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首页|期刊导航|昆明医科大学学报|乳腺癌组织中LDH-C4与CMKLR1的表达及其与临床病理特征、肿瘤标志物和预后的关系

乳腺癌组织中LDH-C4与CMKLR1的表达及其与临床病理特征、肿瘤标志物和预后的关系

龚春梅 熊蓓蓓 李立兰 吴明铭 罗露

昆明医科大学学报2026,Vol.47Issue(6):84-92,9.
昆明医科大学学报2026,Vol.47Issue(6):84-92,9.DOI:10.12259/j.issn.2095-610X.S20260609

乳腺癌组织中LDH-C4与CMKLR1的表达及其与临床病理特征、肿瘤标志物和预后的关系

Expression of LDH-C4 and CMKLR1 in Breast Cancer Tissues and Their Relationship with Clinicopathological Characteristics,Tumor Markers and Prognosis

龚春梅 1熊蓓蓓 1李立兰 1吴明铭 2罗露1

作者信息

  • 1. 成都市双流区第一人民医院/四川大学华西空港医院/肿瘤/介入血管科病区,四川成都 610200
  • 2. 福建医科大学附属第一医院肿瘤内科,福建 福州 350004
  • 折叠

摘要

Abstract

Objective To investigate the expression of lactate dehydrogenase C4(LDH-C4)and chemokine-like receptor 1(CMKLR1)in breast cancer tissues and their relationship with clinical pathological characteristics,tumor markers and prognosis.Methods A prospective cohort study was conducted on 150 patients with breast cancer admitted to the First People's Hospital of Shuangliu District,Chengdu from January 2016 to June 2020.All patients underwent radical mastectomy and cancer tissues and adjacent normal tissues were collected intraoperatively.Immunohistochemical staining was used to detect LDH-C4 and CMKLR1 expression.LDH-C4 and CMKLR1 expression in different tissues was compared,and the relationship between the expression of LDH-C4 and CMKLR1 in cancer tissues and the pathological characteristics,serum tumor markers[carcinoembryonic antigen(CEA),cancer antigen 153(CA153)]of breast cancer patients was analyzed.Follow-up was conducted for 6~60 months.Kaplan-Meier method analysis was performed to analyze the relationship between LDH-C4 and CMKLR1 expression and postoperative progression-free survival(PFS)prognosis.Stratified Cox regression analysis was used to identify factors influencing PFS prognosis,and subgroup analysis of LDH-C4 and CMKLR1 expression with PFS prognosis were performed.Results The positive expression rate of LDH-C4 in breast cancer tissue was 53.33%,significantly higher than the 26.67%in adjacent normal tissue,while the positive expression rate of CMKLR1 was 41.33%,significantly lower than the 89.33%in adjacent normal tissue(x2=22.218,76.083,all P<0.05).In patients with pathological stage Ⅱ-Ⅲ,lymph node metastasis,CEA>5.39 μg/L,and CA153>26.57 U/mL,the positive expression of LDH-C4 was higher,and CMKLR1 positive expression was lower compared to patients with stage I disease,no lymph node metastasis,CEA ≤ 5.39 μg/L,and CA153 ≤ 26.57 U/mL(P<0.05).During the 6~60 month follow-up,33 patients experienced tumor progression.Kaplan-Meier survival analysis showed that the 5-year overall progression-free survival rate in LDH-C4 positive patients was 65.85%,lower than the 92.06%in negative patients,while CMKLR1 positive patients had a rate of 91.67%,higher than the 67.06%in negative patients(Log-rank x2=11.748,8.832,P<0.05).Cox regression analysis showed that pathological stage,lymph node metastasis,CEA,CA153 and LDH-C4 expression were independent risk factors for PFS prognosis,while CMKLR1 expression was an independent protective factor(P<0.05).Stratified Cox proportional hazard regression analysis showed that after adjusting for pathological stage,lymph node metastasis status,CEA and CA153 levels,LDH-C4 positive positively ramained a risk factor for PFS in breast cancer patients(HR=3.082,95%CI:1.889~5.027,P<0.05),while CMKLR1 positivity was a protective factor for PFS(HR=0.902,95%CI:0.825~0.986,P<0.05).Conclusion The expression of LDH-C4 and CMKLR1 is closely associated with pathological stage,lymph node metastasis and serum tumor markers of breast cancer,Together,they constitute a powerful risk network affecting postoperative PFS prognosis and provide a novel theoretical framework for clinical prognostic assessment and precision management after surgery.

关键词

乳腺癌/LDH-C4/CMKLR1/临床病理特征/肿瘤标志物/预后

Key words

Breast cancer/LDH-C4/CMKLR1/Clinicopathological characteristics/Tumor markers/Prognosis

分类

医药卫生

引用本文复制引用

龚春梅,熊蓓蓓,李立兰,吴明铭,罗露..乳腺癌组织中LDH-C4与CMKLR1的表达及其与临床病理特征、肿瘤标志物和预后的关系[J].昆明医科大学学报,2026,47(6):84-92,9.

基金项目

四川省卫生健康科研课题(23PJ319) (23PJ319)

昆明医科大学学报

1003-4706

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