国际肿瘤学杂志
國際腫瘤學雜誌
국제종류학잡지
JOURNAL OF INTERNATIONAL ONCOLOGY
2012年
1期
64-67
,共4页
薛伟明%王占祥%马永会%谭国伟%郭剑锋
薛偉明%王佔祥%馬永會%譚國偉%郭劍鋒
설위명%왕점상%마영회%담국위%곽검봉
神经胶质瘤%表皮生长因子样结构7基因%微血管密度
神經膠質瘤%錶皮生長因子樣結構7基因%微血管密度
신경효질류%표피생장인자양결구7기인%미혈관밀도
Glioma%Epidermal growth factor-like domain 7%Microvessel density
目的 检测表皮生长因子样结构7基因( EGFL7)、微血管密度(MVD)、磷酸化局部黏着斑激酶( FAKpY397)在人脑胶质瘤中的表达,探讨胶质瘤EGFL7与FAKpY397及MVD的相互关系.方法 应用免疫组化法检测56例脑胶质瘤和8例脑外伤内减压脑组织中EGFL7、FAKpY397的表达,用CD34标记计数MVD.结果 EGFL7在脑胶质瘤组织和正常脑组织中的阳性表达率分别为75%和0,差异有统计学意义(χ2=17.45,P<0.01);随着脑胶质瘤恶性程度的增加,EGFL7的表达也明显增强( χ2=26.24,P<0.01).FAKpY397在脑胶质瘤组织和正常脑组织中的阳性表达率分别为73.2%和12.5%,差异有统计学意义(χ2=6.23,P<0.05);随着脑胶质瘤恶性程度的增加,FAKpY397的阳性表达率相应增高(χ2 =6.71,P<0.01).正常脑组织MVD为(15±4)/HP,Ⅰ~Ⅱ级和Ⅲ~Ⅳ脑胶质瘤中MVD分别为(27 ±3)/HP和(60 ±4)/HP,MVD计数在脑胶质瘤组织和正常脑组织中差异有统计学意义(P<0.01),Ⅲ、Ⅳ级脑胶质瘤的MVD计数明显高于Ⅰ、Ⅱ级(P<0.01).EGFL7与FAKpY397在脑胶质瘤的表达呈正相关(r =0.314,P<0.01);EGFL7阳性组与阴性组的MVD分别为(56±4)/HP和(25 ±3)/HP,差异有统计学意义(t=26.55,P<0.01).结论 EGFL7表达与脑胶质瘤的病理分级、MVD及FAKpY397均有良好的正相关性,提示EGFL7基因不仅在脑胶质瘤血管生成中起着重要的调控作用,而且可能直接参与了脑胶质瘤的发生、侵袭发展.
目的 檢測錶皮生長因子樣結構7基因( EGFL7)、微血管密度(MVD)、燐痠化跼部黏著斑激酶( FAKpY397)在人腦膠質瘤中的錶達,探討膠質瘤EGFL7與FAKpY397及MVD的相互關繫.方法 應用免疫組化法檢測56例腦膠質瘤和8例腦外傷內減壓腦組織中EGFL7、FAKpY397的錶達,用CD34標記計數MVD.結果 EGFL7在腦膠質瘤組織和正常腦組織中的暘性錶達率分彆為75%和0,差異有統計學意義(χ2=17.45,P<0.01);隨著腦膠質瘤噁性程度的增加,EGFL7的錶達也明顯增彊( χ2=26.24,P<0.01).FAKpY397在腦膠質瘤組織和正常腦組織中的暘性錶達率分彆為73.2%和12.5%,差異有統計學意義(χ2=6.23,P<0.05);隨著腦膠質瘤噁性程度的增加,FAKpY397的暘性錶達率相應增高(χ2 =6.71,P<0.01).正常腦組織MVD為(15±4)/HP,Ⅰ~Ⅱ級和Ⅲ~Ⅳ腦膠質瘤中MVD分彆為(27 ±3)/HP和(60 ±4)/HP,MVD計數在腦膠質瘤組織和正常腦組織中差異有統計學意義(P<0.01),Ⅲ、Ⅳ級腦膠質瘤的MVD計數明顯高于Ⅰ、Ⅱ級(P<0.01).EGFL7與FAKpY397在腦膠質瘤的錶達呈正相關(r =0.314,P<0.01);EGFL7暘性組與陰性組的MVD分彆為(56±4)/HP和(25 ±3)/HP,差異有統計學意義(t=26.55,P<0.01).結論 EGFL7錶達與腦膠質瘤的病理分級、MVD及FAKpY397均有良好的正相關性,提示EGFL7基因不僅在腦膠質瘤血管生成中起著重要的調控作用,而且可能直接參與瞭腦膠質瘤的髮生、侵襲髮展.
목적 검측표피생장인자양결구7기인( EGFL7)、미혈관밀도(MVD)、린산화국부점착반격매( FAKpY397)재인뇌효질류중적표체,탐토효질류EGFL7여FAKpY397급MVD적상호관계.방법 응용면역조화법검측56례뇌효질류화8례뇌외상내감압뇌조직중EGFL7、FAKpY397적표체,용CD34표기계수MVD.결과 EGFL7재뇌효질류조직화정상뇌조직중적양성표체솔분별위75%화0,차이유통계학의의(χ2=17.45,P<0.01);수착뇌효질류악성정도적증가,EGFL7적표체야명현증강( χ2=26.24,P<0.01).FAKpY397재뇌효질류조직화정상뇌조직중적양성표체솔분별위73.2%화12.5%,차이유통계학의의(χ2=6.23,P<0.05);수착뇌효질류악성정도적증가,FAKpY397적양성표체솔상응증고(χ2 =6.71,P<0.01).정상뇌조직MVD위(15±4)/HP,Ⅰ~Ⅱ급화Ⅲ~Ⅳ뇌효질류중MVD분별위(27 ±3)/HP화(60 ±4)/HP,MVD계수재뇌효질류조직화정상뇌조직중차이유통계학의의(P<0.01),Ⅲ、Ⅳ급뇌효질류적MVD계수명현고우Ⅰ、Ⅱ급(P<0.01).EGFL7여FAKpY397재뇌효질류적표체정정상관(r =0.314,P<0.01);EGFL7양성조여음성조적MVD분별위(56±4)/HP화(25 ±3)/HP,차이유통계학의의(t=26.55,P<0.01).결론 EGFL7표체여뇌효질류적병리분급、MVD급FAKpY397균유량호적정상관성,제시EGFL7기인불부재뇌효질류혈관생성중기착중요적조공작용,이차가능직접삼여료뇌효질류적발생、침습발전.
Objective To test the expression of epidermal growth factor-like domain 7 (EGFL7),microvessel density (MVD) and foeal adhesion kinase pY397 (FAKpY397) in human glioma tissues,and to evaluate their relationship.Methods The expression of EGFL7 and FAKpY397 in 56 cases of human glioma and 8 cases of normal brain tissues were detected by immunohistochemistry test,and MVD was detected by CD34 staining.Results There was a significant difference of the positive rates of EGFL7 between normal brain tissue (0) and gliomas (75%),χ2 =17.45,P <0.01.With the increased pathological grade,the expression level of EGFL7 increased (χ2 =26.24,P < 0.01 ).There was a significant difference of the positive rates of FAKpY397 between normal brain tissue ( 12.5% ) and gliomas (73.2%),χ2 =6.23,P < 0.05.With the increased pathological grade,the expression level of FAKpY397 increased (χ2 =6.71,P < 0.01 ). MVD on normal brain was( 15 ± 4 )/HP,on Ⅰ - Ⅱ grade and Ⅲ -Ⅳ grade gliomas was ( 27 ± 3 )/HPand ( 60 ± 4 )/HP respectively,there was a significant difference on MVD between normal brain tissue and gliomas (P < 0.01 ).Higher level of MVD was found in gliomas with higher grade ( P < 0.01 ).There was a positive correlation between EGFL7 and FAKpY397 expressions in gliomas (r =0.314,P <0.01 ).There was a significant difference on MVD between positive and negative expression of EGFL7 ( t =26.55,P < 0.01 ). MVD was (56 ± 4 )/HP and (25 ± 3 )/HP respectively.Conclusion The expression of EGFL7 of human gliomas has a favorable positive correlation with the degree of malignancy,MVD and FAKpY397.It is indicated that EGFL7not only palys an important regulative role in glioma neovascularization,but also it may participate directly in glioma occurrence and invasion.