Postoperative radiotherapy does not improve survival in patients with Masaoka-Koga stage IIB thymomas: A propensity score matching study based on the SEER database.

This study, based on a population, explored the prognostic value of postoperative radiotherapy (PORT) for Masaoka-Koga IIB stage thymomas. Patients diagnosed with thymoma from 2004 to 2017 in the Surveillance, Epidemiology, and End Results (SEER) database were included in the retrospective study. Through propensity score matching, the baseline characteristics of the patients were successfully matched to mitigate the selection bias of PORT. Survival rates and survival curves were compared between the PORT and non-PORT groups, with potential confounding factors addressed using a multivariate Cox regression model. In this study, 785 cases of IIB stage thymoma were included from the SEER database, and 303 patients were successfully matched between PORT and non-PORT groups through propensity score matching, with no significant differences in baseline characteristics. In the PORT and non-PORT groups, 10-year overall survival rates were 65.2% versus 59.6%, and cancer-specific survival rates were 87.0% vs. 84.4%, PORT did not yield statistically significant improvements in overall survival (P = .275) or cancer-specific survival (P = .336) for stage IIB thymomas. Based on the SEER database, the results of our study indicated that PORT does not confer a significant survival benefit for IIB stage thymomas.

Pulmonary function protection by single-port thoracoscopic segmental lung resection in elderly patients with IA non-small cell lung cancer: A differential matched analysis.

In patients with stage IA non-small cell lung cancer (NSCLC), uniportal video-assisted thoracic surgery (U-VATS) anatomical segmentectomy removes the lung tumor while preserving lung function as much as possible, and it is therefore an alternative to lobectomy. Patients with stage IA NSCLC receiving U-VATS segmental resection at our institution from September 2017 to June 2019 were compared with patients receiving U-VATS lobectomy. A total of 47 patients received segmentectomy and 209 patients received U-VATS lobectomy in the same period. Propensity score matching was conducted to diminish bias. The final study cohort included 42 patients who received segmentectomy and 42 propensity score matching-matched patients who received lobectomy. Perioperative parameters and postoperative complications, length of hospital stay, postoperative forced expiratory volume in 1 s (FEV1), and forced vital capacity (FVC) were compared between the 2 groups. Surgery was successfully completed in all patients. The mean follow-up was for 8.2 months. The postoperative complication rate was comparable between the 2 groups: 31.0% in segmentectomy patients versus 35.7% in lobectomy patients (P = .643). At 1 month after surgery, FEV1% and FVC% were not significantly different between the 2 groups (P > .05). At 3 months after surgery, FEV1 and FVC were higher in segmentectomy patients than in lobectomy patients (FEV1, 82.79% ± 6.36% vs 78.55% ± 5.42%; FVC, 81.66% ± 6.09% vs 78.90% ± 5.58%, P < .05). Patients receiving segmentectomy suffer less pain and have better postoperative lung function and higher quality of life.

CircRPPH1 promotes cell proliferation, migration and invasion of non-small cell lung cancer via the PI3K/AKT and JAK2/STAT3 signalling axes.

Non-small cell lung cancer (NSCLC) has markedly increased morbidity and mortality rates worldwide. Circular RNAs were shown to regulate NSCLC progression. But the underlying pathways of the circRPPH1-mediated regulation of NSCLC still need further exploration. We evaluated circRPPH1 levels in NSCLC tissues and cell lines via qRT-PCR. Moreover, using ectopic plasmid incorporation and siRNA assays, we analysed the circRPPH1-mediated regulation of cell proliferation (CP), cell migration (CM) and cell invasion (CI) in NSCLC cell lines (H1975 and A549 cells), using CCK-8, colony forming, scratch wound and transwell assays, respectively. CircRPPH1 levels were remarkably high in the NSCLC tissues and cell lines. The transfection experiments showed that circRPPH1 overexpression was able to promote CP, CM and CI of NSCLC cells, while CP, CM and CI were significantly restrained by the knockdown of circRPPH1. We also displayed that circRPPH1 knockdown suppressed the cell progression via inactivating the PI3K/AKT and JAK2/STAT3 signalling axes. Subsequently, in vivo experiment in nude mice was demonstrated that the inhibition of circRPPH1 could reduce the tumour growth of NSCLC. circRPPH1 may accelerate the growth and metastasis of NSCLC, in culture conditions and in animal models, by stimulating the PI3K/AKT and JAK2/STAT3 signalling axes, thus promoting the development of NSCLC.

Lung adenocarcinoma organoids harboring EGFR 19Del and L643V double mutations respond to osimertinib and gefitinib: A case report.

INTRODUCTION: It has been well reported that non-small-cell lung cancer (NSCLC) patients with single epithelial growth factor receptor (EGFR) activating mutation have high objective response rate when treated with EGFR-TKIs. However, due to rarity of cases, the response of patients with EGFR double or multiple mutations is not yet well understood. Patient-derived organoid technology has become to a powerful tool in cancer personalized medicine. PATIENT CONCERNS: A 60-year-old nonsmoking female was admitted to hospital for lung cancer after Chest CT. DIAGNOSES: The patient had no obvious clinical symptoms. Postoperative pathology confirmed a stage I of NSCLC. An EGFR double mutation 19Del/L643V was detected in the sequence of patient's cancer specimen. INTERVENTIONS: The patient was in good condition after surgical resection, with no sign of lung cancer recurrence. The patient has not yet started on targeted medicine. OUTCOMES: A lung cancer organoid culture was established from the cancer tissue of the patient, which recapitulated the morphological and molecular characteristics of cancer tissue. The drug sensitivity test showed that the cancer organoids that retained original mutations were sensitive to anticancer agents osimertinib and gefitinib, while resistant to erlotinib and icotinib. CONCLUSION: The uncommon EGFR double mutation exhibits distinctive sensitivities towards different target drugs of EGFR-TKIs. Our findings provide a better understanding of EGFR-TKIs' effects on patient-derived cancer organoids harboring uncommon EGFR double mutation(s).