AbstractBackgroundA growing body of evidence indicates that aberrant expression of miR-107 plays a core role in cancers. This study aims to demonstrate the function of miR-107 and its roles in chemo-drug resistance in breast cancer cells.MethodologyCCK-8 assays were carried out to test the effect of miR-107 mimics on the proliferation of MCF-7 cells. The apoptosis level of each group was detected by flow cytometry. miR-107 level, mRNA levels of Bcl-2/Bax and TRIAP1 were detected by quantitative real-time Polymerase Chain Reaction (qRT-PCR) analysis. Protein levels of Bcl-2/Bax, p-Akt/Akt in MCF-7 cells were detected by using Western Blot. Lastly, the dual luciferase reporter gene assay system was used to confirm interaction between miR-107 and its target gene TRIAP1.ResultsCCK-8 assays indicated that miR-107 mimics augmented Taxol-induced cell viability inhibition. Flow cytometry showed that miR-107 mimics augmented Taxol-induced elevation of cell apoptosis. qRT-PCR analysis revealed that miR-107 mimics inhibited the mRNA expression of Bcl-2 and induced the mRNA level of Bax. Western Blotting indicated that miR-107 mimics inhibited the expression of proteins Bcl-2 and p-Akt, and induced the expression of Bax, while showing no significant effects on Akt. The relative luciferase activity revealed that oncogene TRIAP1 is a potential target gene of miR-107.ConclusionsmiR-107 plays a role in regulating chemo-drug sensitivity in mammary cancer cell by targeting TRIAP1.

Background We describe the clinical features, genetic profile, and their correlation in NSCLC patients. Methods A total of 256 Chinese patients with NSCLC were enrolled in this study. NGS‐based genomic profiling of major lung cancer‐related genes was performed on formalin‐fixed paraffin‐embedded tumor samples. Results Of 256 patients with NSCLC, 219 were adenocarcinoma and most of them were in the early stage. Among patients, 63.3% patients have more than two gene mutations. By analyzing variant allele frequency (VAF), we found that the median VAF has significant differences between squamous cell carcinoma and adenocarcinoma, as well as early stage and advanced stage. The frequency of mutations in EGFR, MET, and RET were significantly higher in nonsmokers than in smokers. Besides, Pearson correlation analysis found that ALK, BRAF, and MET mutations had a strong correlation with age. Notably, higher frequencies of ALK and BRAF alterations were associated with younger age, while more frequent MET mutations appear in the patients at age 55 or older. Conclusion More unique features of cancer driver genes in Chinese NSCLC were identified by next‐generation sequencing. These findings highlighted that it is necessary to carry out targeted detection according to different clinical features for NSCLC.

More than half of new cases of hepatocellular carcinoma (HCC) and associated deaths occurring annually worldwide are recorded in China. Chinese patients with HCC exhibit special characteristics in terms of etiology, leading to differences in prognosis versus Western patients. In recent years, several angiogenesis inhibitors were approved, and immune checkpoint blockers (ICBs) were recommended as second-line therapy for advanced HCC. In addition, the recent success of a combination of atezolizumab with bevacizumab signals resulted in an essential change in the first-line treatment of HCC. We investigated the characteristics of patients with HCC in China and summarized the rapidly emerging relevant clinical data, which relate to the prospects and challenges associated with the use of ICBs in this setting. We further evaluated the efficacy of ICBs in Chinese patients with HCC based on data obtained from global trials, and discussed possible factors influencing the effectiveness of ICBs in patients with HCC in China. Immunotherapy offers new options for the treatment of advanced HCC, though responses varied between patients. Currently, there is a need to discover specific biomarkers for the accurate identification of patients who would more likely benefit from immunotherapy. Furthermore, investigation of patient characteristics in different countries is necessary to provide a clinical practice basis and reference value for the diagnosis and treatment of HCC.

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We presented a 67-year-old nonsmoking female lung adenocarcinoma patient with novel epidermal growth factor receptor (EGFR) A289G/F287_G288insHA cis mutations who responded positively to sintilimab combined with regorafenib and albumin paclitaxel, and sequential treatment of icotinib. Gene mutations in patients were detected by next-generation sequencing (NGS) technology, and changes in gene mutations before and after treatments were observed by ctDNA monitoring. We observed the efficacy of the patient through chest computed tomography (CT) imaging and carcinoembryonic antigen (CEA) level and found that the patient benefited from immunotherapy in combination with antiangiogenesis and chemotherapy for more than 1 year, CEA levels initially fell sharply and then rebounded during the treatment period. After changing to EGFR-TKI therapy, the CEA level of the patient does not only decreased sharply at the initial stage of treatment but also rebounded and increased at the later stage of treatment. The patient was tested for genetic mutations after 4 months of sequential EGFR-TKI therapy and was found to have lost all previous EGFR mutations, which may be the cause of resistance to targeted drug icotinib. We believe that our findings have enriched the EGFR mutation spectrum in NSCLC and highlighted the possible choice for patients harboring this mutation by immunotherapy combined with chemotherapy and antivascular therapy, and EGFR-TKI-targeted therapy.