Since its initial approval by the United States Food and Drug Administration (FDA) in 2014, the indications for the use of the immune checkpoint inhibitors (ICIs) in non-small cell lung cancer (NSCLC) patients has increased. However, to date, there has no report on immune myocarditis caused by the ICI sintilimab. In addition, there has been no literature review on ICI-induced myocarditis in lung cancer patients. This is a case report of an elderly male patient who presented with a productive cough and progressive dysphagia for 3 days. The symptoms started on day 6 after the third cycle of sintilimab treatment for his lung carcinoma. In accordance with his clinical manifestations of progressive dysphagia, a previous history of lung cancer, abnormal electrocardiograph, significantly increased serum myocardial enzyme levels, and normal coronary angiography results, sintilimab-induced myocarditis was diagnosed.Methylprednisolone (80-40 mg) was used to inhibit the immune injury and the patient was safely discharged on the 13th day following admission. Since ICI-induced myocarditis is rare and fatal, we summarized the characteristics of 20 cases of the disease in lung cancer patients to highlight to oncologists, respiratory experts, and cardiologists the serious side effects of the drug when they encounter lung cancer patients using ICIs. Like most ICIs, sintilimab induces severe immune myocarditis and requires corticosteroids therapy, and this should be recognized by doctors in multiple departments.
Three-dimensional (3D) structured organoids have become increasingly promising and effective in vitro models, and there is an urgent need for reliable models to assess health effects of inhaled pollutants on the human airway. In our study, we conducted a toxicity assessment of human airway organoids (hAOs) for tire wear particles (TWPs) as an emerging inhaled pollutant. We induced primary human bronchial epithelial cells (HBECs) to generated human airway organoids, which recapitulated the key features of human airway epithelial cells including basal cells, ciliated cells, goblet cells, and club cells. TWPs generated from the wearing of tire treads were considered a major source of emerging inhaled road traffic-derived non-exhaust particles, but their health effect on the lungs is poorly understood. We used human airway organoids to assess the toxicology of tire wear particles on the human airway. In an exposure study, the inhibitory effect of TWPs on the growth of human airway organoids was observed. TWPs induced significant cell apoptosis and oxidative stress in a dose-dependent manner. From the qPCR analysis, TWPs significantly up-regulated the expression pf genes involved in the inflammation response. Additionally, the exposure of TWPs reduced SCGB1A1 gene expression associated with the function of the club cell and KRT5 gene expression related to the function of basal cells. In conclusion, this was first study using human airway organoids for a toxicological assessment of TWPs, and our findings revealed that human airway organoids provide an evaluation model of inhaled pollutants potentially affecting the lungs.
Asians who develop non-small cell lung cancer (NSCLC) have a chance of approximately 50% of harboring the epidermal growth factor receptor (EGFR) mutation. The G719X mutation in EGFR has 3 subtypes (i.e., G719A, G719C, or G719S), all of them being classified as uncommon EGFR mutations.The EGFR mutation G719X is most often associated with lung adenocarcinoma. Conversely, its occurrence in lung squamous cell carcinoma is rare. Its response to tyrosine kinase inhibitor (TKI) treatment remains unknown. A 50-year-old Asian male with no smoking history was admitted to our hospital (Affiliated Hospital of Qingdao University) with an irritating dry cough and 1 month of progressive dyspnea. The patient was diagnosed with lung squamous cell carcinoma (cT4N3M0, stage IIIC). Lung biopsy revealed the presence of EFGR G719X mutation. The patient received a tracheobronchial stent, targeted therapy, chemotherapy, seed implantation and radiotherapy, and survived for 25.4 months following diagnosis. It is crucial that gene mutation analysis is performed in non-smoking male squamous cell carcinoma patients.Compared to lung adenocarcinoma patients with rare G719X mutation, this lung squamous cell carcinoma patient with G719X-mutant tumor had a higher sensitivity to 2 nd -generation EGFR-TKI treatment, but similar progression-free survival. Importantly, the patient clearly benefited from the used comprehensive treatment plan. This article seeks to shed light on the treatment of lung squamous cell carcinoma patients with the uncommon EGFR G719X mutation.
Background ROS1 gene rearrangement has been reported in several types of cancers, including non-small cell lung cancer (NSCLC). It is reported that tyrosine kinase inhibitors are effective in the treatment of ROS1- rearranged NSCLC. Therefore, the identification of ROS1 rearrangement can be used as potential therapeutic target in lung cancer. Epidemiological data indicates that ROS1 gene rearrangement occurs in approximately 1–2% of NSCLC patients. The small sample sizes of the existing associated studies only represent the characteristics of patients in specific regions or countries, and there is still no latest statistical analysis on ROS1 gene rearrangement anywhere in the world. Methods We conducted a systematic search of the PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), CBM, CNKI, Wanfang, and VIP databases to identify studies on ROS1 gene rearrangement in NSCLC patients from January 1, 2015 to October 27, 2019. We conducted a meta-analysis to investigate the relationship between ROS1 gene rearrangement and clinical characteristics of NSCLC patients. The four clinical features are as follows: gender, smoking status, pathological type, and lung cancer stage. Results Thirty-nine studies constituting of 25,055 NSCLC patients were eligible for inclusion in this meta-analysis. A prominently higher rate of ROS1 gene rearrangement was observed in female NSCLC patients (OR =1.94, 95% CI: 1.62–2.32%, P<0.05), patients with no smoking history (OR =2.82, 95% CI: 2.24–3.55%, P<0.05), patients with adenocarcinoma (OR =1.55, 95% CI: 1.14–2.11%, P<0.05), and patients with stage III–IV disease (OR =1.50, 95% CI: 1.15–1.94%, P<0.05). Our meta-analysis also showed that the prevalence of ROS1 rearrangement in adenocarcinoma was 2.49% (95% CI: 1.92–3.11%), while it was lower in non-adenocarcinoma patients (1.37%). Conclusions ROS1 gene rearrangement was more predominant in female patients, patients without smoking history, patients with adenocarcinoma and patients with advanced-stage disease (stages III to IV).
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