PHOSPHO1 Serves as a Key Metabolism-Related Biomarker in the Tumorigenesis of Diffuse Large B-cell Lymphoma.

OBJECTIVE: Diffuse large B-cell lymphoma (DLBCL) is an aggressive type of non-Hodgkin lymphoma. Due to its genetic heterogeneity and abnormal metabolism, many DLBCL patients have a poor prognosis. This study investigated the key metabolism-related genes and potential mechanisms. METHODS: Differentially expressed genes, differentially expressed transcription factors (TFs), and differentially expressed metabolism-related genes (DEMRGs) of glucose and lipid metabolic processes were identified using the edgeR package. Key DEMRGs were screened by Lasso regression, and a prediction model was constructed. The cell type identification by estimating relative subsets of RNA transcripts algorithm was utilized to assess the fraction of immune cells, and Gene Set Enrichment Analysis was used to determine immune-related pathways. A regulatory network was constructed with significant co-expression interactions among TFs, DEMRGs, immune cells/pathways, and hallmark pathways. RESULTS: A total of 1551 DEMRGs were identified. A prognostic model with a high applicability (area under the curve=0.921) was constructed with 13 DEMRGs. Tumorigenesis of DLBCL was highly related to the neutrophil count. Four DEMRGs (PRXL2AB, CCN1, DECR2 and PHOSPHO1) with 32 TF-DEMRG, 36 DEMRG-pathway, 14 DEMRG-immune-cell, 9 DEMRG-immune-gene-set, and 67 DEMRG-protein-chip interactions were used to construct the regulatory network. CONCLUSION: We provided a prognostic prediction model based on 13 DEMRGs for DLBCL. We found that phosphatase, orphan 1 (PHOSPHO1) is positively regulated by regulatory factor X5 (RFX5) and mediates MYC proto-oncogene (MYC) targeting the V2 pathway and neutrophils.

The Diagnostic and Prognostic Role of Interleukin 12B and Interleukin 6R Gene Polymorphism in Patients With Ankylosing Spondylitis.

OBJECTIVES: Interleukin 23 (IL-23) pathway and IL-1 cluster genes play prominent role in the etiopathology of ankylosing spondylitis (AS). The aim of this study was to investigate the diagnostic and prognostic role of 5 single-nucleotide polymorphisms related to IL-23 pathway and IL-1 cluster genes in AS patients. METHODS: Four hundred thirty-one patients with AS and 206 age- and sex-matched healthy controls were recruited in this prospective cohort study. Five potential single-nucleotide polymorphisms (IL-23R [rs11209026], IL-12B [rs6871626], TYK2 [rs6511701], IL-6R [rs4129267], and IL-1R2 [rs2192752]) related to IL-23 pathway and IL-1 cluster genes by analyzing previous studies were genotyped. Among 431 total AS patients, 198 active cases were treated and followed up for 24 weeks. RESULTS: Frequencies of IL-12B AA (rs6871626) and IL-6R TT (rs4129267) genotypes were increased in AS patients compared with healthy controls (both P < 0.001), and IL-12B A (rs6871626) as well as IL-6R T (rs4129267) allele increased the risk of AS independently (both P < 0.001). The Bath Ankylosing Spondylitis Disease Activity Index score was found to be elevated in AS patients with IL-12B AA (rs6871626) compared with patients with the CA and CC genotypes (P = 0.002 and P < 0.001, respectively), and the Bath Ankylosing Spondylitis Functional Index score was also increased in AS patents with IL-12B AA (rs6871626) than in those with the CA and CC genotypes (P = 0.001 and P < 0.001). In addition, IL-6R T (rs4129267) allele could predict a worse ASAS-20 (Assessment of SpondyloArthritis international Society) response at week 24 as an independent factor by multivariate logistic regression analysis with additive model (P = 0.011). CONCLUSIONS: Interleukin 12B (rs6871626) and IL-6R (rs4129267) gene polymorphisms could serve as promising biomarkers for diagnosis and prognosis in AS patients.

[Experimental study on stimulation of guided bone regeneration by autogenous bone marrow].

OBJECTIVE: To study the effect of autogenous bone marrow on guided bone regeneration (GBR), and evaluate the repairing ability of GBR in bone defect with autogenous bone marrow. METHODS: Ten mm segmental defects were produced in both radii of 18 rabbits. The defect was bridged with a silicon tube. Autogenous bone marrow was injected into the tube on the experimental group at 0, 2, 4 weeks after operation, and peripheral blood into the control group at the same time. The X-ray, gross, histological and biochemical examinations were observed in various times. RESULTS: The new bone formation of experimental group was prior to that of control group; calcium and alkaline phosphatase of experimental group were higher than those of control group. The experimental group had all been healed at the tenth week, but no one healed in control group. CONCLUSION: It can be conclude that autogenous bone marrow can stimulate bone formation and facilitate GBR in bone defect.