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组织TIPE2、Cath-D、GPX3与PTC发病关系及预测术后复发的相关性

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目的 探讨组织免疫负调控分子肿瘤坏死因子α诱导蛋白8样分子2(TIPE2)、组织蛋白酶D(Cath-D)、谷胱甘肽过氧化物酶3(GPX3)与甲状腺乳头状癌(PTC)发病及预测术后复发的相关性。方法 选取2020年6月至2021年12月于新乡市中心医院接受手术治疗的176例(均完成1年随访)PTC患者为PTC组,同期176例甲状腺良性结节患者为对照组,根据PTC患者术后1年复发情况将其分为复发(64例)和未复发(112例)两个亚组。比较两组TIPE2、Cath-D、GPX3表达情况,比较复发和未复发患者癌组织中TIPE2、Cath-D、GPX3表达情况,比较不同病理学参数PTC患者癌组织中TIPE2、Cath-D、GPX3表达情况,分析组织中TIPE2、Cath-D、GPX3表达情况与PTC发病、PTC病理学参数及术后复发的相关性,偏回归分析PTC患者术后复发的影响因素。结果 PTC组癌组织中TIPE2、GPX3阳性表达率低于对照组,Cath-D阳性表达率高于对照组(P<0。05);复发患者癌组织中TIPE2、GPX3阳性表达率低于未复发患者,Cath-D阳性表达率高于未复发患者(P<0。05);不同病理学参数PTC患者癌组织中TIPE2、GPX3阳性表达率比较:Ⅰ~Ⅱ期高于Ⅲ~Ⅳ期,高中分化高于低分化,无淋巴结转移高于有淋巴结转移(P<0。05);不同病理学参数PTC患者癌组织中Cath-D阳性表达率比较:Ⅰ~Ⅱ期低于Ⅲ~Ⅳ期,高中分化低于低分化,无淋巴结转移低于有淋巴结转移(P<0。05);PTC发病、复发、临床分期、分化程度、淋巴结转移与组织中TIPE2、GPX3阳性表达率呈负相关,与Cath-D阳性表达率呈正相关(P<0。05);Logistic回归分析发现,PTC患者癌组织TIPE2、GPX3阳性表达是PTC患者术后复发的保护因素,Cath-D阳性表达为危险因素(p<0。05)。结论 组织中TIPE2、Cath-D、GPX3阳性表达率与PTC发生发展相关,且是PTC患者术后复发的影响因素。
Relationship between TIPE2,Cath-D,GPX3 and incidence of PTC and correlation of predicting postoperative recurrence
[Objective]To investigate the correlation between tumor necrosis factor-alpha-induced protein 8-like 2(TIPE2),cathepsin D(Cath-D),glutathione peroxidase 3(GPX3)and the incidence and postoperative recurrence of papillary thyroid carcinoma(PTC).[Methods]A total of 176 patients with PTC who received surgical treatment in Xinxiang Central Hospital from June 2020 to December 2021(all completed 1-year follow-up)were selected as the PTC group,and 176 patients with benign thyroid nodules during the same period were selected as the control group.According to the recurrence of PTC patients 1 year after surgery,they were divided into two subgroups:recurrence(64 cases)and non-recurrence(112 cases).The expressions of TIPE2,Cath-D and GPX3 in the two groups were compared,the expressions of TIPE2,Cath-D and GPX3 in the cancer tissues of patients with recurrence and those without recurrence were compared,and the expressions of TIPE2,Cath-D and GPX3 in the cancer tissues of patients with different pathological parameters PTC were compared.The correlation between the expression of TIPE2,Cath-D and GPX3 in tissues and the incidence of PTC,pathological parameters of PTC and postoperative recurrence was analyzed,and the influencing factors of postoperative recurrence in PTC patients were analyzed by partial regression.[Results]The positive expression rates of TIPE2 and GPX3 in PTC group were lower than those in control group,and the positive expression rate of Cath-D in PTC group was higher than that in control group(P<0.05).The positive expression rates of TIPE2 and GPX3 in patients with recurrence were lower than those without recurrence,and the positive expression rate of Cath-D was higher than that without recurrence(P<0.05).The positive expression rates of TIPE2 and GPX3 in cancer tissues of PTC patients with different pathological parameters were higher in stage Ⅰ to Ⅱ than in stage Ⅲ to Ⅳ,higher in high and medium differentiation than in low differentiation,higher in no lymph node metastasis than in lymph node metastasis(P<0.05).The incidence,recurrence,clinical stage,differentiation degree and lymph node metastasis of PTC were negatively correlated with the positive expression rate of TIPE2 and GPX3 in tissues,and positively correlated with the positive expression rate of Cath-D(P<0.05).Logistic regression analysis showed that the positive expression of TIPE2 and GPX3 in cancer tissue was a protective factor for postoperative recurrence in PTC patients,and the positive expression of Cath-D was a risk factor(P<0.05).[Conclusion]The positive expression rates of TIPE2,Cath-D and GPX3 in tissues are related to the occurrence and development of PTC,and are the influencing factors for postoperative recurrence of PTC patients.

papillary thyroid carcinomapostoperative recurrenceimmunonegative regulator tumor necrosis factor-alpha-induced protein 8-like 2cathepsin Dglutathione peroxidase 3

杜学铅、张森焱、冯跃庆

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新乡市中心医院头颈乳腺外科,河南新乡 453000

甲状腺乳头状癌 术后复发 免疫负调控分子肿瘤坏死因子α诱导蛋白8样分子2 组织蛋白酶D 谷胱甘肽过氧化物酶3

2024

中国医学工程
中国医药生物技术协会 卫生部肝胆肠外科研究中心

中国医学工程

影响因子:0.504
ISSN:1672-2019
年,卷(期):2024.32(5)
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