Introduction: Central nervous system (CNS) tumors comprise 15-20% of all malignancies occurring in childhood and adolescence. Previous researches have shown that overexpression and amplification of the AURKA gene could induce multiple human malignancies, with which the connection of CNS tumor susceptibility has not been extensively studied.
Material And Methods: In this study, we assessed whether and to what extent AURKA gene single nucleotide polymorphisms (SNPs) (rs1047972 C > T, rs2273535 T > A, rs8173 G > C) were associated with CNS tumor susceptibility, based on a case-control analysis in 191 CNS tumor patients and 248 controls. We determined this correlation using odds ratios (ORs) and 95% confidence intervals (CIs).
Results: AURKA gene rs8173 G > C exhibited a crucial function to CNS tumor susceptibility fall-off (GC/CC vs. GG: adjusted OR = 0.68, 95% CI = 0.46-0.998, P = 0.049). In addition, the combined effect of lowering the risk of developing CNS tumors was more pronounced in carriers with 3 protective genotypes than others (adjusted OR = 0.55, 95% CI = 0.31-0.98, P = 0.044). Further stratification analysis illustrated that the existence of rs8173 GC/CC and three protective genotypes lowered CNS tumor risk in some subgroups.
Conclusions: Our research suggested that the AURKA gene rs8173 G > C could significantly reduce CNS tumor susceptibility in Chinese children. More functional experiments are needed to explore the role of the AURKA gene rs8173 G > C.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8777528 | PMC |
http://dx.doi.org/10.1007/s12672-021-00459-w | DOI Listing |
Front Oncol
December 2024
Department of Pathology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Background: Exonuclease 1 (EXO1), a protein involved in mismatch repair and recombination processes, has been identified as a prognostic biomarker in lung adenocarcinoma (LUAD). Nevertheless, its role in LUAD progression remains elusive. This study seeks to elucidate the functional significance of EXO1 in LUAD and evaluate its potential as a therapeutic target.
View Article and Find Full Text PDFBiology (Basel)
November 2024
Artificial Intelligence and Cyber Futures Institute, Charles Sturt University, Bathurst, NSW 2795, Australia.
Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors globally, significantly affecting liver functions, thus necessitating the identification of biomarkers and effective therapeutics to improve HCC-based disabilities. This study aimed to identify prognostic biomarkers, signaling cascades, and candidate drugs for the treatment of HCC through integrated bioinformatics approaches such as functional enrichment analysis, survival analysis, molecular docking, and simulation. Differential expression and functional enrichment analyses revealed 176 common differentially expressed genes from two microarray datasets, GSE29721 and GSE49515, significantly involved in HCC development and progression.
View Article and Find Full Text PDFSci Rep
January 2025
College of Pharmacy, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon, 34134, Republic of Korea.
Ferroptosis plays a role in tumorigenesis by affecting lipid peroxidation and metabolic pathways; however, its prognostic or therapeutic relevance in pancreatic adenocarcinoma (PAAD) remains poorly understood. In this study, we developed a prognostic ferroptosis-related gene (FRG)-based risk model using cohorts of The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC), proposing plausible therapeutics. Differentially expressed FRGs between tumors from TCGA-PAAD and normal pancreatic tissues from Genotype-Tissue Expression were analyzed to construct a prognostic risk model using univariate and multivariate Cox regression and LASSO analyses.
View Article and Find Full Text PDFExp Cell Res
December 2024
Department of Hematology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China. Electronic address:
Aurora kinase B (AURKB) was reported to assist Aurora kinase A (AURKA) to regulate cellular mitosis. AURKA has been found activated in myeloproliferative neoplasms (MPNs) patients with CALR gene mutation, however, it's unclear whether AURKB displays a compensatory function of AURKA in regulation of CALR mutant cell growth and differentiation. Here, we found that AURKB, similar with AURKA, was aberrantly activated in CALR mutant patients, and displayed a more tolerance to the aurora kinase inhibitor.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Medicine II, University Hospital Tuebingen, Eberhard Karls University, 72074 Tuebingen, Germany.
-rearranged (r) leukemia is characterized by a poor prognosis. Depending on the cell of origin, it differs in the aggressiveness and therapy response. For instance, in adults, volasertib blocking Polo-like kinase 1 (PLK-1) exhibited limited success.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!