Low-grade gliomas (LGGs) are primary invasive brain tumors that grow slowly but are incurable and eventually develop into high malignant glioma. Fc fragment of IgG receptor IIIa (FCGR3A) gene polymorphism may correlate with some cancers’ treatment responses. However, the expression and prognosis value of FCGR3A and correlation with tumor-immune infiltrate in LGG remain unclear. FCGR3A mRNA expression in gastric cancer (GC) was examined using TIMER and GEPIA databases. Correlations between FCGR3A expression and clinicopathological parameters were analyzed using ULACAN and CGGA databases. GEPIA, OncoLnc, and ULACAN databases were used to examine the clinical prognostic significance of FCGR3A in LGG. TIMER was used to analyze the correlations among FCGR3A and tumor-infiltrating immune cells. Signaling pathways related to FCGR3A expression were identified by LinkedOmics. We found that FCGR3A expression was higher in LGG than in normal tissue and was correlated with various clinical parameters. In addition, high FCGR3A expression predicted poor overall survival in LGG. More importantly, FCGR3A expression positively correlated with immune checkpoint molecules, including PD1, PD-L1, PD-L2, CTLA4, LAG-3 and TIM-3, and tumor-associated macrophage (TAM) gene markers in LGG. GO and KEGG pathway analyses indicated that TUBA1C may potentially regulate the pathogenesis of LGG through immune-related pathways. These findings indicated that FCGR3A plays a vital role in the infiltration of immune cells and could constitute a promising prognostic biomarker in LGG patients.
More clinical studies are needed to clarify the risk stratification by the integration of all fusion genes in adult B-cell precursor acute lymphoblastic leukemia (BCP-ALL). A total of 320 consecutive adult Ph-negative BCP-ALL patients who had been tested classical fusions (KMT2A rearrangement and TCF3-PBX1) at diagnosis were further retrospectively screened novel fusion genes (Ph-like, ZNF384 and MEF2D fusions) by multiplex real-time quantitative PCR (RQ-PCR). Classical fusions were identified in 12.5% of patients, while 4.4%, 17.2% and 3.8% of patients were identified Ph-like, ZNF384 and MEF2D fusions, respectively. 1-course CR rate, relapse-free survival (RFS) and overall survival (OS) rates tended to show or showed statistically significant differences among fusion-defined subgroups (P = 0.084, 0.001 and 0.0093, respectively). Based on individual outcomes, patients with KMT2A rearrangement, TCF3-PBX1, Ph-like, and MEF2D fusions were classified into fusion-defined high-risk group (n = 66, 20.6%). High-risk group had significantly lower 3-year RFS and 3-year OS rates than standard-risk group (P 0.001 and = 0.0022), and was an independent adverse prognostic factor for RFS in the entire cohort (P 0.001). In conclusion, the spectrum of fusion genes in the current Chinese cohort was distinct from that in reports from western countries. Detection of fusion genes improved risk stratification in adult Ph-negative BCP-ALL patients.
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