Assessment of the association between D-dimer levels and clinicopathological characteristics of pancreatic cancer and its role in prognosis: A systematic review and meta-analysis.

According to previous studies, D-dimer levels are associated with the prognosis of patients with pancreatic cancer (PC). However, the results of current studies are limited and controversial. Therefore, we performed this meta-analysis to assess the relationship between D-dimer levels and prognostic and pathological characteristics of PC patients. We first searched the databases of PubMed, Embase, The Cochrane Library, Web Of Science, CBM, VIP, CNKI and Wanfang to identify available studies. The relationship between pretreatment d-dimer levels and prognosis in PC patients was assessed using the combined hazard ratio (HR) and 95% confidence interval (CI). The combined odds ratio (OR) and 95% confidence interval (CI) were used in assessing the relationship between pathological characteristics and d-dimer levels in PC patients. Stata 12.0 software was used for all statistical analyses. In total, we included 13 studies involving 2777 patients. The results showed that elevated pre-treatment d -dimer levels were significantly associated with OS deterioration (HR = 1.46 95% CI: 1.34-1.59; p < 0.001). We also performed subgroup analyses based on sample size, d -dimer threshold, follow-up time, and HR source to further validate the prognostic value of pretreatment d -dimer levels in PC. In addition, according to the analysis, high pretreatment d -dimer levels in PC patients were associated with late tumor stage (OR = 4.78, 95% CI 1.73-13.20, p < 0. 005), larger tumor size (OR = 1.72, 95% CI 1.25-2.35, p < 0.005), and distant metastasis of tumor (OR = 5.06, 95% CI 2.45-10.43, p < 0.005) were significantly associated. In contrast, other clinicopathological factors, including age, gender and lymph node metastasis, were not associated with d-dimer levels. In conclusion, we found that high pre-treatment d-dimer levels were associated with a poor prognosis in PC patients, in relation to later tumor stage, larger tumor size and the development of distant metastases. Plasma d-dimer levels can be used as a biomarker of prognosis in PC patients.

Association between immune-related hub genes CD36, CXCL13, FGFR4, GABBR1, LAMP3, MMP12, and PPM1H and colorectal cancer prognosis.

The present study aims to identify immune-related prognostic genes in colorectal cancer (CRC), and to explore potential mechanisms through which these genes regulate CRC progression. We first constructed a prognostic risk model based on seven gene signatures [cluster of differentiation-36 (CD36), chemokine (C-X-C-motif) ligand 13 (CXCL13), fibroblast growth factor receptor 4 (FGFR4), gamma-amino-butyric acid type B receptor 1 (GABBR1), lysosome-associated membrane glycoprotein 3 (LAMP3), recombinant matrix metalloproteinase 12 (MMP12), and protein phosphatase 1H (PPM1H)] using integrated bioinformatic analyses. FGFR4, GABBR1, and LAMP3 were highly expressed in CRC cell lines (in comparison with a normal colonic epithelial cell line), while CD36, CXCL13, MMP12, and PPM1H were weakly expressed. These in vitro expression results were largely consistent with our bioinformatic analysis. A prognostic model was generated to identify a high-risk group with worse survival outcome based on Kaplan-Meier analysis. Our prognostic model showed superior accuracy in both the training and test cohorts. In addition, we found that the low-risk subgroup exhibited greater infiltration by M1 macrophages, CD8+ T cells, CD4+ T cells, and activated NK cells. In conclusion, our findings provide evidence that seven immune-related hub genes can be considered as gene signatures to predict CRC prognosis and to differentiate CRC patient benefit, ultimately serving as a guide for individualized immunotherapy.

Comprehensive analysis of the role of ICOS ( CD278 ) in pan-cancer prognosis and immunotherapy.

BACKGROUND: The immunological checkpoint known as Inducible T Cell Costimulatory Factor (ICOS, Cluster of Differentiation, CD278) is activated and expressed on T cells. Both somatic cells and antigen-presenting cells expressed its ligand, ICOSL (including tumor cells in the tumor microenvironment).It is important for immunosuppression. Uncertainty surrounds the function of ICOS in tumor immunity. METHODS: Several bioinformatics techniques were employed by us to thoroughly examine the expression and prognostic value of ICOS in 33 cancers based on data collected from TCGA and GTEx. In addition, ICOS was explored with pathological stage, tumor-infiltrating cells, immune checkpoint genes, mismatch repair (MMR) genes, DNA methyltransferases (DNMTs), microsatellite instability (MSI),and tumor mutation burden (TMB).In addition,To ascertain the level of ICOS expression in various cells, qRT-PCR was employed. RESULTS: The findings revealed that ICOS expression was up regulation in most cancer types. The high expression of ICOS in tumor samples was related to the poor prognosis of UVM and LGG; The positive prognosis was boosted by the strong expression of ICOS in OV, SARC, SKCM, THYM, UCEC, and HNSC. The result is that the expression of malignancy was revealed by the immune cells' invasion.profile of ICOS in different types of cancer. Different ways that ICOS expression is connected to immune cell infiltration account for variations in patient survival. Additionally, the TMB, MSI, MMR, and DNMT genes as well as ICOS expression are linked in many cancer types.The results of PCR showed that it is highly expressed in gastric, breast, liver and renal cell carcinoma cell lines compared with normal cells. CONCLUSION: This study suggests that ICOS may be a potential tumor immunotherapy target and prognostic marker.

The crosstalking of lactate-Histone lactylation and tumor.

Lactate was once considered to be a by-product of energy metabolism, but its unique biological value was only gradually explored with the advent of the Warburg effect. As an end product of glycolysis, lactate can act as a substrate for energy metabolism, a signal transduction molecule, a regulator of the tumor microenvironment and immune cells, and a regulator of the deubiquitination of specific enzymes, and is involved in various biological aspects of tumor regulation, including energy shuttling, growth and invasion, angiogenesis and immune escape. Furthermore, we describe a novel lactate-dependent epigenetic modification, namely histone lactylation modification, and review the progress of its study in tumors, mainly involving the reprogramming of tumor phenotypes, regulation of related gene expression, mediation of the glycolytic process in tumor stem cells (CSCs) and influence on the tumor immune microenvironment. The study of epigenetic regulation of tumor genes by histone modification is still in its infancy, and we expect that by summarizing the effects of lactate and histone modification on tumor and related gene regulation, we will clarify the scientific significance of future histone modification studies and the problems to be solved, and open up new fields for targeted tumor therapy.