摘要
BACKGROUND： Several studies have shown that midkine directly participates in tumor cell growth and invasion, as well as the regulation of angiogenesis. OBJECTIVE： To investigate midkine expression in meningioma tissue in relation to angiogenesis, invasion, peritumoral edema, and clinicopathology. DESIGN, TIME AND SETTING： The present clinical, case-controlled, neuropathological study was performed at the Laboratory of Molecular Organism, People＇s Hospital of Deyang City between May 2007 and April 2008. MATERIALS： Fifty-two meningioma tissues were classified by WHO tumor classification of the central nervous system, comprising 40 grade Ⅰ meningioma, five grade Ⅱ meningioma, and seven grade Ⅲ meningioma. Ten normal, human cerebral maters were selected from cerebral trauma patients. METHODS： Midkine protein expression and mean microvessel density were detected using immunohistochemical techniques. Simultaneously, all data were statistically analyzed. MAIN OUTCOME MEASURES： Midkine expression and microvessel density in meningiomas and normal cerebral maters. RESULTS： The positive midkine expression rate was 64% in the meningioma tissues. However, midkine expression was not detected in normal cerebral mater tissue. The mean microvessel density was 82.0 ± 22.7 in the meningiomas, and 25.8± 6.2 in the normal cerebral mater tissues. There was significant difference in midkine expression and mean microvessel density between meningioma tissues and human cerebral maters （P 〈 0.05）. Midkine expression positively correlated with microvessel density （r = 0.756, P 〈 0.05）. Midkine expression did not correlate to patient age, gender, or tumor size, location, and shape （P 〉 0.05）. However, it closely correlated with patient clinical condition, pathological grade, invasion, and peritumoral edema （r = 0.3785,0.741 2,0.6518, 0.614 2, P 〈 0.05）. CONCLUSION： Midkine protein was overexpressed in meningiomas and correlated to tumor angiogenesis, invasion, pefitumoral edema, and clinicopathology.
BACKGROUND： Several studies have shown that midkine directly participates in tumor cell growth and invasion, as well as the regulation of angiogenesis. OBJECTIVE： To investigate midkine expression in meningioma tissue in relation to angiogenesis, invasion, peritumoral edema, and clinicopathology. DESIGN, TIME AND SETTING： The present clinical, case-controlled, neuropathological study was performed at the Laboratory of Molecular Organism, People＇s Hospital of Deyang City between May 2007 and April 2008. MATERIALS： Fifty-two meningioma tissues were classified by WHO tumor classification of the central nervous system, comprising 40 grade Ⅰ meningioma, five grade Ⅱ meningioma, and seven grade Ⅲ meningioma. Ten normal, human cerebral maters were selected from cerebral trauma patients. METHODS： Midkine protein expression and mean microvessel density were detected using immunohistochemical techniques. Simultaneously, all data were statistically analyzed. MAIN OUTCOME MEASURES： Midkine expression and microvessel density in meningiomas and normal cerebral maters. RESULTS： The positive midkine expression rate was 64% in the meningioma tissues. However, midkine expression was not detected in normal cerebral mater tissue. The mean microvessel density was 82.0 ± 22.7 in the meningiomas, and 25.8± 6.2 in the normal cerebral mater tissues. There was significant difference in midkine expression and mean microvessel density between meningioma tissues and human cerebral maters （P 〈 0.05）. Midkine expression positively correlated with microvessel density （r = 0.756, P 〈 0.05）. Midkine expression did not correlate to patient age, gender, or tumor size, location, and shape （P 〉 0.05）. However, it closely correlated with patient clinical condition, pathological grade, invasion, and peritumoral edema （r = 0.3785,0.741 2,0.6518, 0.614 2, P 〈 0.05）. CONCLUSION： Midkine protein was overexpressed in meningiomas and correlated to tumor angiogenesis, invasion, pefitumoral edema, and clinicopathology.
