Expression Of MTOR And EIF4E In Glioma: Relationship And Clinical Value

ObjectiveIntracranial tumour in one of the most common diseases in neurosurgery, and the most common malignant tumor is glioma in intracranial tumour. Brain tumour gum can happen at any age, the main age is 30-40 years, in addition, people with 10-20 years are alse common in intracranial tumour. According to the national statistics of brain tumor,35.26%-60.96%(44.69%) intracranial tumour is glioma, Column first,its attacks and relapse rate both are significantly higher than other intracranial tumour. Due to the glioma invasive growth, the operation completely remove is difficult, postoperation relapse rate and mortality rate are both high.In the development human solid tumors, The excessive proliferation of tumor cells is the most important feature. Accompanied by a cell division essential protein replication system activation, Producing lots of protein, to provide the requisite physical infrastructure for cells divide,so synthesis cells protein is essential for tumour cells divide proliferation. Malignant glioma is one of the most malignant tumor in human, Excessive proliferation of a large number of juvenile gum cell is a important pathological trait in malignant tumour. Research shows Mammals mTOR protein plays the regulatory role in the process of tumor cells divide and proliferation. After mTOR was phosphoric, it can be activated. The activated mTOR can phosphoric acid and really the translation of the nuclear factor 4e, the combination of apolipoprotein 4ebpl,4ebpl and is the translation of the nuclear factor to leave the eif4e, Work after the eif4e can activate the translation, to start protein synthesis and promote cell division,play a key role in tumour development.The purpose of this study is to discuss the expression of Mammals mTOR protein and eIF4E in human glioma,and the relationship with pathological classification of human glioma, and to further clarify the molecules mechanism of the development in human brain gum developement, to provide theoretical basis.MethodsThe paraffin-embedded specimens of gliomas were taken from department of neurosurgeon in First Affiliated Hospital of Zhengzhou University from july 2006 to march 2009, including 35 males,29 females, mean age was 3.5 ages to 88 ages,pathological grading was classified according to the standard pathological grades for glioma.GradeⅠ10 cases,gradeⅡ21cases,gradeⅢ22 cases,gradeⅣ11 cases.We take the of method of SP to detect the expression of mTOR protein and eIF4E in glioma and normal brain tissue. Due to glioma GradeⅠandⅡwas not enough, We combined gradeⅠand gradeⅡof glioma to low malignancy group (LMG),and grsdeⅢand grade IV to high malignancy group (HMG).We usedχ2-test and Fisher's exact probabilities in 2×2 table to test the difference between normal brain tissue, low malignancy group and high malignancy group,and to analyze the relevance of mTOR and eif4e with Spearman level analysis. Results1. mTOR:With the increasing of pathological grades of glioma,the positive rate of mTOR was 30.00% for grade 1,38.10% for gradeⅡ,77.27% for gradeⅢ,81.82 % for gradeⅣ.And there was significant deviation between LGG(35.48%) and HGG (79.79%).2. eIF4E:With the increasing of pathological grades of glioma,the positive rate of eIF4E was40.00% for gradeⅠ,47.62% for gradeⅡ,72.73% for gradeⅢ,90.91 % for gradeⅣ.And there was significant deviation between LGG(45.16%) and HGG(78.79%).3. There was significant deviation between mTOR andeIF4E,there was depend-ability between mTOR andeIF4E.Conclusions1. mTOR in normal brain tissue did not express,and the expression of mTOR protein was positively correlated with the glioma malignancy.2.eIF4E in normal brain tissue did not express,and the expression of eIF4E protein was positively correlated with the glioma malignancy.3. There was significant dependability between mTOR and eIF4E. mTOR and eIF4E play a synergistic role in the invasive growth of glioma cells.They are helpful to judge the malignancy,invasion and prognosis of glioma,and become possible new directions in targeted therapy of glioma.