow in the right S1 and #3a lymph nodes were found to increase in size. He was diagnosed with adenosquamous carcinoma in right S1 and relapsing ALK-mutant adenocarcinoma in #3a lymph node. Gefitinib treatment was continued, but due to a renewed increase in the size of the #3a lymph node, the drug was changed to alectinib 16 months postoperatively. Subsequently, the EGFR-mutant adenocarcinomas were found to increase in left S1 despite the decrease in the #3a lymph node size. Nineteen months after the first surgery, the treatment was changed to gefitinib, and repeated treatment with this drug and alectinib administered every 2 months was continued. This approach enabled 39 months of progression-free survival, and no serious adverse events were observed.