The optimal timing for initiating supplemental parenteral nutrition in chemotherapy- induced severe granulocytopenia in patients with lung cancer remains uncertain.A retrospective study was conducted among patients with lung cancer from February 2016 to June 2018. In total, 182 eligible patients were included and divided into 2 groups according to the time of supplemental parenteral nutrition intervention: early initiation (within 72 hours of development of granulocytopenia) and late initiation (over 72 hours). The primary outcomes of the study were bacterial infection and fungal infection, and the secondary outcomes were duration of absolute neutrophil count less than 1.0×109 cells/L, length of hospital stay, mortality rate, and rate of chemotherapy (4 cycles) completion.The incidence rates of bacterial infection and fungal infection were significantly lower among patients who received supplemental parenteral nutrition early than among patients who received it late. No significant difference in mortality was observed between the groups. In addition, compared with late supplemental parenteral nutrition, early supplemental parenteral nutrition was associated with a higher rate of completion of 4 chemotherapy cycles and shorter hospital stays and leukocyte recovery periods in our cohort. Univariate and multivariate logistic regression analyses revealed that the subgroup of patients with an NRS-2002 score of 2 benefited from early supplemental parenteral nutrition.Early supplemental parenteral nutrition after chemotherapy-induced severe granulocytopenia could reduce the risk of infection, improve the likelihood of chemotherapy completion, and shorten hospital stays and leukocyte recovery times.
Oncolytic viruses (OVs) could be the next breakthrough in oncology. The primary objective of this study was to gain a more thorough understanding of OVs in advanced malignancies. This study reviewed 161 clinical studies, including 4,300 patients with advanced cancer. We summarized the antitumor immune response and clinical response to OVs. Moreover, TRAEs, adverse events attributable to OVs, were summarized by grade. 52 (52/161, 32.3%) studies assessed the tumor microenvironment, most of which reported that CD8 + T cells (N = 31) and PD-L1 (N=9) were increased. 60 (60/161, 37.3%) studies reported increased systemic immune responses, including IFN-γ (N=27), IL-6 (N=22) and CD8 + T cells (N=20). A total of 106 (106/161, 65.8%) studies evaluated clinical efficacy in 2,631 patients, with objective response and disease control rates of 621 (23.6%) and 1603 (60.9%), respectively. Subgroup analysis showed an objective response in 352 (30.8%) and disease control in 704 (62.2%) of 1143 patients in the HSV subgroup. The percentages of patients with objective response and disease control for different administration routes, including intratumoral injection (25.8%; 62.2%) and intravenous injection (20.2%; 56.8%), and for different treatment options, including combination therapy (31.3%; 69.8%) and OVs monotherapy (17.8%; 54.3%), were summarized. For different combination therapies, OVs plus immunotherapy may be promising, with objective response and disease control at elevated proportions (39.6%; 66.3%). Moreover, OVs demonstrated a manageable safety profile, with most TRAEs being grade 1-2. In summary, OVs that activate innate and specific immune responses that ultimately enhance the antitumor response deserve further investigation.
Background: Increasing bodies of evidence reveal that targeting a programmed cell death protein 1 (PD-1) monoclonal antibody is a promising immunotherapy for lung adenocarcinoma.Although PD receptor ligand 1 (PDL1) expression is widely recognized as the most powerful predictive biomarker for anti-PD-1 therapy, its regulatory mechanisms in lung adenocarcinoma remain unclear.Therefore, we conducted this study to explore differentially expressed genes (DEGs) and elucidate the regulatory mechanism of PDL1 in lung adenocarcinoma.Methods: The GSE99995 data set was obtained from the Gene Expression Omnibus (GEO) database.Patients with and without PDL1 expression were divided into PDL1-positive and PDL1-negative groups, respectively.DEGs were screened using R.The Gene Ontology (GO) database and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed using the Database for Annotation, Visualization and Integrated Discovery .Protein-protein interaction (PPI) networks of DEGs was visualized using Cytoscape, and the MNC algorithm was applied to screen hub genes.A survival analysis involving Gene Expression Profiling Interactive Analysis was used to verify the GEO results.Mutation characteristics of the hub genes were further analyzed in a combined study of five datasets in The Cancer Genome Atlas (TCGA) database.Results:In total, 869 DEGs were identified, 387 in the PDL1-positive group and 482 in the PDL1negative group.GO and KEGG analysis results of the PDL1-positive group mainly exhibited enrichment of biological processes and pathways related to cell adhesion and peroxisome proliferators-activated receptors (PPAR) signaling pathway, whereas biological process and pathways associated with cell division and repair were mainly enriched in the PDL1negative group.The top 10 hub genes were screened during the PPI network analysis.Notably, survival analysis revealed BRCA1, mainly involved in cell cycle and DNA damage responses, to be a novel prognostic indicator in lung adenocarcinoma.Moreover, the
Background: Increasing bodies of evidence reveal that targeting a programmed cell death protein 1 (PD-1) monoclonal antibody is a promising immunotherapy for lung adenocarcinoma.Although PD receptor ligand 1 (PDL1) expression is widely recognized as the most powerful predictive biomarker for anti-PD-1 therapy, its regulatory mechanisms in lung adenocarcinoma remain unclear.Therefore, we conducted this study to explore differentially expressed genes (DEGs) and elucidate the regulatory mechanism of PDL1 in lung adenocarcinoma.Methods: The GSE99995 data set was obtained from the Gene Expression Omnibus (GEO) database.Patients with and without PDL1 expression were divided into PDL1-positive and PDL1-negative groups, respectively.DEGs were screened using R.The Gene Ontology (GO) database and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed using the Database for Annotation, Visualization and Integrated Discovery .Protein-protein interaction (PPI) networks of DEGs was visualized using Cytoscape, and the MNC algorithm was applied to screen hub genes.A survival analysis involving Gene Expression Profiling Interactive Analysis was used to verify the GEO results.Mutation characteristics of the hub genes were further analyzed in a combined study of five datasets in The Cancer Genome Atlas (TCGA) database.Results:In total, 869 DEGs were identified, 387 in the PDL1-positive group and 482 in the PDL1negative group.GO and KEGG analysis results of the PDL1-positive group mainly exhibited enrichment of biological processes and pathways related to cell adhesion and peroxisome proliferators-activated receptors (PPAR) signaling pathway, whereas biological process and pathways associated with cell division and repair were mainly enriched in the PDL1negative group.The top 10 hub genes were screened during the PPI network analysis.Notably, survival analysis revealed BRCA1, mainly involved in cell cycle and DNA damage responses, to be a novel prognostic indicator in lung adenocarcinoma.Moreover, the
Background: Increasing bodies of evidence reveal that targeting a programmed cell death protein 1 (PD-1) monoclonal antibody is a promising immunotherapy for lung adenocarcinoma.Although PD receptor ligand 1 (PDL1) expression is widely recognized as the most powerful predictive biomarker for anti-PD-1 therapy, its regulatory mechanisms in lung adenocarcinoma remain unclear.Therefore, we conducted this study to explore differentially expressed genes (DEGs) and elucidate the regulatory mechanism of PDL1 in lung adenocarcinoma.Methods: The GSE99995 data set was obtained from the Gene Expression Omnibus (GEO) database.Patients with and without PDL1 expression were divided into PDL1-positive and PDL1-negative groups, respectively.DEGs were screened using R.The Gene Ontology (GO) database and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed using the Database for Annotation, Visualization and Integrated Discovery .Protein-protein interaction (PPI) networks of DEGs was visualized using Cytoscape, and the MNC algorithm was applied to screen hub genes.A survival analysis involving Gene Expression Profiling Interactive Analysis was used to verify the GEO results.Mutation characteristics of the hub genes were further analyzed in a combined study of five datasets in The Cancer Genome Atlas (TCGA) database.Results:In total, 869 DEGs were identified, 387 in the PDL1-positive group and 482 in the PDL1negative group.GO and KEGG analysis results of the PDL1-positive group mainly exhibited enrichment of biological processes and pathways related to cell adhesion and peroxisome proliferators-activated receptors (PPAR) signaling pathway, whereas biological process and pathways associated with cell division and repair were mainly enriched in the PDL1negative group.The top 10 hub genes were screened during the PPI network analysis.Notably, survival analysis revealed BRCA1, mainly involved in cell cycle and DNA damage responses, to be a novel prognostic indicator in lung adenocarcinoma.Moreover, the
Background: Increasing bodies of evidence reveal that targeting a programmed cell death protein 1 (PD-1) monoclonal antibody is a promising immunotherapy for lung adenocarcinoma.Although PD receptor ligand 1 (PDL1) expression is widely recognized as the most powerful predictive biomarker for anti-PD-1 therapy, its regulatory mechanisms in lung adenocarcinoma remain unclear.Therefore, we conducted this study to explore differentially expressed genes (DEGs) and elucidate the regulatory mechanism of PDL1 in lung adenocarcinoma.Methods: The GSE99995 data set was obtained from the Gene Expression Omnibus (GEO) database.Patients with and without PDL1 expression were divided into PDL1-positive and PDL1-negative groups, respectively.DEGs were screened using R.The Gene Ontology (GO) database and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed using the Database for Annotation, Visualization and Integrated Discovery .Protein-protein interaction (PPI) networks of DEGs was visualized using Cytoscape, and the MNC algorithm was applied to screen hub genes.A survival analysis involving Gene Expression Profiling Interactive Analysis was used to verify the GEO results.Mutation characteristics of the hub genes were further analyzed in a combined study of five datasets in The Cancer Genome Atlas (TCGA) database.Results:In total, 869 DEGs were identified, 387 in the PDL1-positive group and 482 in the PDL1negative group.GO and KEGG analysis results of the PDL1-positive group mainly exhibited enrichment of biological processes and pathways related to cell adhesion and peroxisome proliferators-activated receptors (PPAR) signaling pathway, whereas biological process and pathways associated with cell division and repair were mainly enriched in the PDL1negative group.The top 10 hub genes were screened during the PPI network analysis.Notably, survival analysis revealed BRCA1, mainly involved in cell cycle and DNA damage responses, to be a novel prognostic indicator in lung adenocarcinoma.Moreover, the
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