Search

Background: Usage of immune checkpoint inhibitors (ICIs) has prolonged the overall survival (OS) of patients with extensive‐stage small‐cell lung cancer (ES‐SCLC). In clinical trials, males accounted for a large proportion, leading to the uncertainty of its efficacy in female patients. We therefore conducted this study to explore the efficacy and safety of using ICIs in female patients with ES‐SCLC. Methods: We retrospectively enrolled female SCLC patients and subdivided them into two groups. Group A (n = 40) was defined as ES‐SCLC patients who received first‐line standard chemotherapy with or without ICIs. Group B (n = 47) included relapsed SCLC patients who were administered with second‐line therapies. Kaplan–Meier methodology was used to calculate survival analysis. Chi‐squared tests were used to analyze the incidence of adverse events (AEs). Results: Median progression‐free survival (PFS) and median OS favored the ICI‐contained cohorts (Group A PFS: 8.3 vs. 6.1 months; OS: not reached vs. 11.3 months; Group B PFS: 15.1 vs. 3.3 months; OS: 35.3 vs. 8.3 months), especially in those patients who received second‐line immunotherapies. Patients who received immunotherapy had a slightly higher incidence rate of grade ≥3 AEs (Group A: 71.4% vs. 46.2%; Group B: 44.5% vs. 13.2%). Those who developed grade ≥3 AEs in first‐line ICIs cohort had a more favorable survival (PFS: 8.3 vs. 3.2 months; OS: not reached vs. 5.1 months). Conclusions: Our study suggested that female ES‐SCLC patients treated with immunotherapy tended to achieve a relatively longer survival. The incidence of AEs (grade ≥3) was higher in women patients receiving ICIs, which requires monitoring more closely. [ABSTRACT FROM AUTHOR]

Background: Triosephosphate isomerase 1 (TPI1), as a widely involved glycolytic enzyme, plays a significant role in glucose metabolism and is highly expressed in various tumors. However, its role in lung adenocarcinoma (LUAD) remains incompletely understood. Methods: Through bioinformatic analysis, we identified a positive association between high expression of TPI1 and metastasis in LUAD. Western blot, RT‐qPCR, wound healing assays and transwell experiments, were employed to investigate potential mechanisms. Results: In this study, bioinformatic analysis showed that high expression of TPI1 was associated with poor prognosis in LUAD patients. We examined the expression of TPI1 in 29 paired LUAD tissues and found that TPI1 expression was higher in LUAD tissues than in paired adjacent noncancerous tissues. Meanwhile, overexpression of TPI1 promoted the epithelial‐mesenchymal transition (EMT) process in LUAD cells, while silencing TPI1 weakened the EMT process. Furthermore, TPI1 was shown to regulate EMT through the MAPK/ERK signaling pathway. Conclusion: TPI1 promotes LUAD metastasis by activating the MAPK/ERK signaling pathway. [ABSTRACT FROM AUTHOR]

Exosomes can carry various kinds of RNAs to mediate intercellular communication. Circular RNA (circRNA) special AT‐rich sequence‐binding protein 2 (circSATB2) was identified as an oncogene in lung cancer. This study was performed to explore the association of circSATB2 with exosomes and the regulatory mechanism of circSATB2. Exosomes could transmit circSATB2 into lung cancer cells. Exosomes enhanced cell proliferation, invasion, and migration by carrying circSATB2. Exosomal circSATB2 abrogated the inhibitory effect of short hairpin (sh)‐circSATB2 on lung cancer progression. Moreover, circSATB2 promoted tumor growth in vivo via exosomes. CircSATB2 interacted with microRNA‐330‐5p (miR‐330‐5p) and miR‐330‐5p targeted pseudopodium enriched atypical kinase 1 (PEAK1). In addition, circSATB2 affected the PEAK1 level via sponging miR‐330‐5p in lung cancer cells. All results suggested that exosomal transfer of circSATB2 contributed to the malignant development of lung cancer by acting as a sponge of miR‐330‐5p to upregulate PEAK1. [ABSTRACT FROM AUTHOR]

Background: For advanced nonsquamous non‐small cell lung cancer (NSCLC), the mechanisms of resistance to first‐line immunotherapy are not clear. Immune checkpoint inhibitors (ICIs) in combination with agents targeting other pathways may serve as second‐line therapy options. Apatinib (a vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor) could increase the efficacy of camrelizumab (an ICI agent). The efficacy and safety of this combination regimen as a second‐line therapy for NSCLC patients after failure on first‐line immunotherapy has not previously been evaluated. Methods: In this single‐arm, multicenter, phase II trial, metastatic nonsquamous NSCLC patients previously treated with single‐agent ICI or ICI plus chemotherapy will be enrolled. Participants will receive intravenous camrelizumab 200 mg D1 and oral apatinib 250 mg D1‐21 for a 21‐day cycle. The study treatment will continue until disease progression, unacceptable toxicity, or withdrawal of consent. The primary endpoint is progression‐free survival by investigator. Secondary endpoints are overall survival, objective response rate, disease control rate, duration of response by investigator, quality of life, safety, and toxicity. Conclusions: This trial will provide evidence of the benefit of treatment with camrelizumab combined with apatinib in advanced nonsquamous NSCLC patients who were previously treated with first‐line immunotherapy. [ABSTRACT FROM AUTHOR]

Background: Non‐small cell lung cancer (NSCLC) is one of the most malignant cancers worldwide and its pathogenesis is not completely clear. In this study, we explored the functions and mechanisms of exosomes transferring miR‐3180‐3p in NSCLC progression. Methods: The expression levels of miR‐3180‐3p in NSCLC tissues and paracarcinoma tissues was obtained from the GEO database (GEO: GSE53882). Exosomes derived from A549 cells were identified. Proliferation, migration and invasion were measured after treatment with exosomal miR‐3180‐3p or transfection using miR‐3180‐3p mimics. The relationship between miR‐3180‐3p and forkhead box P4 (FOXP4) was predicted using a bioinformatic tool and measured using a dual‐luciferase reporter gene assay and western blotting. Finally, a mouse xenograft model of NSCLC cells was established to verify the function of exosomal miR‐3180‐3p in vivo. Results: We found that miR‐3180‐3p decreased in both NSCLC cell lines and patient tissues. Overexpression of miR‐3180‐3p or treatment with exosomal miR‐3180‐3p significantly suppressed cell proliferation and metastasis in NSCLC cell lines. Subsequently, we found miR‐3180‐3p downregulated FOXP4 protein expression levels. Furthermore, the volumes and weights of nude mouse tumors expressing exosomal miR‐3180‐3p were significantly reduced. Conclusions: Exosomal miR‐3180‐3p suppresses NSCLC progression by downregulating FOXP4 expression. Key points: Significant findings of the study: We found that exosomal miR‐3180‐3p suppressed NSCLC progression and also identified a miR‐3180‐3p target gene. These findings provide a foundation to determine innovative therapeutic strategies. What this study adds: This study contributes to research investigating exosomal containing miRNAs. [ABSTRACT FROM AUTHOR]

Anatomical segment‐based or subsegmental resection for early lung cancer surgery has been used in selected cases, although postoperative complications of bronchopleural fistula sometimes occur. Persistent air leaks can cause complications such as empyema and aspiration pneumonia, resulting in prolonged patient hospitalization. The traditional treatment for postoperative bronchopleural fistula is reoperation, but the advent of bronchoscopic interventional therapy usually prevents patients from needing a second operation. This article details a case of thoracoscopic segmentectomy of the left lower lung dorsal segment resulting in residual subsegmental pleural fistula, and because the use of pleural adhesives made the patient's fistula inappropriate for surgical repair, we finally used bronchoscopic injury of the airway mucosa combined with an absorbable gelatin sponge and an autologous blood closure method for successful treatment. [ABSTRACT FROM AUTHOR]

Kirsten rat sarcoma viral oncogene homolog (KRAS) is one of the most common mutant oncogenes in non‐small cell lung cancer (NSCLC). The survival of patients with KRAS mutations may be much lower than patients without KRAS mutations. However, due to the complex structure and diverse biological properties, it is difficult to achieve specific inhibitors for the direct elimination of KRAS activity, making KRAS a challenging therapeutic target. At present, with the tireless efforts of medical research, including KRAS G12C inhibitors, immunotherapy and other combination strategies, this dilemma is expected to an end. In addition, inhibition of the downstream signaling pathways of KRAS may be a promising combination strategy. Given the rapid development of treatments, understanding the details will be important to determine the individualized treatment options, including combination therapy and potential resistance mechanisms. The survival of patients with KRAS mutations may be much lower than patients without KRAS mutations. At present, with the tireless efforts of medical research, including KRAS G12C inhibitors, immunotherapy and other combination strategy, this dilemma of KRAS mutated NSCLC is expected to an end. [ABSTRACT FROM AUTHOR]

Background This study was conducted to explore programmed cell death-ligand-1 ( PD-L1) expression and fibroblast growth factor receptor 1 ( FGFR1) amplification in stage IIIB/IV lung squamous cell carcinoma ( SQC). Correlations between PD-L1 and FGFR1, and with clinicopathological characteristics, efficacy of platinum-based chemotherapy, and prognosis were analyzed. Methods One hundred and twenty-eight consecutive stage III/IV SQC patients were enrolled in this study from 2009 to 2014. Seventy-eight patients received platinum-based chemotherapy. Immunohistochemistry was used to assess PD-L1 expression and fluorescence in situ hybridization was applied to detect FGFR1 amplification. Results PD-L1 expression was detected in 61.7% (79/128) of lung SQC patients. Smokers had significantly higher PD-L1 expression rates than non-smokers (66.1% vs. 44.0%, P = 0.042, respectively). The objective response and disease control rates for platinum-based chemotherapy were not significantly different between PD-L1 negative and positive patients (43.3% vs. 36.2%, P = 0.434; 80.0% vs. 78.7% P = 0.840, respectively); however, overall survival in PD-L1-negative patients was significantly longer than in PD-L1-positive patients (41.5 vs. 19.3 months, P = 0.001). Twenty-five percent (32/128) of patients displayed FGFR1 amplification, with a lower rate in stage III patients compared to stage IV (17.1% vs. 36.5%, P = 0.013, respectively). There was no significant difference in FGFR1 amplification levels between overall response, disease control or overall survival rates. No correlation was observed between PD-L1 expression and FGFR1 amplification ( P = 0.916). Conclusion PD-L1 expression may function as a prognostic factor in Chinese stage III/IV SQC patients. FGFR1 amplification is more prevalent in late stage SQC patients but does not predict chemotherapy response. There is no apparent correlation between PD-L1 expression and FGFR1 amplification. [ABSTRACT FROM AUTHOR]

Background The aim of this study was to compare the short-term outcomes and three-year survival between dual-incision esophagectomy ( DIE) and total minimally invasive Mc Keown esophagectomy ( MIME) for esophageal cancer patients with negative upper mediastinal lymph nodes requiring esophagectomy and neck anastomosis. Methods One hundred and fifty patients underwent DIE, while 361 patients received total MIME. Perioperative outcomes and three-year survival were compared in unmatched and propensity score matched data between two groups. Results Both unmatched and matched analysis demonstrated that there were no significant differences in the number of lymph nodes harvested, or major or minor complication rates between the DIE and MIME groups. Compared with patients who underwent DIE, patients who underwent total MIME had longer operation duration (310 minutes vs. 345 minutes; P = 0.002). However, there was significantly less intraoperative blood loss in the total MIME compared with the DIE group (191 m L vs. 287 m L, respectively; P < 0.001). Kaplan- Meier analysis demonstrated a trend that patients who underwent MIME had longer overall (79.5% vs. 64.1%; P = 0.063) and disease-free three-year survival (65.3% vs. 82.8%; P = 0.058) compared with patients who underwent DIE. Conclusions Both total MIME and DIE are feasible for the surgical treatment of esophageal cancer patients with negative upper mediastinal lymph nodes requiring esophagectomy and neck anastomosis. However, MIME was associated with better overall and disease-free three-year survival compared with DIE. [ABSTRACT FROM AUTHOR]