中华检验医学杂志
中華檢驗醫學雜誌
중화검험의학잡지
CHINESE JOURNAL OF LABORATORY MEDICINE
2011年
8期
676-680
,共5页
陈葆国%李伯利%章卫国%石卫武%郑瑞%罗文达
陳葆國%李伯利%章衛國%石衛武%鄭瑞%囉文達
진보국%리백리%장위국%석위무%정서%라문체
白血病%髓样%急性%抗原%CD44%细胞外信号调节MAP激酶类%磷酸化酶类
白血病%髓樣%急性%抗原%CD44%細胞外信號調節MAP激酶類%燐痠化酶類
백혈병%수양%급성%항원%CD44%세포외신호조절MAP격매류%린산화매류
Leukemia,myeloid acute%Antigens,CD44%Extracellular signal-regulated MAP kinases%Phosphorylases
目的 探讨CD44v6和p-ERK1/2在AML中的表达及临床意义.方法 应用流式细胞仪检测22名健康对照者及152例AML患者骨髓原始细胞上CD44v6及p-ERK1/2的表达.对其中129例AML患者进行了跟踪随访,分析CD+44v6和CD-44v6对AML患者的复发率以及生存时间是否存在影响.结果 22名健康对照者中,各有1例(4.5%)CD44v6和p-ERK1/2阳性.152例AML患者中,55例(36.2%)CD44v6阳性,97例(64.5%)p-ERK1/2阳性.AML患者组骨髓原始细胞p-ERK1/2的MFI为14(7~58),高于健康对照组的8(6~10),差异有统计学意义(U=4.2,P<0.01).CD+44v6 AML患者p-ERK1/2的MFI为28(15~61),高于CD-44v6 AML患者的18(6~37),差异有统计学意义(U=6.7,P<0.01).CD44v6的MFI与p-ERK1/2的MFI呈显著性正相关(ra=0.7,P<0.01).对129例AML患者进行了4~65个月的随访,其中CD-44v6患者的复发率为32.1%(26/81),低于CD+44v6患者的复发率81.3%(39/48),差异有统计学意义(x2=29.1,P<0.01).生存分析表明,CD+44v6AML患者平均生存时间为(28.5±1.8)个月,CD-44v6AML患者平均生存时间为(51.2±2.0)个月,差异有统计学意义(x2=48.2,P<0.01).结论 CD44v6阳性的AML患者生存时间明显缩短、预后差.CD44v6可能通过上调p-ERK1/2水平促进白血病细胞增殖.
目的 探討CD44v6和p-ERK1/2在AML中的錶達及臨床意義.方法 應用流式細胞儀檢測22名健康對照者及152例AML患者骨髓原始細胞上CD44v6及p-ERK1/2的錶達.對其中129例AML患者進行瞭跟蹤隨訪,分析CD+44v6和CD-44v6對AML患者的複髮率以及生存時間是否存在影響.結果 22名健康對照者中,各有1例(4.5%)CD44v6和p-ERK1/2暘性.152例AML患者中,55例(36.2%)CD44v6暘性,97例(64.5%)p-ERK1/2暘性.AML患者組骨髓原始細胞p-ERK1/2的MFI為14(7~58),高于健康對照組的8(6~10),差異有統計學意義(U=4.2,P<0.01).CD+44v6 AML患者p-ERK1/2的MFI為28(15~61),高于CD-44v6 AML患者的18(6~37),差異有統計學意義(U=6.7,P<0.01).CD44v6的MFI與p-ERK1/2的MFI呈顯著性正相關(ra=0.7,P<0.01).對129例AML患者進行瞭4~65箇月的隨訪,其中CD-44v6患者的複髮率為32.1%(26/81),低于CD+44v6患者的複髮率81.3%(39/48),差異有統計學意義(x2=29.1,P<0.01).生存分析錶明,CD+44v6AML患者平均生存時間為(28.5±1.8)箇月,CD-44v6AML患者平均生存時間為(51.2±2.0)箇月,差異有統計學意義(x2=48.2,P<0.01).結論 CD44v6暘性的AML患者生存時間明顯縮短、預後差.CD44v6可能通過上調p-ERK1/2水平促進白血病細胞增殖.
목적 탐토CD44v6화p-ERK1/2재AML중적표체급림상의의.방법 응용류식세포의검측22명건강대조자급152례AML환자골수원시세포상CD44v6급p-ERK1/2적표체.대기중129례AML환자진행료근종수방,분석CD+44v6화CD-44v6대AML환자적복발솔이급생존시간시부존재영향.결과 22명건강대조자중,각유1례(4.5%)CD44v6화p-ERK1/2양성.152례AML환자중,55례(36.2%)CD44v6양성,97례(64.5%)p-ERK1/2양성.AML환자조골수원시세포p-ERK1/2적MFI위14(7~58),고우건강대조조적8(6~10),차이유통계학의의(U=4.2,P<0.01).CD+44v6 AML환자p-ERK1/2적MFI위28(15~61),고우CD-44v6 AML환자적18(6~37),차이유통계학의의(U=6.7,P<0.01).CD44v6적MFI여p-ERK1/2적MFI정현저성정상관(ra=0.7,P<0.01).대129례AML환자진행료4~65개월적수방,기중CD-44v6환자적복발솔위32.1%(26/81),저우CD+44v6환자적복발솔81.3%(39/48),차이유통계학의의(x2=29.1,P<0.01).생존분석표명,CD+44v6AML환자평균생존시간위(28.5±1.8)개월,CD-44v6AML환자평균생존시간위(51.2±2.0)개월,차이유통계학의의(x2=48.2,P<0.01).결론 CD44v6양성적AML환자생존시간명현축단、예후차.CD44v6가능통과상조p-ERK1/2수평촉진백혈병세포증식.
Objective To investigate expressions of CDev6 and p-ERK1/2 in AML patients and its clinical significance.Methods Expressions of CD44v6 and p-ERK1/2 on bone marrow blasts in 152 AML patients and 22 normal controls were determined by flow cytometry.Meanwhile,the effects of CD44v6 expression(CD+44v6 and CD-44v6) on relapse rate and survival time were analyzed by following up of 129 AML patients.Results Double positive expressions of CD44v6 and p-ERK1/2 were observed in 4.5%(1/22) of the normal bone marrow blasts while single positive expression of CD44v6 and p-ERK1/2 was observed in 36.2%(55/162) and 64.5%(97/162) of AML patients,respectively.The MFI of p-ERK1/2 expression on blast cells in AML patients was [14(7 -58)],which was higher than that in normal controls [8(6 - 10),U =4.2,P<0.01].Furthermore,MFI of p-ERK1/2 expression on blast cells in CD+44v6 AML patients was [28(15-61)] ,which was significantly higher than that in CD-44v6 AML patients [18(6- 37),U =6.7,P<0.01].A strong correlation was obtained between CD44v6 and p-ERK1/2 expression(rs = 0.7,P< 0.01).Among 129 patients followed up for 4 to 65 months,the data also revealed that the relapse rate of CD-44v6 AML patients was 32.1%(26/81) ,which was much lower than that in CD44v6 AML patients [81.3%(39/48),x2 = 29.13,P< 0.01).And the overall survival in CD44v6 AML patients was(28.5 ± 1.8)months,which was significantly worse than that of CD44v6 AML patients [(51.2±2.0) months,x2 =48.2,P< 0.01).Conclusion CD44v6 expression was associated with a poor survival in AML patients,and CD44v6 might promote the expansion of leukemic blast cells by up-regulating p-ERK1/2.