摘要
目的探讨急性髓系白血病(AML)病人外周血中CC类趋化因子22(CCL22)、叉头框蛋白P1(FOXP1)表达水平及其预后预测价值。方法选择2018年5月至2019年5月在孝感市中心医院、华中科技大学医学院附属同济医院及咸宁市中心医院确诊的68例AML病人设为观察组,另取同期健康体检者68例作为对照组,采用酶联免疫法测定外周血CCL22,FOXP1表达水平,分析其与临床特征的关系;采用Pearson法分析AML病人外周血中CCL22,FOXP1表达的相关性;采用Kaplan-Meier生存分析法分析CCL22,FOXP1表达与总体生存时间(OS)的关系;采用Cox比例风险回归模型分析病人预后死亡的影响因素。结果与对照组相比,观察组CCL22[(600.27±62.89)ng/L比(756.84±100.86)ng/L],FOXP1[(56.02±13.68)ng/L比(103.06±22.16)ng/L]表达均明显升高(t=10.86,14.90,均P<0.05);CCL22,FOXP1表达水平与AML病人年龄、性别、染色体预后、血红蛋白(HGB)、血小板计数(PLT)、FMS样酪氨酸激酶3-内部串联重复基因(FLT3-ITD)、核仁磷酸蛋白基因1(NPM1)突变无关(χ^(2)=0.06~2.95,均P>0.05),与脾肿大、白细胞计数(WBC)有关(χ^(2)=5.90~8.59,均P<0.05);Pearson法分析结果显示,AML病人外周血中CCL22与FOXP1表达呈正相关(r=0.27,P<0.05);Kaplan-Meier法分析结果显示,AML病人外周血CCL22,FOXP1高表达组3年生存率均低于低表达组(47.06%比70.59%,44.12%比73.53%)(χ^(2)=6.50,P<0.05);多因素logistic回归分析结果显示,CCL22,FOXP1是影响AML病人预后的独立危险因素(P<0.05)。结论CCL22,FOXP1在AML病人外周血中呈高表达,CCL22,FOXP1高表达组病人3年生存率均低于低表达组,二者有望成为AML病人预后评估的分子标志物。
Objective To investigate the expression levels of C-C class chemokine 22(CCL22)and forkhead box P1(FOXP1)in pe-ripheral blood of patients with acute myeloid leukemia(AML)and their prognostic value.Methods From May 2018 to May 2019,68 AML patients diagnosed in Xiaogan Central Hospital,Tongji Hospital affiliated to Huazhong University of Science and Technology School of Medicine,and Xianning Central Hospital were gathered as the research group,another 68 healthy people who came to our hospital for physical examination were gathered as the control group.The expression levels of CCL22 and FOXP1 in peripheral blood were determined by enzyme-linked immunosorbent assay,and their relationship with clinical characteristics was analyzed;Pearson method was used to analyze the correlation of CCL22 and FOXP1 expression in peripheral blood of AML patients;Kaplan-Meier surviv-al analysis was used to analyze the relationship between the expression levels of CCL22 and FOXP1 in peripheral blood of AML pa-tients and overall survival time(OS);Cox proportional hazards regression model was used to analyze the influencing factors of prognosis and death of patients.Results Compared with healthy subjects(control group),the expressions of CCL22[(600.27±62.89)ng/L vs.(756.84±100.86)ng/L]and FOXP1[(56.02±13.68)ng/L vs.(103.06±22.16)ng/L]in peripheral blood of AML patients were obviously in-creased(t=10.86,14.90,all P<0.05);the expression levels of CCL22 and FOXP1 were not related to age,gender,chromosomal prognosis,hemoglobin(HGB),and platelet count(PLT)in AML patients(χ^(2)=0.06-2.95,all P>0.05),but were related to splenomegaly and white blood cell count(WBC)(χ^(2)=5.90-8.59,all P<0.05);the results of Pearson analysis showed that the expressions of CCL22 and FOXP1 in peripheral blood of AML patients were positively correlated(r=0.27,P<0.05);the results of Kaplan-Meier analysis showed that the 3-year survival rates of the high expression groups of CCL22 and FOXP1 in peripheral blood of AML patients were lower than those of the low expression group(47.06%vs.70.59%,44.12%vs.73.53%)(χ^(2)=6.50,P<0.05);multivariate logistic regression analysis showed that CCL22 and FOXP1 were independent risk factors affecting the prognosis of AML patients(P<0.05).Conclusions CCL22 and FOXP1 are highly expressed in the peripheral blood of AML patients.The 3-year survival rates of CCL22 and FOXP1 high expression groups were lower than those of low expression groups,and they may become molecular markers for prognostic evaluation of AML patients.
作者
胡婕
刘瑞菡
王高翔
熊婷
黄欣
程利民
HU Jie;LIU Ruihan;WANG Gaoxiang;XIONG Ting;HUANG Xin;CHENG Limin(Department of Hematology,Xiaogan Central Hospital,Xiaogan,Hubei 432099,China;Department of Laboratory Medicine,Xiaogan Central Hospital,Xiaogan,Hubei 432099,China;Department of Hematology,Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology,Wuhan,Hubei 430030,China;Department of Hematology,Xianning Central Hospital,Xianning,Hubei 437199,China)
出处
《安徽医药》
CAS
2024年第2期371-375,共5页
Anhui Medical and Pharmaceutical Journal
基金
孝感市自然科学计划立项项目(XGKJ2022010036)。
作者简介
通信作者:程利民,男,主任医师,研究方向为血液内科疾病,Email:hgwei16@163.com。
