Apatinib (Aitan®, brand name in China) is a new anti-antiangiogenic agent that has recently been approved for the treatment of advanced gastric cancer (GC) in China. Nevertheless, its therapeutic efficacy against other types of advanced solid tumors remains unclear. This meta-analysis examines the short-term efficacy and safety of apatinib or combination therapy for GC, hepatocellular carcinoma (HCC) and non-small-cell lung cancer (NSCLC); and provides a discussion of its anti-angiogenesis therapy applications. Seven clinical studies met the inclusion criteria. The treatment of cancers using apatinib was more successful compared to therapy without apatinib. Both objective response rates (ORRs) and disease control rates (DCRs) were significantly improved in the apatinib group compared to those in the control group (RR=2.18, 95% CI 1.30–3.65; RR=2.09, 95% CI 1.21–3.60). The DCR of 850 mg qd and 750 mg qd were higher than those in the control group (P<0.05). Based on the short-term acute adverse reactions of apatinib, significant differences between groups were found for hypertension, urine protein, hand foot syndrome, and gastrointestinal reactions (diarrhea), while no significant differences were found for myelosuppression, nausea and vomiting. Moreover, the results showed that apatinib prolonged patient survival (HR=0.38, 95% CI: 0.28–0.52), and the effect was more pronounced in patients treated with 750 mg qd or 850 mg qd of apatinib than in those treated with a dose of ≤500 mg qd. Additionally, compared to its second-line application, the third-line application was shown to further reduce the risk ratio in patients. Furthermore, overall survival was longer in patients treated with apatinib. Apatinib was shown to have certain short-term effects and survival benefits on GC, HCC, and NSCLC with controllable adverse effects.

Background Cervical cancer as one of the most common malignant tumors lead to bad prognosis among women. Some researches already focus on the carcinogenesis and pathogenesis of cervical cancer, but it is still necessary to identify more key genes and pathways. Methods Differentially expressed genes were identified by GEO2R from the gene expression omnibus (GEO) website, then gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyzed by DAVID. Meanwhile, protein–protein interaction network was constructed by STRING, and both key genes and modules were found in visualizing network through Cytoscape. Besides, GEPIA did the differential expression of key genes and survival analysis. Finally, the expression of genes related to prognosis was further explored by UNLCAN, oncomine, and the human protein atlas. Results Totally 57 differentially expressed genes were founded, not only enriched in G1/S transition of mitotic cell cycle, mitotic nuclear division, and cell division but also participated in cytokine–cytokine receptor interaction, toll‐like receptor signaling pathway, and amoebiasis. Additionally, 12 hub genes and 3 key modules were screened in the Cytoscape visualization network. Further survival analysis showed that TYMS (OMIM accession number ), MCM2 (OMIM accession number ), HELLS (OMIM accession number ), TOP2A (OMIM accession number ), and CXCL8 (OMIM accession number ) were associated with the prognosis of cervical cancer. Conclusion This study aim to better understand the characteristics of some genes and signaling pathways about cervical cancer by bioinformatics, and could provide further research ideas to find new mechanism, more prognostic factors, and potential therapeutic targets for cervical cancer.

Background:With the development of research on cancer genomics and microenvironment, a new era of oncology focusing on the complicated gene regulation of pan-cancer research and cancer immunotherapy is emerging. This study aimed to identify the common gene expression characteristics of multiple cancers -lung cancer, liver cancer, kidney cancer, cervical cancer, and breast cancer -and the potential therapeutic targets in public databases. Material/Methods:Gene expression analysis of GSE42568, GSE19188, GSE121248, GSE63514, and GSE66272 in the GEO database of multitype cancers revealed differentially expressed genes (DEGs). Then, GO analysis, KEGG function, and path enrichment analyses were performed. Hub-genes were identified by using the degree of association of protein interaction networks. Moreover, the expression of hub-genes in cancers was verified, and hub-generelated survival analysis was conducted. Finally, infiltration levels of tumor immune cells with related genes were explored. Results:We found 12 cross DEGs in the 5 databases (screening conditions: "adj p<0.05" and "logFC>2 or logFC<-2"). The biological processes of DEGs were mainly concentrated in cell division, regulation of chromosome segregation, nuclear division, cell cycle checkpoint, and mitotic nuclear division. Furthermore, 10 hub-genes were obtained using Cytoscape: TOP2A, ECT2, RRM2, ANLN, NEK2, ASPM, BUB1B, CDK1, DTL, and PRC1. The high expression levels of the 10 genes were associated with the poor survival of these multiple cancers, as well as ASPM, may be associated with immune cell infiltration. Conclusions:Analysis of the common DEGs of multiple cancers showed that 10 hub-genes, especially ASPM and CDK1, can become potential therapeutic targets. This study can serve as a reference to understand the characteristics of different cancers, design basket clinical trials, and create personalized treatments.

Background: Limited therapeutic options are available for advanced LUAD without driver gene mutations. Anti-CDK therapy has shown effectiveness in several kind of cancers, however, the mechanisms still need to be elucidated. Materials and Methods: The lncRNA associated with CDK1 and the immunomodulatory factors that regulate CDK1 were found by bioinformatics analysis and experimental verification. The prognostic model and immune resistance mechanism of lung adenocarcinoma were revealed by single cell analysis, immune infiltration analysis, and signal pathway analysis. Results: LINC00261 was found to be an important CDK1-related lncRNA with a better prognosis in LUAD. In addition, high CDK1 expression indicates a poor immunotherapy response, which may be associated with overexpression of CXCL8. CXCL8 decreased in patients who were immunotherapy-responsive but increased in patients who were immunotherapy-resistant. Signaling pathway analysis suggested that increased CXCL8 and decreased LINC00261 may participate in hypoxia-induced tumor angiogenesis and cause a poor prognosis for the patients. CXCL8 and CDK1 may change G2-M transformation and EMT and promote tumor proliferation. Conclusion: This study explained that LINC00261, CDK1, and CXCL8 may have a mutual regulation relationship, which affects the occurrence of LUAD and the efficacy of immunotherapy.

No abstract