Esophageal cancer (EC) is the sixth most deadly cancer, and its incidence is still increasing year by year. Although the researches on the molecular mechanisms of EC have been widely carried out and incremental progress has been made, its overall survival rate is still low. There is cumulative evidence showing that the esophageal microenvironment plays a vital role in the development of EC. In precancerous lesions of the esophagus, high-risk environmental factors can promote the development of precancerous lesions by inducing the production of inflammatory factors and the recruitment of immune cells. In the tumor microenvironment, tumor-promoting cells can inhibit anti-tumor immunity and promote tumor progression through a variety of pathways, such as bone marrow-derived suppressor cells (MDSCs), tumor-associated fibroblasts (CAFs), and regulatory T cells (Tregs). The formation of extracellular hypoxia and acidic microenvironment and the change of extracellular matrix stiffness are also important factors affecting tumor progression and metastasis. Simultaneously, primary tumor-derived cytokines and bone marrow-derived immune cells can also promote the formation of pre-metastasis niche of EC lymph nodes, which are beneficial to EC lymph node metastasis. Further research on the specific mechanism of these processes in the occurrence, development, and metastasis of each EC subtype will support us to grasp the overall pre-cancerous prevention, targeted treatment, and metastatic assessment of EC.

Background: Pulmonary carcinosarcomas (PCSs) are a heterogeneous group of non-smallcell lung carcinomas (NSCLCs) with aggressiveness and a poor prognosis. Although genetic mutations of some common lung cancer subtypes have been extensively studied, the molecular characteristics of PCSs and the existence of abnormal target genes are unknown. Methods: In this study, the clinical and molecular characterization in 3 pulmonary sarcomatoid carcinomas (PSCs) were presented using microscope analysis and next-generation sequencing (NGS) analysis. Results: The results revealed a carcinosarcomas subtype presenting squamous cell carcinoma and sarcoma components in all 3 cases. NGS analysis showed that 182, 316 and 230 shared mutations were detected between sarcoma and lung carcinoma from 3 patients. Two identical alterations in two genes (CSMD3 and RYR3) that were all shared by the two components in 3 patients. Tumor suppressor gene TP53 (5/6, 83%) showed the highest mutation frequency for driver genes here. Additionally, we focused on an LYST mutation which was mainly present in the sarcoma components. Moreover, the clonal evolution and signature analysis confirm that lung squamous cell carcinoma and sarcoma in each PCS patient may have come from a common ancestor, and mutagenesis was possibly related to indirect effects of tobacco, age or other unknown factors. Conclusion: Our results indicate that genetic analysis and molecular targeted therapy are necessary for the identification and treatment of these rare lung tumors. CSMD3 and LYST, as common mutation genes, may be a potential therapeutic target in PCS.

OBJECTIVES To compare the perioperative and follow-up outcomes of patients with myasthenia gravis (MG) receiving subxiphoid-subcostal or unilateral thoracoscopic thymectomy and to identify the factors affecting MG prognosis. METHODS From January 2013 to December 2019, a total of 137 consecutive MG patients received subxiphoid-subcostal thoracoscopic thymectomy (STT, n = 65) or conventional unilateral thoracoscopic thymectomy (UTT, n = 72). The primary outcomes of this study were perioperative complications, duration and expenses of hospitalization, VAS score and complete stable remission (CSR). RESULTS The patients receiving STT had significantly shorter drainage duration and postoperative hospital stay and lower hospitalization expenses (P < 0.01). Pain scores on postoperative Days 1, 3, 7 and 14 were significantly lower in patients undergoing STT (P < 0.01). The average follow-up was 54.3 ± 24.18 months, with a CSR rate of 30.6% and an overall effective rate of 87.3%. Through uni- and multivariable analyses, shorter symptom duration and Myasthenia Gravis Foundation of America (MGFA) class I were independent predictors for CSR in MG patients receiving thymectomy. CONCLUSIONS The present study not only showed that STT was a safe and feasible technique for MG, with a potentially faster postoperative recovery, lower hospitalization expenses, less postoperative pain and equivalent remission rate, but also revealed that shorter symptom duration and MGFA class I were favourable prognostic factors for CSR.

Tumor metastasis is still an insurmountable obstacle in tumor treatment. Lung cancer represents one of the most common malignancies with high morbidity worldwide. hnRNPA1 has been reported to be involved in the regulation of tumor metastasis, while its specific role in tumor metastasis seems to be controversial and its molecular mechanism in lung cancer metastasis remains to be further elucidated. In this study, we confirmed that knockdown of the hnRNPA1 led to enhanced migration, invasion and EMT transition in lung cancer cells. Bioinformatics analysis of the GSE34992 dataset revealed that hnRNPA1 may regulate the alternative splicing (AS) of LAS1L exon 9. Further AGE assays and RIP assays revealed that hnRNPA1 can directly bind to the LAS1L pre-mRNA to inhibit the splicing of LAS1L exon 9. The RNA pull-down assays showed that hnRNPA1 can specifically bind to the two sites (UAGGGU(WT1) and UGGGGU(WT3)) of LAS1L Intron 9. Further Transwell assays indicated that the expression ratio of LAS1L-L/LAS1L-S regulated by hnRNPA1 can further promote the migration, invasion and EMT transition in lung cancer cells. Moreover, hnRNPA1 expression showed significant heterogeneity in lung cancer tissues, which may contain new research directions and potential therapeutic targets. Our results indicate that hnRNPA1 can affect the metastasis of lung cancer cells by modulating the AS of LAS1L exon 9, highlighting the potential significance of hnRNPA1 in lung cancer metastasis.