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Clinical Features and Differential Gene Screening of Invasive Behaviors between Glioma and Brain Metastasis

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Objective: To analyze invasive behaviors between glioma and Brain Metastasis (BM), and to screen invasive differentially expressed genes. Methods: Patients diagnosed pathologically with glioma or BM divided into low-grade glioma groups (n = 19), high-grade glioma group (n = 18), and BM group (n = 15). The survival period was determined. The clinical characteristics were retrospectively analyzed to draw Kaplan-Meier survival curve. Glioma and BM samples were obtained for RNA sequencing. By GO, KEGG, PubMed, and GeneCard, invasive genes were theoretical selected. Correlation between invasive genes and pathological grade was performed. The expression level of invasive genes was verified. Results: The survival curve found that the clinical invasive behavior related to short lifetime includes: size, edema range, blood supply, vascular invasion, grade, and Ki 67 expression. Theoretical analysis finally found that the expression levels of CALM3, CAMK2A, CAMK2B, and PRKCG were negatively correlated with pathological grade (P< 0.01), of which CALM3 was highly correlated with BM (P< 0.01). CALM3 mRNA was significantly down-regulated in BM (P< 0.05), and PRKCG mRNA was significantly down-regulated in both glioma and BM (P< 0.05). Conclusion: The clinical invasive behavior between glioma and BM have significantly shortened the median survival time of patients. Down-regulation of CALM3 suggested a higher correlation with BM, meanwhile Down-regulation of PRKCG played a role in glioma and BM The detection of CALM3 and PRKCG may be helpful for invasive behavior and provide a reference for the targeted therapy in glioma and BM.
Title: Clinical Features and Differential Gene Screening of Invasive Behaviors between Glioma and Brain Metastasis
Description:
Objective: To analyze invasive behaviors between glioma and Brain Metastasis (BM), and to screen invasive differentially expressed genes.
Methods: Patients diagnosed pathologically with glioma or BM divided into low-grade glioma groups (n = 19), high-grade glioma group (n = 18), and BM group (n = 15).
The survival period was determined.
The clinical characteristics were retrospectively analyzed to draw Kaplan-Meier survival curve.
Glioma and BM samples were obtained for RNA sequencing.
By GO, KEGG, PubMed, and GeneCard, invasive genes were theoretical selected.
Correlation between invasive genes and pathological grade was performed.
The expression level of invasive genes was verified.
Results: The survival curve found that the clinical invasive behavior related to short lifetime includes: size, edema range, blood supply, vascular invasion, grade, and Ki 67 expression.
Theoretical analysis finally found that the expression levels of CALM3, CAMK2A, CAMK2B, and PRKCG were negatively correlated with pathological grade (P< 0.
01), of which CALM3 was highly correlated with BM (P< 0.
01).
CALM3 mRNA was significantly down-regulated in BM (P< 0.
05), and PRKCG mRNA was significantly down-regulated in both glioma and BM (P< 0.
05).
Conclusion: The clinical invasive behavior between glioma and BM have significantly shortened the median survival time of patients.
Down-regulation of CALM3 suggested a higher correlation with BM, meanwhile Down-regulation of PRKCG played a role in glioma and BM The detection of CALM3 and PRKCG may be helpful for invasive behavior and provide a reference for the targeted therapy in glioma and BM.

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