With the continuous development of immunotherapy, researchers have paid more attention to the specific immune regulatory mechanisms of various immune responses in different diseases. As a novel and vital innate immune signal pathway, the cGAS-STING signal pathway activated by nucleic acid substances, interplays with other immune responses, by which it participates in regulating cancer, autoimmune and inflammatory diseases, microbial and parasitic infectious diseases, and other diseases. With the exception of its role in innate immunity, the growing list of researches demonstrated expanding roles of the cGAS-STING signal pathway in bridging the innate immunity (macrophage polarization) with the adaptive immunity (T lymphocytes differentiation). Macrophages and T lymphocytes are the most representative cells of innate immunity and adaptive immunity, respectively. Their polarization or differentiation are involved in the pathogenesis and progression of various diseases. Here we mainly summarized recent advanced discoveries of how the cGAS-STING signal pathway regulated macrophages polarization and T lymphocytes differentiation in various diseases and vaccine applications, providing a promising direction for the development and clinical application of immunotherapeutic strategies for related diseases.
Abstract. We analyzed the changes in mitochondrial DNA (mtDNA) copy numbers and the shifting of mtDNA D310 sequence variations (D310 mutation) with their relationships to pathological status and the expression levels of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor-2 (HER-2/neu), tumor-suppressor protein p53 and cellular proliferation protein Ki-67 in breast invasive ductal carcinoma (BIDC), respectively. Fifty-one paraffin-embedded BIDCs and their paired non-cancerous breast tissues were dissected for DNA extraction. The mtDNA copy number and mtDNA D310 sequence variations were determined by quantitative real-time polymerase chain reaction (q-PCR) and PCR-based direct sequencing, respectively. The expression levels of ER, PR, HER-2/neu, p53 and Ki-67 were determined by immunohistochemical (IHC) staining. Compared to the paired non-cancerous breast tissues, 24 (47.1%) BIDCs had elevated mtDNA copy numbers and 29 (56.9%) harbored mtDNA D310 mutations. Advanced T-status (p=0.056), negative-ER (p=0.005), negative-PR (p=0.007), positive-p53 (p=0.050) and higher Ki-67 (p=0.004) expressions were related to a higher mtDNA copy ratio. In addition, advanced T-status (p=0.019) and negative-HER-2/neu expression (p=0.061) were associated with mtDNA D310 mutations. In conclusion, higher mtDNA copy ratio and D310 mutations may be relevant biomarkers correlated with pathological T-status and the expression levels of ER, PR, HER-2/neu, p53 and Ki-67 in BIDCs.
Introduction: Diet is closely related to the occurrence of esophageal cancer (EC). Dietary Inflammatory Index (DII), as a novel index that describes the inflammatory potential of diet, was widely used in many diseases. Objective: To systematically analyze the relationship between DII and the risk of esophageal cancer. Methods: We mainly searched relative studies in PubMed, Cochrane library, Web of Science, and other literature database. The random-effect model was used for meta-analysis, and subgroup analysis and sensitivity analysis were used to detect the origin of heterogeneity. Results: We finally obtained 6 articles (8 studies). All studies were case-control studies which consisted of 1961 cases and 3577 controls. In this study, compared with the lowest DII category, the highest DII category had a higher risk of esophageal cancer, and the pooled odds ratio (OR) of the 8 studies were 2.54 (95% confidence interval (CI): 1.90–3.40; I 2 = 65.7%, P = .005). Furthermore, regardless of the differences in published year, DII components, geographic location, and study quality, there was still an increased risk of esophageal cancer in the highest DII category compared with the lowest DII category. Conclusions: Our results inferred that DII was positively correlated with esophageal cancer risk and it could be used as a tool to predict the esophageal cancer risk and evaluate human health.
Background: Sub-total/total gastrectomy with lymph node dissection (LND) remains an effective therapeutic strategy for resectable gastric adenocarcinomas (GACs). Despite the prognostic significance of positive lymph nodes (PLNs) defined in N-status, few have appraised the impacts of negative lymph nodes (NLNs) and the percentage of NLN (=number of NLNs/number of total lymph nodes [TLNs], %), as well as the extent of TLNs to be dissected in GACs. Methods: We retrospectively analyzed 62 GAC patients (mean age of 67.1 years; 41 men) undergoing primary sub-total/total gastrectomy from a single institute. Candidate variables, including the number of NLNs (≤9 and >9) and the percentage of NLN (≤37.5, 37.5-80.6 and >80.6, %), were evaluated to determine their prognostic impacts and hazard ratios (HRs). Results: Under the multivariate Cox proportional-hazards regression model, tumor length exceeding 4 cm (p = 0.017; HR = 2.828), perineural invasion (p = 0.037; HR = 3.182), and lower percentage of NLN (p = 0.016 and p = 0.060; HRs = 1.000, 0.327, and 0.333 for subgroups ≤37.5, 37.5-80.6, and >80.6, respectively) were three independent predictors with elevated HRs for poor prognosis. GAC patients with the percentage of NLN > 80.6 were highly related to those with NLNs > 9 (p < 0.001), and GAC patients with NLNs > 9 were highly related to those with TLNs > 15 (p < 0.001). For all 62 GAC or 42 N(+) GAC patients, those who underwent LND with TLNs>15 tended to have more PLNs (p = 0.018, p = 0.003) and more NLNs (p < 0.001, p = 0.029) than did those with TLNs ≤ 15. Among the 42 GAC patients with TLNs > 15, a lower percentage of NLN (p = 0.026 and p = 0.015; HRs = 1.000, 0.272, and 0.180 for subgroups ≤37.5, 37.5-80.6, and >80.6, respectively) remained an independent predictor of poor prognosis. Conclusion: The percentage of NLN could predict the prognosis of GAC patients properly. However, an accurate percentage of NLN needs a minimal requirement of TLNs > 15 to detect an adequate number of PLNs and sufficient number of NLNs.
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