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 = 0.378 5, 0.741 2, 0.651 8, 0.614 2, P < 0.05). CONCLUSION: Midkine protein was overexpressed in meningiomas and correlated to tumor angiogenesis, invasion, peritumoral 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. METHODS: Midkine protein expression and mean microvessel density were detected using immunohistochemical techniques. Simultaneously, all data were copied analyzed. MAIN OUTCOME MEASURES: Midkine e 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 5, 0.741 2, 0.651 8, 0.614 2, P <0.05). CONCLUSION: Midkine protein was overexpressed in meningiomas and correlated to tumor angiogenesis, invasion, peritumoral edema, an d clinicopathology.