Adjuvant chemotherapy has long been indicated to extend survival in completely resected stage IB to IIIA non‐small cell lung cancer (NSCLC). However, there is accumulating evidence that chemotherapy or chemoradiotherapy can induce epithelial‐to‐mesenchymal transition (EMT) in disseminated or circulating NSCLC cells. Here, we describe the first case of EMT as the cause of recurrence and metastasis in a patient with resected stage IIB lung adenosquamous carcinoma after adjuvant chemotherapy. We review the literature and explore the possible mechanisms by which EMT occurs in disseminated tumor cells (DTC) or circulating tumor cells (CTC) in response to adjuvant chemotherapy (cisplatin) as a stressor. We also explore the possible therapeutic strategies to reverse EMT in patients with recurrence. In summary, although adjuvant cisplatin‐based chemotherapy in resected NSCLC does extend survival, it may lead to the adverse phenomenon of EMT in disseminated tumor cells (DTC) or circulating tumor cells (CTC) causing recurrence and metastasis.

Neoadjuvant chemotherapy is a therapeutic option for potentially resectable non‐small cell lung cancer (NSCLC). The role of neoadjuvant targeted therapy (NTT) remains less explored. This case highlights the use of neoadjuvant osimertinib in a case of advanced NSCLC. A 67‐year‐old woman had a left lower lobe lung mass measuring 5.0 × 5.1 × 7.0 cm with an enlarged subcarinal lymph node (LN) on her positron emission tomography scan. Following biopsy, a diagnosis of stage IIIB N2 (cT3N2M0) EGFR exon 19 deletion mutation‐positive lung adenocarcinoma was established. NTT using osimertinib 80 mg once daily was commenced. Subsequent re‐imaging at 3 months (ycT2bN2M0), 6 months (ycT1cN2M0) and 9 months showed tumour downstaging and resolution of the subcarinal LN (ycT1cN0M0). She underwent left lower lobectomy with systematic nodal dissection. All surgical specimens demonstrated no evidence of malignant cells (ypT0N0). Osimertinib could be the preferred NTT for potentially resectable NSCLC.

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Anti-N-Methyl D-Aspartate Receptor (NMDAR) Encephalitis is

Introduction: In non-small cell lung cancer (NSCLC), there may be a relationship between programmed death-ligand 1 (PD-L1) expression, driver mutations and cigarette smoking. Methods: In this single-center retrospective study, the relationship between common driver mutations (EGFR mutation and ALK rearrangement) and PD-L1 expression in advanced NSCLC according to the patients’ smoking history was examined. Light, moderate and heavy smokers were patients who had smoked <20, 20-39, and >40 pack-years, respectively. The level of PD-L1 expression, assessed using Ventana SP263 monoclonal antibody assay, was defined by the tumor proportion score (TPS) as follows: high expression (TPS ≥50%), low expression (TPS 1% - 49%) and no expression (TPS <1%). Results: 101 (52.9%) of 191 patients were never smokers. EGFRmutations were more common in never smokers [65 (64.4%) of 101 patients] than in smokers [16 (17.8%) of 90 patients] (P<0.0001). A higher proportion of smokers had high PD-L1 expression [24 (26.7%) of 90] compared to never smokers [14 (13.9%) of 101] (P=0.042). High PD-L1 expression was seen in 32 of 110 patients (29.1%) with EGFRwild-type tumors but only in 6 of 81 (7.4%) patients with tumors harbouring sensitising EGFR mutations (P<0.0001). Among the 90 smokers, a higher proportion of heavy smokers [19 (35.8%) of 53] than non-heavy smokers [5 (13.5%) of 37] had high PD-L1 expression (P = 0.034). Conclusions: High PD-L1 expression in NSCLC is more common in smokers than in never smokers, in EGFRwild-type than EGFR-mutant NSCLC and in heavy smokers among smokers.