Metabolic disorders and abnormal immune function changes occur in tumor tissues and cells to varying degrees. There is increasing evidence that reprogrammed energy metabolism contributes to the development of tumor suppressive immune microenvironment and influences the course of gastric cancer (GC). Current studies have found that tumor microenvironment (TME) also has important clinicopathological significance in predicting prognosis and therapeutic efficacy. Novel approaches targeting TME therapy, such as immune checkpoint blockade (ICB), metabolic inhibitors and key enzymes of immune metabolism, have been involved in the treatment of GC. However, the interaction between GC cells metabolism and immune metabolism and how to make better use of these immunotherapy methods in the complex TME in GC are still being explored. Here, we discuss how metabolic reprogramming of GC cells and immune cells involved in GC immune responses modulate anti-tumor immune responses, as well as the effects of gastrointestinal flora in TME and GC. It is also proposed how to enhance anti-tumor immune response by understanding the targeted metabolism of these metabolic reprogramming to provide direction for the treatment and prognosis of GC.
Background:The 5-year overall survival rate in metastatic prostate adenocarcinoma (PRAD) is extremely low. Genomic studies of PRAD have improved our understanding of disease biology. However, the role of immune checkpoint genes (ICGs) in PRAD remains unclear.Methods: Univariate and multivariate analyses were used to analyze genes associated with metastasisfree survival (MFS) in The Cancer Genome Atlas (TCGA)-PRAD dataset. The expressions of ADORA2A and TNFRSF18 were detected via immunohistochemical assay and real-time fluorescence quantitative PCR (RT-PCR) assay in our in-house cohort. The expression of long non-coding RNAs (lncRNAs) AL139287.1, SLC9A3-AS1, and SNHG12 were detected via RT-PCR assay in our in-house cohort. Stepwise regression, Cox regression, and nomogram analyses were used to evaluate the prognostic role of these genes in both the TCGA dataset and in-house cohort. The "pRRophetic" R package was used to evaluate drug sensitivity in the TCGA cohort according to the gene mRNA expression level.Results: In our study, univariate and multivariate analyses revealed that the mRNA expressions of two ICGs, ADORA2A and TNFRSF18, were independent factors affecting MFS in PRAD patients. A prognostic 2-ICG model predicted the MFS of PRAD patients with medium-to-high accuracy in the TCGA dataset and in-house cohort. The expressions of AL139287.1, SLC9A3-AS1, and SNHG12 were correlated with ADORA2A and TNFRSF18. A prognostic lncRNA-ICG model predicted the MFS of PRAD patients with medium-to-high accuracy in the TCGA dataset and in-house cohort. In addition, correlation analyses between the sensitivity of doxorubicin, erlotinib, gemcitabine, or vinorelbine and AL139287.1, SLC9A3-AS1, SNHG12, ADORA2A, and TNFRSF18 were conducted.Conclusions: Our results provide new targets for predicting tumor metastasis in PRAD and treating patients with metastatic PRAD.
Background To investigate the association between XRCC1 Arg194Trp, Arg280His and Arg399Gln polymorphisms and breast cancer (BC) risk, fifteen previous meta-analyses and large amounts of original articles had been published but drew conflicting conclusions. Because of lacking credibility analysis, the positive results of the previous meta-analyses were quite suspicious. Objectives We performed an updated meta-analysis to solve the controversy in compliance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Methods All results of the current meta-analysis were evaluated comprehensively based on concerning credibility. Results With 74 studies including 31,166 cases and 34,669 controls, XRCC1 Arg399Gln polymorphism significantly increased BC risk in overall and subgroups (Asians, Indians, Africa, Asia and North America), and it was again demonstrated in Asians and Asia by further sensitivity analyses. As 45 studies with 17,239 cases and 19,026 controls pooled to explore the role of Arg194Trp polymorphism in BC risk, no significant results were found in overall and any ethnicity and geographic region, and there was a decreased BC risk in post-menopausal and an increased BC risk in pre-menopausal. The Arg280His polymorphism analyses, involving 18 studies with 9,571 cases and 10,108 controls, did not find an association with BC risk in overall and any ethnicity and region, but an increased BC risk was found in overall and Asians living in Asia in sensitivity analyses. However, all significant results were taken for less credible after we comprehensively analyzed with heterogeneity characteristics, the quality of involved studies and Bayesian false-discovery probability (BFDP) to evaluate the credibility of significant results. Conclusion The issue about false-positive results should be taken seriously and more high-quality original studies still have plenty of value to be significantly developed.
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