Search

Objective To investigate the effect and mechanism of targeted regulation of phosphatase and tensin homolog (PTEN) and phosphatidylinositol 3-kinase (PI3K) on the proliferation and apoptosis of nephroblastoma cells. Methods Posto-perative tumor tissue and normal paracancerous tissue were collected from 15 children with nephroblastoma, and Western blotting and quantitative real-time PCR were used to measure the protein and mRNA expression levels of PTEN and PI3K in tissue. Nephroblastoma SK-NEP-1 cells were divided into control group (group A, transfected with NC siRNA and Flag empty vector), PTEN overexpression group (group B, transfected with NC siRNA and Flag-PTEN expression vector), PI3K knockdown group (group C, transfected siPI3K and Flag empty vector), a nd combined targeting group (group D, transfected siPI3K and FLAG-PTEN). Western blotting was used to measure the expression levels of PI3K, protein kinase A (AKT), and phosphorylated AKT (p-AKT) in SK-NEP-1 cells at 24 h after transfection; CCK-8 assay was used to observe the proliferation of SK-NEP-1 cells at 24, 48, and 72 h of intervention; flow cytometry was used to observe apoptosis rate and cell cycle at 24 h after transfection. Results Compared with normal paracancerous tissue, nephroblastoma tumor tissue showed significant increases in the protein and mRNA expression levels of PI3K (t=22.862,7.098,P

Objective To investigate the effect of laparoscopic surgery in the treatment of periappendiceal abscess in children. Methods A retrospective analysis was performed for 106 children with periappendiceal abscess who underwent laparosco-pic three-hole surgery in Department of Pediatric General Surgery in our hospital from January 2017 to May 2023. These children were analyzed in terms of age, sex, time of onset, clinical symptoms, auxiliary examination, surgery, and postoperative review. Results The 106 children had a mean intraoperative blood loss of (8.55±3.52)mL, an operation duration of (65.05±10.80)min, and a length of postoperative hospital stay of (10.60±1.50)d. Among these children, 5 had postoperative incision infection and 8 had residual abscess in the abdominal cavity, all of whom were cured after conservative anti-inflammatory treatment. Postoperative pathology showed 82 cases of appendiceal gangrene and 24 cases of suppurative inflammation. All children underwent reexamination at the outpatient service of our hospital at 1, 3, and 6 months after discharge; physical examination showed no obvious positive signs, and ultrasound showed no obvious fluid seepage and abdominal mass in the abdominal cavity. Conclusion Laparoscopic surgery has the advantages of low intraoperative blood loss, a short length of hospital stay, and few postoperative complications in the treatment of periappendiceal abscess in children, and therefore, it is recommended for the treatment of such children.

The nucleotide excision repair (NER) system is one of the main ways to protect organisms from DNA damage caused by endogenous and exogenous carcinogens. NER deficiency increases genome mutations, chromosomal aberrations, and cancer viability. However, the genetic association between Wilms tumor and NER pathway gene polymorphisms needs to be further validated. We assessed the associations between 19 NER gene polymorphisms and Wilms tumor susceptibility in 416 cases and 936 controls from East China via the TaqMan method. We found that xeroderma pigmentosum group D (XPD) rs238406 and rs13181 significantly decreased the risk of Wilms tumor [adjusted odds ratio (OR) = 0.59, 95% confidence interval (CI) = 0.46–0.75, p <.0001; adjusted OR = 0.63, 95% CI = 0.44–0.89, p = .009, respectively]. Furthermore, the rs751402 and rs2296147 polymorphisms in the xeroderma pigmentosum group G (XPG) gene were significantly correlated with an increased risk for Wilms tumor (adjusted OR = 1.47, 95% CI = 1.03–2.09, p = .034; adjusted OR = 2.14, 95% CI = 1.29–3.56, p = .003, respectively). Expression quantitative trait loci (eQTL) analysis revealed that these four polymorphisms may affect the expression of genes that are adjacent to XPD and XPG. Our study provides evidence that XPD and XPG gene polymorphisms are associated with Wilms tumor risk. Nonetheless, these findings should be confirmed in a larger sample size. [ABSTRACT FROM AUTHOR]

Objective: Nucleotide excision repair (NER) plays a vital role in maintaining genome stability, and the effect of NER gene polymorphisms on hepatoblastoma susceptibility is still under investigation. This study aimed to evaluate the relationship between NER gene polymorphisms and the risk of hepatoblastoma in Eastern Chinese Han children., Methods: In this five-center case-control study, we enrolled 966 subjects from East China (193 hepatoblastoma patients and 773 healthy controls). The TaqMan method was used to genotype 19 single nucleotide polymorphisms (SNPs) in NER pathway genes, including ERCC1 , XPA , XPC , XPD , XPF , and XPG . Then, multivariate logistic regression analysis was performed, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were utilized to assess the strength of associations., Results: Three SNPs were related to hepatoblastoma risk. XPC rs2229090 and XPD rs3810366 significantly contributed to hepatoblastoma risk according to the dominant model (adjusted OR=1.49, 95% CI=1.07-2.08, P=0.019; adjusted OR=1.66, 95% CI=1.12-2.45, P=0.012, respectively). However, XPD rs238406 conferred a significantly decreased risk of hepatoblastoma under the dominant model (adjusted OR=0.68, 95% CI=0.49-0.95; P=0.024). Stratified analysis demonstrated that these significant associations were more prominent in certain subgroups. Moreover, there was evidence of functional implications of these significant SNPs suggested by online expression quantitative trait loci (eQTLs) and splicing quantitative trait loci (sQTLs) analysis., Conclusions: In summary, NER pathway gene polymorphisms ( XPC rs2229090, XPD rs3810366, and XPD rs238406) are significantly associated with hepatoblastoma risk, and further research is required to verify these findings., (Copyright ©2024 Chinese Journal of Cancer Research. All rights reserved.)

Metastasis is a hallmark of malignant neuroblastoma and is the main reason for therapeutic failure and recurrence of the tumor. The CXC chemokine receptor-4 (CXCR4), a Gi protein-coupled receptor for the ligand CXCL12/stromal cell-derived factor-1α (SDF-1α), is expressed in various types of tumor. This receptor mediates the homing of tumor cells to specific organs that express the ligand, CXCL12, for this receptor and plays an important role in tumor growth, invasion, metastasis and angiogenesis. In the present study, the inflammatory cytokine, tumor necrosis factor‑α (TNF‑α) upregulated CXCR4 expression in neuroblastoma cells and increased migration to the CXCR4 ligand SDF‑1α. In addition, this effect was dependent upon NF-κB transcriptional activity, as blocking the NF-κB pathway with pyrrolidinedithiocarbamic acid ammonium salt suppressed TNF-α‑induced upregulation of CXCR4 expression and reduced the migration towards the CXCR4 ligand, SDF-1α. Treating neuroblastoma cells with TNF-α resulted in the activation of nuclear factor-kappa B (NF-κB) and subsequently, the translocation of NF-κB from the cytoplasm to the nucleus. Using immunohistochemistry, NF‑κB and CXCR4 were significantly correlated with each other (P=0.0052, Fisher's exact test) in a cohort of neuroblastoma samples (n=80). The present study indicates that the inflammatory cytokine, TNF-α, partially functions through the NF‑κB signaling pathway to upregulate CXCR4 expression to foster neuroblastoma cell metastasis. These findings indicate that effective inhibition of neuroblastoma metastasis should be directed against the inflammatory cytokine-induced NF‑κB/CXCR4/SDF‑1α signaling pathway.