ABSTRACT
Objective To explore expression of HMGB1 in glioma tissue of glioma-related epilepsy patients. Methods Immunohistochemistry was used to detect the expression of HMGB1 in the tissues from 82 glioma-related epi?lepsy patients (glioma-related epilepsy group), 80 glioma patients (glioma without epilepsy group), 80 intractable epilepsy patients (epilepsy control group) epileptogenic foci tissue and 20 normal controls (negative control group). Results HMGB1 in glioma tissue of glioma-related epilepsy group was significantly higher than that in glioma tissue of glioma without epilepsy grou p (χ2=16.944, P<0.001), especially in low pathological grade glioma tissue. HMGB1 was higher in glioma tissue of glioma-related epilepsy group than in epileptogenic foci tissue of epilepsy control group (χ2=26.094, P<0.001). Expression of HMGB1 in glioma tissue of glioma without epilepsy group (χ2=32.273, P<0.001) and epileptogenic foci tissue of epilepsy control group ( χ2=22.236,P<0.001) was higher than in normal brain tissue of negative control group. In glioma-related epilepsy group, HMGB1 was positively correlated with seizures duration(r=0.365,P=0.001), sei? zures frequency (r=0.531,P=0.000) and pathological grade of glioma tissue (r=0.265,P=0.016). Conclusions HMGB1 is highly expressed in glioma tissues of glioma-related epilepsy; HMGB1 expression is closely related with seizures; and HMGB1 in glioma tissue may contribute to the formation of glioma-related epilepsy.
ABSTRACT
@#Objective To investigate the application of tissue microarray (TMA) technique in human brain gliomas. Methods The TMAs containing 50 glioma specimens of all pathological grades were constructed. The immunohistochemistry and in situ hybridization techniques were used to detect the expressions of Ki-67, mutant P53 protein and wild-type p53 mRNA. Results The expression of Ki-67 was significantly associated with the pathological grades (P<0.05). There was significant correlation between the expression of mutant P53 protein and wild-type p53 mRNA (P<0.001), as well as p53 mutation and Ki-67 (P<0.05). Conclusion It's feasible and valuable to utilize TMA technique in research on human brain gliomas.