Background: Immune checkpoint inhibitors (ICIs) can cause severe immune‐related adverse events (irAEs). However, biomarkers for irAEs common to different types of ICIs and cancers have not been reported. This study examined whether eosinophils can be used as a predictor of irAEs.Methods: Six hundred fourteen patients with cancer (esophageal, gastric, head and neck, lung, melanoma, renal cell, urothelial, and other cancer) received anti‐PD‐1, anti‐PD‐L1, or anti‐CTLA‐4 plus anti‐PD‐1 therapy. The patients were divided into two groups depending on whether they experienced irAEs (irAE group) or not (non‐irAE group). Eosinophils were examined before the two‐course treatment.Results: Patients in the irAE group who received anti‐PD‐1 or anti‐CTLA‐4 plus anti‐PD‐1 therapy had higher eosinophils before the two‐course treatment than those in the non‐irAE group (p < 0.05). The eosinophils in the anti‐PD‐L1 therapy group tended to increase in the irAE group. Furthermore, eosinophils in gastric, head and neck, lung, melanoma, renal, and urothelial cancers were significantly higher in the irAE group than in the non‐irAE group (p < 0.05). The optimal cutoff value for eosinophils against irAEs was 3.0% (area under the curve = 0.668). In multivariate analyses, eosinophils of ≥3.0% were an independent factor for irAEs (odds ratio: 2.57, 95% CI: 1.79–3.67).Conclusion: An increased eosinophil before the two‐course treatment may be a predictor of irAEs in various cancers treated with different ICIs.

Durvalumab, an anti‐programmed cell death‐ligand 1 (PD‐L1) antibody, is currently used in the maintenance therapy for patients with stage III non‐small cell lung cancer after platinum‐based chemoradiotherapy. A 69‐year‐old male with lung adenocarcinoma, clinical stage IIIA, was treated with chemoradiotherapy. As the treatments progressed, his dry cough gradually subsided. After chemoradiotherapy had been completed, we started durvalumab administration. One month later, his dry cough relapsed and persisted. Based on the changes of his blood eosinophil counts, we clinically diagnosed him with asthma. A 71‐year‐old male with lung adenocarcinoma, clinical stage IIIB, was treated with chemoradiotherapy. After completing chemoradiotherapy, we initiated durvalumab administration. After 6 months, his dry cough was noticed to involve wheezing. Based on his spirometric values and the fraction of exhaled nitric oxide, a clinical diagnosis of asthma was established. Asthma should be considered as one of the possible side effects when immune checkpoint inhibitors are used in cancer treatment.

Background: When considering the effects of dupilumab on severe chronic rhinosinusitis with nasal polyps (CRSwNPs), dupilumab is expected to achieve CRSwNPs remission. The aim of this study was to assess the rate of remission of CRSwNPs with comorbid asthma and its predictors on a 24-month course of dupilumab. Methods: Adult patients with severe CRSwNPs and comorbid asthma who had completed a 24-month course of dupilumab were included in this post hoc analysis. The primary outcome was the rate of CRSwNPs remission at 12 and 24 months of dupilumab. The secondary outcome was to identify factors associated with CRSwNPs remission at 12 and 24 months. Based on the European criteria and a previous definition, remission was defined as the absence of symptoms, improved quality of life, no need for surgery, no exacerbations, recovery of olfactory function, and inactive disease by nasal endoscopy for ≥12 months. A rigorous six-component remission, including olfactory testing, was initially used. Results: Of 16 patients, 4 (25%) and 5 (31%) achieved six-component remission of CRSwNPs at 12 and 24 months, respectively. Patients with shorter disease duration and better olfactory function at baseline achieved six-component remission of CRSwNPs more frequently than those without at 24 months (both p < 0.05). Conclusions: Remission of severe CRSwNPs with comorbid asthma is attainable with a 24-month course of dupilumab.

Background: Actionable tumor genomic alterations, primarily EGFR mutations, occur in nearly 70% of Japanese advanced nonsquamous non‐small cell lung cancer (NSCLC) patients. Standard assessment of tumor tissue includes rapid testing for EGFR mutations, ALK fusions and ROS1 fusions. We conducted a prospective observational study (WJOG13620L) of follow‐on next‐generation sequencing of circulating tumor DNA (ctDNA) in patients without driver alterations after EGFR testing.Methods: Patients with untreated advanced (Stage IIIB–IV or relapsed) nonsquamous NSCLC without EGFR mutations according to single‐plex testing of tumor tissue, were enrolled into this study. Patients with other known driver mutations or who underwent comprehensive genomic profiling were excluded. Plasma was analyzed by Guardant360, and the primary endpoint was the proportion of patients with pathogenic gene alterations in at least one of nine genes.Results: Among the 72 patients enrolled, ALK and ROS1 fusions were tested in 86.1% and 65.2%, respectively. Alterations in pre‐defined genes were detected in 21 patients (29.2%; 95% confidence interval: 19.0–41.1, p < 0.001 [one‐sided null hypothesis proportion of 10%]), including RET fusion (n = 1) and mutations in KRAS (n = 11), EGFR (n = 5), ERBB2 (n = 3), and BRAF (n = 1). Median time from sample submission to results was 8 days (range, 5–17 days).Conclusion: Rapid follow‐on comprehensive testing of ctDNA should be considered prior to first‐line treatment for patients with advanced nonsquamous NSCLC when no alterations are detected after single‐plex tissue testing.