摘要
目的探讨癌胚抗原(CEA)、脂联素联合瘦素对结直肠癌的临床诊断价值。方法采用病例对照研究,选取新诊断的结直肠癌患者40例为试验组,40例非结直肠癌患者作为对照组,对研究对象的血清CEA、脂联素、瘦素的水平进行检测。利用ROC曲线评价瘦素联合脂联素对结直肠癌的诊断价值。结果试验组脂联素水平低于对照组,瘦素、CEA水平明显高于对照组,差异均具有统计学意义(P<0.05)。脂联素联合瘦素ROC曲线下面积达到0.714±0.058,特异性77.5%,敏感性65.7%。脂联素、瘦素联合CEA ROC曲线下面积达到0.818±0.048,特异性82.5%,敏感性89.5%。瘦素、脂联素cut off值分别为11.53、9.08μg/mL。结论 CEA、脂联素及瘦素三者联合筛查可显著提高结直肠癌的检出率。
Objective To explore the diagnostic value of carcinoembryonic antigen(CEA),adiponectin combined with leptin in colorectal cancer.Methods The case control study was adopted.Forty cases newly diagnosed as colorectal cancer were selected.Forty cases of non-colorectal cancer were selected according to 1∶1 matching proportion.Serum levels of CEA,adiponectin and leptin were measured in the study subjects.The ROC curve was used to evaluate the diagnostic value of adiponectin combined with leptin for colorectal cancer.Results Serum level of adiponectin in the experimental group was lower than that in the control group,while the CEA and leptin levels were higher than those in the control group,the difference between the two groups was statistically significant(P<0.05).The area under the curve of adiponectin combined with leptin reached 0.714±0.058,its specificity and sensitivity were 77.5% and 65.7% respectively.The area under the curve of adiponectin,leptin combined with CEA reached 0.818±0.048,its specificity and sensitivity were 82.5% and 89.5% respectively.The cut-off values of leptin and adiponectin were 11.53μg/mL and 9.08μg/mL respectively.Conclusion The combined screening of CEA,adiponectin and leptin can significantly improve the detection rate of colorectal cancer.
引文
[1]Ferlay J,Steliarova FE,Lortet TJ,et al.Cancer incidence and mortality patterns in Europe:estimates for 40countries in 2012[J].Eur J Cancer,2013,49(6):1374-1403.
[2]Ning Y,Wang L,Giovannucci L.A quantitative analysis of body mass index and colorectal cancer:findings from 56observational studies[J].Obes Rev,2010,11(1):19-30.
[3]Fenton I,Birmingham M,Hursting D,et al.Adiponectin blocks multiple signaling cascades associated with leptininduced cell proliferation in Apc Min/+colon epithelial cells[J].Int J Cancer,2008,122(11):2437-2445.
[4]向德森,张敬,肖杰,等.脂联素基因多态性与结直肠癌发病风险关联性研究[J].重庆医学,2015,44(25):3493-3496.
[5]陈卫中,倪宗瓒,潘晓平,等.用ROC曲线确定最佳临界点和可疑值范围[J].现代预防医学,2005,32(7):729-731.
[6]Crawshaw P,Augestad M,Keller S,et al.Multivisceral resection for advanced rectal cancer:outcomes and experience at a single institution[J].Am J Surg,2015,209(3):526-531.
[7]Sugiyama M,Takahashi H,Hosono K,et al.Adiponectin inhibits colorectal cancer cell growth through the AMPK/mTOR pathway[J].Int J Oncol,2009,34(2):339-344.
[8]Kim AY,Lee YS,Kim HK,et al.Adiponectin represses colon cancer cell proliferation via AdipoR1-and-R2-mediated AMPK activation[J].Mol Endocrinol,2010,24(7):1441-1452.
[9]Xu XT,Xu Q,Tong JL,et al.Meta-analysis:circulating adiponectin levels and risk of colorectal cancer and adenoma[J].J Dig Dis,2011,12(4):234-244.
[10]Saxena NK,Sharma D,Ding XK,et al.Concomitant activation of the JAK/STAT,PI3K/AKT,and ERK signaling is involved in leptin-mediated promotion of invasion and migration of hepatocellular carcinoma cells[J].Cancer Res,2007,67(6):2497-2507.
[11]Huang XF,Chen JZ.Obesity,the PI3K/Akt signal pathway and colon cancer[J].Obes Revi,2009,10(6):610-616.
[12]Ogunwobi OO,Beales IL.Cyclo-oxygenase-independent inhibition of apoptosis and stimulation of proliferation by leptin in human colon cancer cells[J].Dig Dis Sci,2007,52(8):1934-1945.
[13]Bjrbaek C,Uotani S,Da Silva B,et al.Divergent signaling capacities of the long and short isoforms of the leptin receptor[J].J Biol Chem,1997,272(51):32686-32695.
[14]Quintas-Cardama A,Verstovsek S.Molecular pathways:JAK/STAT pathway:mutations,inhibitors,and resistance[J].Clin Cancer Res,2013,19(8):1933-1940.
[15]Tae CH,Kim SE,Jung SA,et al.Involvement of adiponectin in early stage of colorectal carcinogenesis[J].BMC Cancer,2014,14(12):811-815.