Stable incidence of childhood and adult glioma in the Netherlands, 1989–2003
M.P.W.A. HoubenKatja K.H. AbenJohannes L. TeepenAntoinette Y. N. Schouten–van MeeterenC. C. TijssenCornelia M. van DuijnJ.W.W. Coebergh
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Time trends in the incidence of glioma may reflect changes in the prevalence of environmental risk factors for glioma. We therefore investigated trends in the incidence of childhood and adult glioma in the Netherlands from 1989 to 2003. We used population-based incidence data from the Netherlands Cancer Registry. We calculated European standardised incidence rates for glioma, and stratified for age, gender and glioma subgroups. Changes in the incidence were estimated by calculating the Estimated Annual Percentage Change. Similar to other countries, the overall incidence of glioma was fairly stable in the Netherlands during the period 1989 to 2003, for both children and adults. In adult astrocytic glioma, a significantly increasing incidence of high-grade astrocytoma was balanced by simultaneous decreases of low-grade astrocytoma, astrocytoma with unknown malignancy grade and glioma of uncertain histology. Most of these time trends can be explained by improving detection and diagnostic precision. Stable incidence rates of adult and childhood glioma suggest that no major changes in environmental risk factors have occurred, which influenced the incidence of glioma in the studied period.Tumor progression
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Malignant glioma is the most common and aggressive primary brain tumor and the overall prognosis for glioma patients remains poor. Clarification of the molecular mechanism responsible for glioma progression is critical for the effective treatment of glioma. Melanoma antigen gene (MAGE)-A2 (MAGEA2) is a member of the MAGE-A family proteins widely studied for cancer vaccine development and identification of tumor markers. However, MAGEA2 clinical significance and biological function in glioma remain unclear, especially for the prognosis of glioma patients. This study investigates MAGEA2 expression in glioma tissue samples and its significance in predicting glioma patient prognosis. MAGEA2 protein expression in tissue samples was measured by immunohistochemistry and western blotting, and MAGEA2 mRNA expression was determined by real-time polymerase chain reaction. Our results confirmed that MAGEA2 mRNA and protein expression levels were upregulated in glioma tissues, compared with normal brain tissue. The high expression of MAGEA2 in glioma tissues significantly correlated with World Health Organization advanced grade. Univariate and multivariate analyses revealed that high MAGEA2 expression is an independent prognostic factor for glioma patient poor overall survival. The P53 mRNA expression levels were downregulated in glioma tissues compared to noncancerous brain tissue and MAGEA2 expression negatively correlated with P53 expression. Taken together, our results suggest that MAGEA2 plays an oncogenic role in glioma progression, and they provide insight into MAGEA2 application as a novel predictor of clinical outcomes and a potential glioma biomarker.
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Objective:To study the expression of 5-lipoxygenase(5-LOX)and Ki-67 in astrocytoma and the correlation between 5-LOX and Ki-67.Methods: The expressions of 5-LOX and Ki-67 were detected by immunohistochemistry in 60 paraffinaceous specimen with astrocytoma,including 33 with low potential malignancy tumor and 27 with high potential malignancy tumor.RT-polymerase chain reaction(RT-PCR) was used in 60 cases of fresh astrocytoma.The 14 normal brain tissues subjected to cerebral trauma were control.Results: The normal brain tissue was negative or only had a low expression for 5-LOX and Ki-67.66.7%(40/60) and 71.7%(43/60) of astrocytomas were positive for 5-LOX and Ki-67 respectively.The positive rates of 5-LOX and Ki-67 were significantly higher in the high potential malignancy group than in the low potential malignancy group(P0.01).The 5-LOX positive reaction was correlated with Ki-67(γ=0.875,P0.01).The contents of 5-LOX and Ki-67 mRNA were significantly higher in astrocytoma tissues than in the normal brain tissues(P0.01)and also higher in the high potential malignancy group than in the low potential malignancy(P0.01).The 5-LOX mRNA level correlated with Ki-67 mRNA level(γ=0.781,P0.01).Conclusion: The expressions of 5-LOX and Ki-67 are related to the malignancy of astrocytoma,and they may coordinate with each other in the development and progression of astrocytoma.
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Glioma incidence in the US seems to have stabilized over the past 20 years. It's also not clear whether changes in glioblastoma incidence are associated with glioma mortality trends. Our study investigated trends in glioma incidence and mortality according to tumor characteristics.This study obtained data from the Surveillance, Epidemiology, and End Results-9 (SEER-9) registries to calculate glioma incidence and mortality trends. Annual percent changes (APC) and 95% CIs were calculated using the Joinpoint program.62,159 patients (34,996 males and 55,424 whites) were diagnosed with glioma during 1975-2018, and 31,922 deaths occurred from 1995-2018. Glioblastoma (32,893 cases) and non-glioblastoma astrocytoma (17,406 cases) were the most common histologic types. During the study period, the incidence of glioma first experienced a significant increase (APC=1.8%, [95% CI, 1.3% to 2.3%]) from 1975 to 1987, and then experienced a slight decrease (APC=-0.4%, [95% CI, -0.5% to -0.3%]) from 1987 to 2018, while the APC was 0.8% for glioblastoma, -2.0% for non-glioblastoma astrocytoma, 1.1% for oligodendroglial tumors, 0.7% for ependymoma and -0.3% for glioma NOS during the study period. Glioblastoma incidence increased for all tumor size and tumor extension except for distant. From 1995 to 2018, glioma mortality declined 0.4% per year (95% CI: -0.6% to -0.2%) but only increased in patients older than 80 years [APC=1.0%, (95% CI, 0.4% to 1.6%)].Significant decline in glioma incidence (1987-2018) and mortality (1995-2018) were observed. Epidemiological changes in non-glioblastoma astrocytoma contributed the most to overall trends in glioma incidence and mortality. These findings can improve understanding of risk factors and guide the focus of glioma therapy.
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Objective: To investigate the expressions of p53,Ki67,VEGF and MMP-9 in glioma tissues,and their correlations with glioma malignancy.Methods: The expression of p53,Ki67,VEGF and MMP-9 in 10 cases of normal brain tissues and 38 cases of glioma were assessed by immunohistochemistry,and their correlations with glioma malignancy were statistically analyzed. Results: The expression of Ki67 and MMP-9 was correlated with glioma malignancy(P0.05).There was no statistically significant difference between other biological markers with glioma malignancy.There was a positive correlation between VEGF and MMP-9(P0.05).In addition,the expression of p53 had a positive correlation with the expression of Ki67,VEGF and MMP-9,respectively(P0.05). Conclusion: The expression of Ki67 and MMP-9 were two objective biological markers for estimating the glioma malignancy.
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Abstract Background: Glioma is a type of malignant cancer in the central nervous system. New predictive biomarkers have been investigated in recent years, but the clinical prognosis in glioma remains poor. The function of CPLX2 in glioma and the probable molecular mechanism of tumor suppression was the focus of this investigation. Methods: The glioma transcriptome profile is downloaded from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases were performed to analyze the expression of CPLX2 in glioma. RT-qPCR was performed to detect the expression of CPLX2 in 68 glioma subjects, these patients who have been followed up. Kaplan-Meier survival analyses were done to evaluate the effect of CPLX2 on the prognosis of glioma patients. The CPLX2 knockdown and overexpressed cell lines were constructed to investigate the effect of CPLX2 on glioma. The cell growth, colony formation, and tumor formation in xenograft were performed. Results: The expression of CPLX2 was downregulated in glioma and negatively correlated to the grade of glioma. The higher expression of CPLX2 predicted a longer survival through the analysis of Kaplan-Meier survival curves. Overexpressed CPLX2 impaired tumorigenesis in glioma progression both in vivo and in vitro . Knocking down of CPLX2 promoted the proliferation of the glioma cells. The analysis of GSEA and co-expression analysis revealed that CPLX2 may affect the malignancy of glioma by regulating hypoxia and inflammation pathway. Conclusions: Our data indicated that CPLX2 functioned as a tumor suppressor and could be used as a potential prognostic marker in glioma.
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Time trends in the incidence of glioma may reflect changes in the prevalence of environmental risk factors for glioma. We therefore investigated trends in the incidence of childhood and adult glioma in the Netherlands from 1989 to 2003. We used population-based incidence data from the Netherlands Cancer Registry. We calculated European standardised incidence rates for glioma, and stratified for age, gender and glioma subgroups. Changes in the incidence were estimated by calculating the Estimated Annual Percentage Change. Similar to other countries, the overall incidence of glioma was fairly stable in the Netherlands during the period 1989 to 2003, for both children and adults. In adult astrocytic glioma, a significantly increasing incidence of high-grade astrocytoma was balanced by simultaneous decreases of low-grade astrocytoma, astrocytoma with unknown malignancy grade and glioma of uncertain histology. Most of these time trends can be explained by improving detection and diagnostic precision. Stable incidence rates of adult and childhood glioma suggest that no major changes in environmental risk factors have occurred, which influenced the incidence of glioma in the studied period.
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Glioma is a tumor of the brain. Although the clinical regimens and surgical techniques for glioma have improved, therapies of advanced glioma remain challenging, carrying dismal overall survival and therapeutic success rates. Evidence has shown that miRNAs played important roles in glioma development. The current study aimed at investigating the function of a novel cancerogenic miRNA, miR-93, in glioma progression by investigating the expression and mechanism of it.qRT-PCR was conducted to assess the miR-93 expression and the mRNA expression of target gene in glioma tissues and cells. The invasion and migration abilities of the glioma cells were determined by transwell assays. Luciferase reporter assay was performed to confirm the target of miR-93.The results indicated that miR-93 expression in glioma tissues and cells was increased significantly than that in normal brain tissues and cells. Furthermore, miR-93 promoted glioma cell migration and invasion. RBL2 was recognized as a direct target of miR-93 in glioma cells, and overexpression of RBL2 could reverse the stimulative effect of miR-93 in glioma cell.The above findings suggested that miR-93 together with RBL2 could be diagnostic targets and novel prognostic markers for glioma.
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