高级搜索

进展期食管胃结合部恶性肿瘤主动脉旁淋巴结转移患者的危险因素及预后分析

牛权, 毕小刚

牛权, 毕小刚. 进展期食管胃结合部恶性肿瘤主动脉旁淋巴结转移患者的危险因素及预后分析[J]. 肿瘤防治研究, 2024, 51(11): 918-925. DOI: 10.3971/j.issn.1000-8578.2024.24.0272
引用本文: 牛权, 毕小刚. 进展期食管胃结合部恶性肿瘤主动脉旁淋巴结转移患者的危险因素及预后分析[J]. 肿瘤防治研究, 2024, 51(11): 918-925. DOI: 10.3971/j.issn.1000-8578.2024.24.0272
NIU Quan, BI Xiaogang. Risk Factors and Prognosis of Patients with Para-Aortic Lymph Node Metastasis of Advanced Esophagogastric Junction Malignancy[J]. Cancer Research on Prevention and Treatment, 2024, 51(11): 918-925. DOI: 10.3971/j.issn.1000-8578.2024.24.0272
Citation: NIU Quan, BI Xiaogang. Risk Factors and Prognosis of Patients with Para-Aortic Lymph Node Metastasis of Advanced Esophagogastric Junction Malignancy[J]. Cancer Research on Prevention and Treatment, 2024, 51(11): 918-925. DOI: 10.3971/j.issn.1000-8578.2024.24.0272

进展期食管胃结合部恶性肿瘤主动脉旁淋巴结转移患者的危险因素及预后分析

详细信息
    作者简介:

    牛权(1992-),男,硕士,住院医师,主要从事胃肠胰恶性肿瘤研究,ORCID: 0009-0006-0769-2005

    通讯作者:

    毕小刚(1963-),男,硕士,主任医师,教授,主要从事消化道恶性肿瘤研究,E-mail: 310070682@qq.com,ORCID: 0009-0004-2267-4425

  • 中图分类号: R735

Risk Factors and Prognosis of Patients with Para-Aortic Lymph Node Metastasis of Advanced Esophagogastric Junction Malignancy

More Information
  • 摘要:
    目的 

    通过对比进展期食管胃结合部恶性肿瘤患者一般临床病理特征及区域淋巴结转移状态,探讨患者主动脉旁淋巴结转移阳性的危险因素及其预后。

    方法 

    收集224例手术根治性切除食管胃结合部恶性肿瘤患者临床病理资料,对影响第16组淋巴结转移的危险因素进行单因素χ2检验和多因素Logistic回归分析。生存分析采用Kaplan-Meier法,生存率比较采用Log rank检验。

    结果 

    (1)单因素分析见Siewert分型、肿瘤大小、病理分期、T分期、N分期与主动脉旁淋巴结转移阳性相关(均P<0.05)。多因素分析发现Siewert分型、肿瘤大小均是其转移阳性的独立危险因素(均P<0.001)。(2)纳入的17组区域淋巴结与主动脉旁淋巴结转移相关的单因素分析中,除No.5、No.6、No.111、No.112组淋巴结与主动脉旁淋巴结转移阳性不相关(均P>0.05),剩余13组区域淋巴结均与其相关。多因素分析发现,No.7、No.11p、No.110组淋巴结均是其转移阳性的独立危险因素(均P<0.05)。进一步分析发现,当至少其中一组区域淋巴结转移时,阳性转移率高达47.4%(3组均阴性时仅4.7%)。(3)主动脉旁淋巴结转移阳性患者术后1年、3年累积生存率分别为76.5%、8.1%,阴性患者分别为98.3%、76.8%。Log rank检验表明两组总生存率存在明显差异(P<0.001)。

    结论 

    (1)进展期食管胃结合部恶性肿瘤患者术前检查应明确患者的肿瘤分型及大小,建议SiewertⅡ、Ⅲ型和肿瘤直径>6 cm的患者行主动脉旁淋巴结清扫术。(2)术中行No.7、No.11p、No.110淋巴结冰冻活检病理,发现转移阳性后行主动脉旁淋巴结清扫术,有助于术中对清扫主动脉旁淋巴结的判断。

     

    Abstract:
    Objective 

    To determine the risk factors and prognostic survival of patients with para-aortic lymph node metastasis of advanced esophagogastric junction malignancy by comparing their general clinicopathological characteristics and regional lymph node metastasis status with those of patients with negative para-aortic lymph node metastasis.

    Methods 

    This single-center retrospective case study collected the clinical and pathological data of 224 patients with esophagogastric junction malignant tumors undergoing radical resection. Single factor affecting lymph node metastasis in group 16 was analyzed by chi square test, and multiple factors were examined using logistic regression. Kaplan-Meier method was used for survival analysis, and Log rank test was used for survival rate comparison.

    Results 

    Among the 224 patients with advanced esophagogastric junction malignant tumors, (1) Univariate analysis showed that Siewert classification, tumor diameter, pathological stage, T stage, and N stage were associated with positive para-aortic lymph node metastasis (P<0.05). Meanwhile, multivariate logistic analysis showed that Siewert type and tumor diameter were independent risk factors for positive metastasis (P<0.05); (2) Among the 17 groups of regional lymph nodes with para-aortic lymph node metastasis, univariate analysis revealed that No.5, No.6, No.111, and No.112 lymph nodes were not correlated with positive para-aortic lymph node metastasis (P>0.05). The remaining 13 groups of regional lymph nodes were all associated with para-aortic lymph node metastasis. Meanwhile, multivariate logistic analysis revealed that No.7, No.11p, and No.110 lymph nodes were independent risk factors for metastasis (P<0.05). When the regional lymph node metastasis in these three groups was negative, the positive rate of para-aortic lymph node metastasis was only 4.7%. When at least one of these groups had regional lymph node metastasis, the positive metastasis rate was up to 47.4%; (3) The 1- and 3-year cumulative survival rates of the patients with positive para-aortic lymph node metastasis after surgery were 76.5% and 8.1%, respectively, and those in negative patients were 98.3% and 76.8%, respectively. Log rank test showed a significant difference in overall survival rate between the patients with positive and negative para-aortic lymph node metastasis (P<0.001).

    Conclusion 

    (1) Preoperative examination of patients with advanced esophagogastric junction malignant tumors should clarify the tumor type and maximum diameter. Patients with Siewert type Ⅱ and Ⅲ and maximum tumor diameter of >6 cm are recommended to undergo para-aortic lymph node dissection. (2) Frozen biopsy of lymph nodes of No.7 and No.11p is performed during the operation, and the para-aortic lymph nodes should be dissected if the metastasis is found to be positive, which is helpful for the clinical surgeon to judge the dissection of the para-aortic lymph nodes.

     

  • 乳腺癌是女性最常见的恶性肿瘤[1-2],新疆维吾尔族乳腺癌的发病率近年呈明显上升趋势,且发病趋向年轻化[3]。不同民族乳腺癌具有不同的遗传易感性[4],因此这种遗传背景上的差异对阐明维吾尔族女性乳腺癌发生发展具有重要意义。

    Notch1信号转导通路与乳腺癌相关性有大量文献报道[5-9],课题组前期实验结果发现Notch1信号通路中的配体JAG1分子与新疆汉族女性乳腺癌发生发展密切相关[10],并且JAG1基因甲基化是调控汉族乳腺癌的重要机制之一[11-12]。甲基化是表观遗传学修饰,不同种族人群中的基因甲基化谱及甲基化率可能存在差异[13-16]。新疆汉族与维吾尔族这两个民族具有不同的遗传背景,推测其乳腺癌患者的DNA甲基化水平存在不同的民族差异性,关于JAG1基因的甲基化状态与维吾尔族乳腺癌发生发展的相关性,目前尚未见相关报道。

    因此,本研究以维吾尔族乳腺癌为研究对象,应用MALDI-TOF MS和免疫组织化学技术检测JAG1基因总体水平及单个CpG位点定量甲基化率以及JAG1蛋白表达,以探讨JAG1分子在维吾尔族乳腺癌变进展过程中的作用。

    收集新疆维吾尔自治区人民医院1989年1月至2009年4月手术切除、石蜡包埋的维吾尔族女性乳腺标本,经过伦理委员会批准和受试者知情同意。其中,乳腺普通型导管增生(usual ductal hyperplasia, UDH)15例、非典型性导管增生(atypical ductal hyperplasia, ADH)15例、导管原位癌(ductal carcinoma in situ, DCIS)15例、浸润性导管癌(invasive ductal carcinoma, IDC)50例。收集乳腺癌患者的年龄、组织学分级、淋巴结转移、临床分期、雌孕激素受体水平、HER2表达等临床病理参数。

    EZ-96甲基化试剂盒购自美国Zymo Research公司,JAG1抗体购自美国Santa Cruz公司,SP试剂盒购自福建迈新生物开发有限公司,DAB显色液购自北京中杉金桥生物技术有限公司,MassCLEAVE试剂盒和SAP试剂购自美国Sequenom公司,Mass ARRAY质谱仪购自Sequenom公司。

    检测JAG1基因单个CpG位点定量甲基化水平,该基因CpG位点位于启动子上游-1 396 bp~-1 083 bp之间的CpG岛区域,包括28个CpG位点即15个CpG单位,CpG位点示意图参照文献[11]。首先应用显微切割技术将乳腺组织中UDH和ADH分离出来,提取总DNA,应用MALDI-TOF MS法定量检测单个CpG位点DNA甲基化值。提取出的DNA经亚硫酸氢盐处理,未发生甲基化的胞嘧啶转变为尿嘧啶而甲基化的胞嘧啶保持不变,PCR扩增,引物序列见文献[11],虾碱性磷酸酶处理,处理后的产物体外转录最终成为腺嘌呤,然后再利用特异性的T切酶将甲基化和非甲基化区域剪切成不同的小片段,使发生甲基化CpG位点和非甲基化CpG位点之间相差16 Da,区分甲基化与非甲基化,放入基质芯片中检测,MassARRAY质谱仪收集质谱图,用Epityper TM software v1.0.5软件进行分析。

    石蜡包埋乳腺组织切片脱蜡至水,内源性抗原修复,3%双氧水室温孵育30 min阻断过氧化物酶,JAG1抗体(稀释度1:300)孵育过夜,加二抗,DAB溶液显色,苏木精对比染色,中性树胶封片。人肺癌组织为阳性对照,PBS替代一抗作为阴性对照[17]

    乳腺癌细胞或正常上皮细胞胞质出现黄色颗粒为阳性表达,阳性细胞所占比例≤5%为0分,5%~25%为1分, > 25%~50%为2分, > 50%~75%为3分, > 75%~100%为4分。细胞染色无着色为0分,浅黄色颗粒为1分,棕黄色颗粒为2分,棕褐色颗粒为3分。阳性评分由阳性细胞百分数和阳性强度相乘。总分小于4分为低表达,总分大于或等于4分为高表达[10]

    实验数据采用SPSS 20.0软件分析,Kruskal-Wallis H检验分析JAG1基因总体和单个位点甲基化率在乳腺四组组织之间的比较、两组之间的甲基化率比较以及甲基化率与分级和分期之间的相关性。非参数U检验比较甲基化与ER、PR、HER2之间的关系。卡方检验或Fisher精确检验分析JAG1蛋白和临床病理特征的相关性。Spearman秩和检验分析JAG1蛋白表达和甲基化的相关性。所有检验均以P < 0.05为差异有统计学意义。

    MassARRAY质谱仪收集JAG1基因样本甲基化质谱图,见图 1A,EpiTYPERv1.0.5软件对其15个CpG单位进行甲基化定量分析,包括甲基化率图,见图 1B~1C

    图  1  JAG1基因甲基化质谱图及定量分析
    Figure  1  Mass spectrometry and quantitative analysis of JAG1 gene methylation
    A : MALDI-TOF-MS mass spectrum of a sample from IDC; B: methylation percentage of CpG site in IDC group; C: methylation levels of CpG loci in IDC group

    JAG1基因在维吾尔族乳腺UDH、ADH、DCIS和IDC组织样本中甲基化变化见图 2JAG1基因总甲基化水平为该基因15个CpG单位甲基化平均值,这15个CpG单位位于该基因CpG岛丰富的启动子区,虽然不能准确代表总的甲基化水平,但可以作为该基因总甲基化定量水平的一个简单有用的参考指标。JAG1基因总甲基化水平从UDH、ADH、DCIS到IDC逐渐降低,四组之间差异有统计学意义(P=0.003),四组之间两两比较,IDC与DCIS组分别与UDH组之间差异有统计学意义,其余各组之间差异不明显。

    图  2  JAG1基因总甲基化率在乳腺UDH、ADH、DCIS、IDC组中的变化
    Figure  2  Overall methylation rates of JAG1 gene in usual ductal hyperplasia(UDH), atypical ductal hyperplasia(ADH), ductal carcinoma in situ (DCIS), and invasive ductal carcinoma (IDC) groups of breast tissues
    UDH: usual ductal hyperplasia; ADH: atypical ductal hyperplasia; DCIS: ductal carcinoma in situ; IDC: invasive ductal carcinoma

    JAG1基因单个CpG单位的甲基化值在乳腺不同病变组中呈现不同的水平。JAG1大部分CpG单位的甲基化率在IDC组中均低于DCIS、ADH及UDH,并且CpG_11.12、CpG_14.15、CpG_18.19位点的甲基化率在四组之间比较差异有统计学意义(均P < 0.05)。CpG_3.4.5位点甲基化率在IDC和UDH中分别为15.7%和23.7%,CpG_20.21.22位点甲基化率在IDC和UDH分别为21.9%和26.0%,甲基化水平相对较高,CpG_8.9.10位点甲基化率在IDC和UDH组中均为4.9%,甲基化水平较低,见图 3

    图  3  JAG1基因单个CpG位点甲基化值在乳腺UDH、ADH、DCIS、IDC组中的变化
    Figure  3  Single CpG site methylation values of JAG1 gene in UDH, ADH, DCIS, IDC groups of breast tissues
    A: CpG_1; B: CpG_2; C: CpG_3.4.5; D: CpG6; E: CpG_7; F: CpG_8.9.10; G: CpG_11.12; H: CpG_13; I: CpG_14.15; J: CpG_16.17; K: CpG_18.19; L: CpG_20.21.22; M: CpG_23.24.25; N: CpG_26; O: CpG_27.28

    在48例乳腺癌组织中,JAG1基因总甲基化水平在乳腺癌高分级、淋巴结转移、低分期和Luminal A型(ER+,PR+,HER2-)组中是降低的,但没有统计学意义。然而就单个CpG位点而言,CpG_1甲基化水平从1级到2级至3级逐渐降低且差异有统计学意义(P=0.011);CpG_8.9.10位点甲基化率在无腋窝淋巴结转移组显著高于有腋窝淋巴结转移组(P=0.0014);CpG_16.17位点甲基化率从Ⅰ期到Ⅱ期至Ⅲ期呈逐渐升高趋势且差异有统计学意义(P=0.026);CpG_13、CpG_26位点甲基化在Luminal A型组明显低于HER2过表达组(ER-,PR-,HER2+)(均P=0.049),见表 1

    表  1  JAG1基因甲基化与临床病理参数的关系
    Table  1  Relationship between JAG1 gene methylation and clinicopathological characteristics
    下载: 导出CSV 
    | 显示表格

    JAG1蛋白在维吾尔族乳腺UDH、ADH、DCIS及IDC组中的表达见图 4。JAG1分子的阳性表达定位于乳腺上皮细胞或癌细胞的细胞质和胞膜,从UDH到IDC这一癌变过程中的表达逐渐增强。

    图  4  JAG1蛋白在乳腺UDH、ADH、DCIS、IDC组中的表达(SP×200)
    Figure  4  Expression of JAG1 protein in UDH, ADH, DCIS and IDC groups of breast tissues (SP×200)
    A: UDH; B: ADH; C: DCIS; D: IDC

    分析JAG1蛋白在四组中的表达,结果发现JAG1蛋白在四组中的表达逐渐升高,差异有统计学意义(P=0.015)。四组之间两两比较,UDH、ADH和DCIS组分别与IDC组比较差异有统计学意义,见表 2

    表  2  乳腺普通型导管增生、非典型性导管增生、导管原位癌和浸润性导管癌中JAG1蛋白表达结果
    Table  2  Expression of JAG1 protein in UDH, ADH, DCIS and IDC from breast tissues
    下载: 导出CSV 
    | 显示表格

    从UDH到IDC这一癌变过程中的JAG1蛋白表达率逐渐升高,同时相对应组中的甲基化水平逐渐降低,JAG1蛋白在四组中的总表达水平与基因总甲基化水平之间呈显著负相关(r=-0.674, P < 0.001),并且每一组中蛋白表达和甲基化水平也呈显著负相关,见表 3

    表  3  JAG1蛋白的表达和甲基化的变化
    Table  3  Changes of JAG1 protein expression and methylation
    下载: 导出CSV 
    | 显示表格

    JAG1基因在维吾尔族女性乳腺UDH、ADH、DCIS和IDC组中的甲基化水平逐渐降低,以CpG_11.12、CpG_14.15、CpG_18.19位点甲基化率降低为明显,并且乳腺普通型上皮增生组分别与原位癌组和浸润癌组之间差异有统计学意义,提示JAG1基因低甲基化有可能促进乳腺上皮细胞的癌变和浸润,此结果与前期课题组研究汉族乳腺癌的结论相一致[12]。维吾尔族中CpG_11.12、CpG_14.15、CpG_18.19位点低甲基化可能在乳腺癌变早期阶段和晚期浸润阶段发挥了更加重要的作用,而汉族乳腺组织中CpG_27.28和CpG_23.24.25位点在促进乳腺癌变过程中发挥了重要作用[12],说明JAG1甲基化与乳腺癌的发生在维吾尔族和汉族中存在民族异质性。

    JAG1甲基化和维吾尔族乳腺癌患者临床病理特征之间的相关性显示,CpG_1甲基化率在低分化组中显著降低,说明JAG1基因CpG_1位点低甲基化在乳腺癌的恶性进展过程中可能发挥了关键的作用;CpG_8.9.10在有腋窝淋巴结转移组中的甲基化率明显下降,提示JAG1基因CpG_8.9.10位点低甲基化提高了乳腺癌转移的能力;而CpG_16.17却在晚期乳腺癌组织中的甲基化率明显升高,说明JAG1基因特异性位点的低甲基化率在维吾尔族乳腺癌不同分期阶段可能发挥不同的作用;并且CpG_13和CpG_26甲基化率还与ER、PR、HER2的表达状态显著相关,提示JAG1基因CpG_13、CpG_26低甲基化水平可能与女性激素水平及预后有关。由此提示JAG1基因位点可能是影响乳腺癌发生进展的不同关键DNA区段,但要证实这一结论,有必要进一步检测该DNA区段甲基化水平是否调控基因的表达进而影响乳腺癌的生物学行为。我们前期结果发现汉族乳腺癌患者中JAG1基因低甲基化率促进乳腺癌进展[12],与本研究结果相一致,同时也与其他的研究结论相符合[18-19],本研究发现了JAG1基因在维吾尔族乳腺癌中有特异性甲基化位点,在其地区和民族中未见相关报道。

    JAG1蛋白在维吾尔族乳腺癌变过程的组织(即从UDH、ADH、DCIS到IDC)中的表达逐渐升高,浸润癌中表达最强,提示JAG1分子在乳腺癌中扮演一个癌基因角色,并且与其甲基化水平呈显著负相关,推测JAG1基因低甲基化促进其蛋白表达,进而促进乳腺癌的发生发展。这与我们在汉族乳腺癌中的研究结果相一致[12]

    本研究表明,JAG1基因低甲基化率可能促进了维吾尔族女性乳腺癌的发生发展,并且可能通过JAG1蛋白高表达而实现,但其具体机制还需进一步研究。

    Competing interests: The authors declare that they have no competing interests.
    利益冲突声明:
    所有作者均声明不存在利益冲突。
    作者贡献:
    牛 权:数据收集、整理、统计分析,文章撰写
    毕小刚:文章审阅及修改
  • 图  1   食管胃结合部腺癌患者生存曲线图

    Figure  1   Kaplan-Meier survival analysis of patients with adenocarcinoma of esophagogastric junction

    表  1   患者一般临床病理资料

    Table  1   General clinicopathological data of patients

    Variable n=224(%)
    Gender
    Male 190(84.8)
    Female 34(15.2)
    Age(years) 64.45(40-89)
    Siewert type
    8(3.6)
    151(67.4)
    65(29.0)
    Neoadjuvant chemotherapy
    Yes 16(7.1)
    No 208(92.9)
    Maximum tumor diameter(cm)
    Mean 4.64(1-13)
    Degree of differentiation(adenocarcinoma)
    G1 7(3.1)
    G2 66(29.5)
    G3 52(23.2)
    G4 99(44.2)
    Pathologic stage
    Ⅱa 41(18.3)
    Ⅱb 47(21.0)
    Ⅲa 44(19.6)
    Ⅲb 33(14.7)
    Ⅲc 7(3.1)
    52(23.2)
    T stage
    T2 18(8.0)
    T3 115(51.3)
    T4a 87(38.8)
    T4b 4(1.8)
    N stage
    N0 51(22.8)
    N1 42(18.8)
    N2 54(24.1)
    N3 77(34.4)
    Surgical modality
    Proximal gastrectomy 72(32.1)
    Total gastrectomy 152(67.9)
    下载: 导出CSV

    表  2   一般临床病理资料与第16组淋巴结转移相关的单因素分析

    Table  2   Univariate analysis of general clinicopathological data related to No.16 lymph node metastasis

    Variable n (%) No.16 positive
    metastasis rate/
    % (n)
    χ2 P
    Gender 0.598 0.439
    Male 190(84.8) 23.7(45)
    Female 34(15.2) 17.6(6)
    Age (years) 0.734 0.392
    ≥70 64(28.6) 26.6(17)
    <70 160(71.4) 21.3(34)
    Siewert type 15.514 <0.001
    8(3.6) 12.5(1)
    151(67.4) 15.9(24)
    65(29.0) 40.0(26)
    Neoadjuvant
    chemotherapy
    0.049 0.764
    Yes 16(7.1) 25.0(4)
    No 208(92.9) 22.6(47)
    Maximum tumor
    diameter(cm)
    15.750 <0.001
    >6 38(17.0) 47.4(18)
    ≤6 186(83.0) 17.7(33)
    Degree of
    differentiation
    0.794 0.373
    G1-2 73(32.6) 19.2(14)
    G3-4 151(67.4) 24.5(37)
    Pathologic stage 218.422 <0.001
    Ⅱ-Ⅲ 172(76.8) 0.0(0)
    52(23.2) 98.1(51)
    T stage 5.770 0.015
    T2 18(8.0) 0.0(0)
    T3-T4 206(92.0) 24.8(51)
    N stage 46.880 <0.001
    N0-N1 93(41.5) 0.0(0)
    N2-N3 131(58.5) 38.9(51)
    下载: 导出CSV

    表  3   患者一般临床病理资料与第16组淋巴结转移相关的多因素Logistic分析

    Table  3   Multivariate Logistic analysis of general clinicopathological data of patients related to No.16 lymph node metastasis

    Variable Regression coefficient Standard error Wald Degree of freedom P
    OR (95%CI)
    Siewert type
    1.174 0.320 13.472 1 <0.001 3.235 (1.728-6.055)
    Maximum tumor diameter 1.429 0.377 14.332 1 <0.001 4.173 (1.992-8.742)
    下载: 导出CSV

    表  4   各区域淋巴结与第16组淋巴结转移相关的单因素分析

    Table  4   Univariate analysis of lymph nodes in each region associated with No.16 lymph node metastasis

    Station Positive rate in
    each group
    /%(n)
    No.16 positive
    metastasis rate
    /%(n)
    χ2 P
    No.1 53.1(119) 37.0(44) 29.140 <0.001
    No.2 15.6(35) 40.0(14) 7.005 0.008
    No.3 63.8(143) 32.9(47) 22.938 <0.001
    No.4 20.1(45) 51.1(23) 25.727 <0.001
    No.5 1.3(3) 66.7(2) 3.332 0.131
    No.6 1.3(3) 66.7(2) 3.332 0.131
    No.7 36.2(81) 49.4(40) 51.112 <0.001
    No.8a 12.5(28) 67.9(19) 36.998 <0.001
    No.8p 4.5(10) 90.0(9) 26.907 <0.001
    No.9 9.4(21) 81.0(17) 44.613 <0.001
    No.10 6.3(14) 78.6(11) 26.446 <0.001
    No.11p 16.5(37) 67.6(25) 50.587 <0.001
    No.11d 3.6(8) 62.5(5) 7.448 0.016
    No.12 3.1(7) 85.7(6) 24.511 <0.001
    No.110 12.9(29) 75.9(22) 53.405 <0.001
    No.111 0.4(1) 100(1) 3.407 0.228
    No.112 2.2(5) 60.0(3) 4.032 0.079
    Notes: No.1: right lymph node of cardia; No.2: left lymph node of cardia; No.3: lymph nodes on the lesser curvature of the stomach; No.4: lymph nodes on the greater curvature of the stomach; No.5: suprapyloric lymph nodes; No.6: subpyloric lymph nodes; No.7: lymph nodes of left gastric artery; No.8a: anterior superior lymph nodes of common hepatic artery; No.8p: posterior lymph nodes of common hepatic artery; No.9: celiac trunk lymph nodes; No.10: splenic hilum lymph nodes; No.11p: proximal splenic artery lymph node; No.11d: distal splenic artery lymph nodes; No.12: lymph nodes within the hepatoduodenal ligament; No.110: periesophageal lymph nodes in the lower thoracic region; No.111: supradiaphragmatic lymph nodes; No.112: posterior mediastinal lymph nodes.
    下载: 导出CSV

    表  5   各组淋巴结与第16组淋巴结转移相关的多因素Logistic分析

    Table  5   Multivariate Logistic analysis of lymph nodes in each group associated with No.16 lymph node metastasis

    Station Regression coefficient Standard error Wald Degree of freedom P OR (95%CI)
    No.1 1.264 0.656 3.718 1 0.054 3.541(0.979-12.800)
    No.2 −0.644 0.733 0.771 1 0.380 0.525(0.125-2.211)
    No.3 1.064 0.753 1.999 1 0.157 2.899(0.663-12.676)
    No.4 0.410 0.635 0.418 1 0.518 1.508(0.435-5.229)
    No.7 1.108 0.563 3.877 1 0.049 3.029(1.005-9.126)
    No.8a 1.098 0.715 2.358 1 0.125 2.998(0.738-12.175)
    No.8p 0.745 1.510 0.243 1 0.622 2.106(0.109-40.655)
    No.9 1.153 0.832 1.919 1 0.166 3.168(0.620-16.191)
    No.10 1.099 0.996 1.217 1 0.270 3.002(0.426-21.162)
    No.11p 1.651 0.648 6.496 1 0.011 5.214(1.464-18.563)
    No.11d 1.648 1.074 2.353 1 0.125 5.195(0.633-42.641)
    No.12 1.789 1.243 2.356 1 0.131 5.196(0.725-40.256)
    No.110 2.407 0.646 13.881 1 <0.001 11.101(3.129-39.383)
    下载: 导出CSV

    表  6   No.7、No.11p、No.110与第16组淋巴结转移率的关系

    Table  6   Relationship between the rate of lymph node metastasis between No.7, No.11p, No.110 and No.16

    Lymph node metastasis status in No.7, No.11p, No.110 No.16 lymph node metastasis status No.16 positive metastasis rate (%)
    Metastasis (–) Metastasis(+)
    All negative results 123 6 4.7
    Positive results for at least a regional of lymph nodes 50 45 47.4
    下载: 导出CSV

    表  7   第16组淋巴结转移患者生存分析时间的平均值

    Table  7   Mean value of the survival analysis time of patients with No.16 lymph node metastasis

    No.16 lymph node
    metastasis status
    Estimate Standard
    error
    95%CI
    Negative 59.780 1.926 56.005-63.555
    Positive 18.998 1.644 15.776-22.220
    Population 50.000 1.952 46.173-53.826
    下载: 导出CSV
  • [1]

    Rodriguez GM, DePuy D, Aljehani M, et al. Trends in epidemiology of esophageal cancer in the US, 1975-2018[J]. JAMA Netw Open, 2023, 6(8): e2329497. doi: 10.1001/jamanetworkopen.2023.29497

    [2] 中国医师协会内镜医师分会腹腔镜外科专业组, 国际食管疾病学会中国分会, 中国食管胃结合部腺癌研究协作组, 等. 食管胃结合部腺癌外科治疗中国专家共识(2024年版)[J]. 中华胃肠外科杂志, 2024, 27(2): 109-126. [Laparoscopic Surgery Group of the Endoscopist Branch in the Chinese Medical Doctor Association (CMDA), Chinese Society for Diseases of the Esophagus (CSDE), China Esophageal Gastric Junction Adenocarcinoma Research Collaboration Group, et al. Chinese expert consensus on the surgical treatment for adenocarcinoma of esophagogastric junction (Edition 2024)[J]. Zhonghua Wei Chang Wai Ke Za Zhi, 2024, 27(2): 109-126.] doi: 10.3760/cma.j.cn441530-20231212-00213

    Laparoscopic Surgery Group of the Endoscopist Branch in the Chinese Medical Doctor Association (CMDA), Chinese Society for Diseases of the Esophagus (CSDE), China Esophageal Gastric Junction Adenocarcinoma Research Collaboration Group, et al. Chinese expert consensus on the surgical treatment for adenocarcinoma of esophagogastric junction (Edition 2024)[J]. Zhonghua Wei Chang Wai Ke Za Zhi, 2024, 27(2): 109-126. doi: 10.3760/cma.j.cn441530-20231212-00213

    [3]

    Sung H, Ferlay J, Siegel RL, et al. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries[J]. CA Cancer J Clin, 2021, 71(3): 209-249. doi: 10.3322/caac.21660

    [4]

    Manabe N, Matsueda K, Haruma K. Epidemiological Review of Gastroesophageal Junction Adenocarcinoma in Asian Countries[J]. Digestion, 2022, 103(1): 29-36. doi: 10.1159/000519602

    [5]

    Hosokawa Y, Kinoshita T, Konishi M, et al. Clinicopathological features and prognostic factors of adenocarcinoma of the esophagogastric junction according to Siewert classification: experiences at a single institution in Japan[J]. Ann Surg Oncol, 2012, 19(2): 677-683. doi: 10.1245/s10434-011-1983-x

    [6]

    Hasegawa S, Yoshikawa T. Adenocarcinoma of the esophagogastric junction: incidence, characteristics, and treatment strategies[J]. Gastric Cancer, 2010, 13(2): 63-73. doi: 10.1007/s10120-010-0555-2

    [7]

    Nomura E, Sasako M, Yamamoto S, et al. Gastric Cancer Surgical Study Group of the Japan Clinical Oncology Group. Risk factors for para-aortic lymph node metastasis of gastric cancer from a randomized controlled trial of JCOG9501[J]. Jpn J Clin Oncol, 2007, 37(6): 429-433. doi: 10.1093/jjco/hym067

    [8]

    Kurokawa Y, Takeuchi H, Doki Y, et al. Mapping of Lymph Node Metastasis From Esophagogastric Junction Tumors: A Prospective Nationwide Multicenter Study[J]. Ann Surg, 2021, 274(1): 120-127. doi: 10.1097/SLA.0000000000003499

    [9]

    de Manzoni G, Di Leo A, Roviello F, et al. Tumor site and perigastric nodal status are the most important predictors of para-aortic nodal involvement in advanced gastric cancer[J]. Ann Surg Oncol, 2011, 18(8): 2273-2280. doi: 10.1245/s10434-010-1547-5

    [10]

    Liang H, Deng J. Evaluation of rational extent lymphadenectomy for local advanced gastric cancer[J]. Chin J Cancer Res, 2016, 28(4): 397-403. doi: 10.21147/j.issn.1000-9604.2016.04.02

    [11]

    Fujitani K, Miyashiro I, Mikata S, et al. Pattern of abdominal nodal spread and optimal abdominal lymphadenectomy for advanced Siewert type Ⅱ adenocarcinoma of the cardia: results of a multicenter study[J]. Gastric Cancer, 2013, 16(3): 301-308. doi: 10.1007/s10120-012-0183-0

    [12]

    Goto H, Tokunaga M, Miki Y, et al. The optimal extent of lymph node dissection for adenocarcinoma of the esophagogastric junction differs between Siewert type Ⅱ and Siewert type Ⅲ patients[J]. Gastric Cancer, 2014, 18(2): 375-381.

    [13]

    Yoshikawa T, Takeuchi H, Hasegawa S, et al. Theoretical therapeutic impact of lymph node dissection on adenocarcinoma and squamous cell carcinoma of the esophagogastric junction[J]. Gastric Cancer, 2016, 19(1): 143-149. doi: 10.1007/s10120-014-0439-y

    [14]

    Wang JB, Lin MQ, Li P, et al. The prognostic relevance of parapyloric lymph node metastasis in Siewert type Ⅱ/Ⅲ adenocarcinoma of the esophagogastric junction[J]. Eur J Surg Oncol, 2017, 43(12): 2333-2340. doi: 10.1016/j.ejso.2017.08.017

    [15]

    Cai MZ, Lv CB, Cai LS, et al. Priority of lymph node dissection for advanced esophagogastric junction adenocarcinoma with the tumor center located below the esophagogastric junction[J]. Medicine (Baltimore), 2019, 98(51): e18451. doi: 10.1097/MD.0000000000018451

    [16]

    Chen XD, Chen QC, Xu R, et al. Therapeutic value of lymph node dissection for Siewert type Ⅱ and Ⅲ adenocarcinoma: meta-analysis[J]. BJS Open, 2024, 8(1): zrad138. doi: 10.1093/bjsopen/zrad138

    [17]

    Junfeng Z, Yingxue H, Peiwu Y. Systematic review of risk factors for metastasis to para-aortic lymph nodes in gastric cancer[J]. Surg Oncol, 2013, 22(4): 210-216. doi: 10.1016/j.suronc.2013.10.003

    [18]

    Dong YP, Deng JY. Advances in para-aortic nodal dissection in gastric cancer surgery: A review of research progress over the last decade[J]. World J Clin Cases, 2020, 8(13): 2703-2716. doi: 10.12998/wjcc.v8.i13.2703

    [19]

    Sasako M, Sano T, Yamamoto S, et al. D2 lymphadenectomy alone or with para-aortic nodal dissection for gastric cancer[J]. N Engl J Med, 2008, 359(5): 453-462. doi: 10.1056/NEJMoa0707035

    [20]

    Liu K, Yang K, Zhang W, et al. Changes of Esophagogastric Junctional Adenocarcinoma and Gastroesophageal Reflux Disease Among Surgical Patients During 1988-2012: A Single-institution, High-volume Experience in China[J]. Ann Surg, 2016, 263(1): 88-95. doi: 10.1097/SLA.0000000000001148

    [21]

    Yabusaki H, Nashimoto A, Matsuki A, et al. Comparison of the surgical treatment strategies for Siewert type Ⅱ squamous cell carcinoma in the same area as esophagogastric junction carcinoma: data from a single Japanese high-volume cancer center[J]. Surg Today, 2014, 44(8): 1522-1528. doi: 10.1007/s00595-013-0773-4

    [22]

    Hasegawa S, Yoshikawa T, Rino Y, et al. Priority of lymph node dissection for Siewert type Ⅱ/Ⅲ adenocarcinoma of the esophagogastric junction[J]. Ann Surg Oncol, 2013, 20(13): 4252-4259. doi: 10.1245/s10434-013-3036-0

    [23]

    Zhang C, He Y, Schwarz RE, et al. Evaluation of para-aortic nodal dissection for locoregionally advanced gastric cancer with 1-3 involved para-aortic nodes[J]. Chin Med J (Engl), 2014, 127(3): 435-441. doi: 10.3760/cma.j.issn.0366-6999.20130664

图(1)  /  表(7)
计量
  • 文章访问数:  634
  • HTML全文浏览量:  2070
  • PDF下载量:  160
  • 被引次数: 0
出版历程
  • 收稿日期:  2024-03-27
  • 修回日期:  2024-05-12
  • 录用日期:  2024-09-09
  • 刊出日期:  2024-11-24

目录

/

返回文章
返回
x 关闭 永久关闭