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Pulmonary chronic graft-versus-host disease (cGVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a devastating complication and often diagnosed at a late stage when lung dysfunction is irreversible. Identifying patients before transplant who are at risk may offer improved strategies to decrease the mortality. Bronchiolitis obliterans syndrome (BOS) is the typical manifestation of pulmonary cGVHD, which is clinically diagnosed by pulmonary function test (PFT). This study aimed to evaluate the predictive value of PFT pre-HSCT for BOS.
By conducting a meta-analysis of relevant clinical studies on the treatment of advanced gastric cancer (GC) using laparoscopic and open surgeries, we aimed to evaluate the impact of these two surgical approaches on postoperative surgical site infections (SSIs) in patients with advanced GC. We aimed to provide evidence-based support for preventing SSIs in postoperative patients with advanced GC. From database establishment until May 2023, we systematically searched PubMed, Cochrane Library, MEDLINE, Embase, China National Knowledge Infrastructure, and Wanfang Data databases for relevant studies comparing laparoscopic and open surgeries for the treatment of advanced GC. Two researchers independently performed the literature screening and data extraction based on predefined inclusion and exclusion criteria. The meta-analysis was conducted using STATA 17.0. Twenty articles involving 3084 patients met the inclusion criteria, including 1462 patients in the laparoscopic group and 1622 cases in the open surgery group. The meta-analysis results revealed that the incidence of postoperative SSIs was significantly lower in the laparoscopic group than in the open surgery group (odds ratio = 0.341, 95% confidence interval: 0.219-0.532, p < 0.001). The current evidence indicates that laparoscopic radical gastrectomy can significantly reduce the incidence of postoperative site infections in patients with advanced GC.
MEK1/ERK signaling pathway plays an important role in most tumor progression, including colorectal cancer (CRC), however, MEK1-targeting therapy has little effective in treating CRC patients, indicating there may be a complex mechanism to activate MEK1/ERK signaling pathway except RAS activated mechanism.
Mesenchymal stromal cells (MSCs) function as a formidable regulator of inflammation and tissue homeostasis and expanded MSCs are shown to be effective in treating various inflammatory diseases. Their therapeutic effects require the existence of certain inflammatory cytokines. However, in the absence of sufficient proinflammatory stimuli or in the presence of anti-inflammatory medications, MSCs are animated to promote immune responses and unable to alleviate inflammatory disorders. In this study, it is demonstrated that steroid co-administration interferes the efficacy of MSCs in treating acute graft-versus-host disease (aGvHD). Molecular analysis reveals that vascular endothelial growth factor C (VEGF-C) is highly induced in MSCs by steroids and TNFα and VEGF-C in turn promotes CD8+ T cell response. This immune promoting effect is abolished by blockade or specific genetic ablation of VEGFR3 in CD8+ T cells. Additionally, administration of VEGF-C alone exacerbates aGvHD progression through eliciting more vigorous CD8+ T cell activation and proliferation. Further studies demonstrate that VEGF-C augments the PI3K/AKT signaling process and the expression of downstream genes, such as Cyclin D1. Thus, the data demonstrate that steroids can reverse the immunosuppressive effect of MSCs via promoting VEGF-C-augmented CD8+ T cell response and provide novel information for designing efficacious MSC-based therapies.
The tumourigenesis of various cancers is influenced by epigenetic deregulation. Among 591 epigenetic regulator factors (ERFs) examined, AF9 showed significant inhibition of malignancy in colorectal cancer (CRC) based on our wound healing assays. However, the precise role of AF9 in CRC remains to be explored.
Background: Tumor-associated macrophages (TAMs) are one of the most prominent tumor-infiltrating immune cells in the tumor microenvironment (TME) of CRC and play a vital role in the progression of CRC. BST2 was predicted to be associated with the infiltration of TAMs. However, its potential function by which CRC cells and TAMs interact with each other still needs further investigation. Methods: The target genes in CRC were selected by bioinformatics screening. The level of bone marrow stromal cell antigen 2 (BST2) in CRC cells and tissues was determined by qRT‒PCR, Western blotting, and immunohistochemistry staining. In vitro and in vivo assays were applied to clarify the function of BST2. Results: In this study, according to bioinformatics analysis, a nomogram based on the risk score (constructed by BST2 and CAV1 (caveolin-1)) and clinical features was built and displayed satisfactory prognostic value. Upregulated BST2 was significantly related to Braf mutation, dMMR/MSI-H, CMS1 subtype, and immune response and was a potential biomarker for predicting immune checkpoint blockade therapy. Silencing BST2 in CRC obviously restrained CRC progression and M2 TAM polarization. The infiltration of TAMs was positively correlated with the high expression of BST2, and depletion of TAMs alleviated the protumoural effect of BST2 in CRC in vivo. In vitro experiments revealed that a reduction in BST2 in CRC inhibited CRC proliferation and migration and also M2 polarization. Conclusion: These findings indicated that BST2 played a vital role in CRC progression and might be a predictable marker for immunotherapy.
Aerobic glycolysis is a common metabolic phenotype in tumors that helps cancer cells adjust to severe living conditions and can aid metastasis in several types of carcinomas, including colorectal cancer (CRC). Long non-coding RNAs (lncRNAs) can influence tumor biology and have been previously used to assess patients' outcomes and to identify potential therapeutic targets. However, despite the importance of glycolysis-related lncRNAs (GRLs) in the development of CRC, studies on their use as prognostic markers are still limited. Herein, we applied a series of bioinformatic analyses to screen potential prognostic lncRNAs for colorectal cancer. Out of all lncRNAs screened, nine GRLs were selected to constitute a prognostic signature. Based on the signature, two molecular subtypes were classified with distinct prognostic outcomes and excellent diagnostic accuracy (The 1-, 3- and 5-year AUC are 0.756, 0.716, and 0.721, respectively). The prognostic value of this signature was further validated using another cohort. The enriched molecular pathways, immune infiltration, and mutation landscape were also significantly different between the two groups. The different drug sensitivity results between the two groups suggest a potential strategy for precise treatment. Furthermore, we confirmed that AFAP1-AS1 could regulate aerobic glycolysis and metastasis of CRC cells. Overall, we developed a glycolysis-related lncRNA (GRL) signature and suggested that this signature could offer a predictive value and identify potential therapeutic targets for cancer therapy.
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