前哨淋巴结活检与乳腺癌分子分型的关系

Relationship between sentinel lymph node biopsy and molecular typing of breast cancer

摘要:

目的 探讨前哨淋巴结活检结果与乳腺癌分子分型的关系。方法 选取2015 年1 月—2018 年 12 月于东莞市松山湖中心医院接受全乳切除术或保乳术加前哨淋巴结活检的302 例早期乳腺癌患者作为 研究对象，采用免疫组织化学法检测肿瘤组织中雌激素受体（ER）、孕激素受体（PR）、人体表皮生长因 子受体-2（Her-2）、Ki-67 的表达，并将患者划分为Luminal A 型、Luminal B 型、HER-2 阳性型及三阴 性型。分析前哨淋巴结转移与患者分型的关系。结果 患者中Luminal A 型134 例、Luminal B 型91 例、 Her-2 阳性型32 例及三阴性型45 例，各亚型中前哨淋巴结阳性者分别有31、37、7 及6 例。前哨淋巴结 阳性组年龄≤ 52 岁、T2 期、Luminal B 型占比均高于阴性组（P <0.05），TNM 分期是前哨淋巴结阳性的危 险因素[Ol ^ R=3.531（95% CI ：1.936，6.438），P =0.000]，Luminal A 型[Ol ^ R=0.242（95% CI ：0.121，0.483）， P =0.000]、年龄[Ol ^ R=0.202（95% CI ：0.101，0.405），P =0.000] 是其保护因素。前哨淋巴结阳性组年龄≤ 52 岁、T2 期、Luminal B 型占比均高于阴性组（P <0.05）， 年龄[Ol ^ R=0.250（95% CI ：0.063，0.987）， P =0.000] 是前哨淋巴结阳性数的保护因素。检出组年龄≤ 52 岁、T2 期、阳性前哨淋巴结数量≥ 2 枚、前哨 淋巴结宏转移者占比均高于未检出组（P <0.05），前哨淋巴结阳性数量≥ 2 枚[Ol ^ R=27.926（95% CI ：6.433， 121.222），P =0.000]、前哨淋巴结宏转移[Ol ^ R=10.662（95% CI ：1.620，70.177），P =0.014] 是非前哨淋巴结转 移的危险因素。结论 分子分型与前哨淋巴结阳性有一定关系，其中Luminal A 型患者前哨淋巴结阳性风险 低于Luminal B 型患者，但分子分型与是否伴非前哨淋巴结转移无关。

Abstract:

Objective To investigate the relationship between sentinel lymph node biopsy results and molecular typing of breast cancer. Methods Totally 302 patients with early breast cancer treated with total mastectomy or breast conserving surgery plus sentinel lymph node biopsy from January 2015 to December 2018 were enrolled in this study. The expression of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor (HER) -2 and Ki-67 were detected by immunohistochemistry. Then patients were divided into Luminal A type, Luminal B type, HER- 2 positive type and three negative types. The relationship between sentinel lymph node metastasis and molecular type was analyzed. Results Among 302 patients, 81 were sentinel lymph node positive and 221 were sentinel lymph node negative. Among them, 134 (44.37%) were Luminal A, where 31 (23.13%) were sentinel lymph node positive; 91 (30.13%) were Luminal B, where 37 (40.66%) were sentinel lymph node positive; 32 (10.60%) were HER-2 positive, where 7 (21.88%) were sentinel lymph node positive; 45 (14.90%) were tri-negative, where 6 (16.22%) were sentinel lymph node positive. the proportion of positive sentinel lymph nodes in age ≤ 52 years, T2 stage and Luminal B type was higher than that in negative group (P < 0.05). TNM stage was the risk factor of sentinel lymph node positive [Ol ^ R = 3.531, (95% CI: 1.936, 6.438), P = 0.000]; meanwhile, Luminal A [(Ol ^ R = 0.242, (95% CI: 0.121, 0.483), P = 0.000], and age [Ol ^ R = 0.202, (95% CI: 0.101, 0.405), P = 0.000] were the protective factors; age [Ol ^ R = 0.250, (95% CI: 0.063, 0.987), P = 0.000] was the protective factor of positive sentinel lymph nodes; the age of detection group ≤ 52 years old, T2 stage, the number of positive sentinel lymph nodes ≥ 2, the proportion of sentinel lymph nodes macrometastases were higher than that of non detection group (P < 0.05); the number of sentinel lymph nodes positive ≥ 2 [Ol ^ R = 27.926, (95% CI: 6.433, 121.222), P = 0.000], the number of sentinel lymph nodes macrometastases [Ol ^ R = 10.662, (95% CI: 1.620, 70.177), P = 0.014] were the risk factors of non sentinel lymph node metastasis. Conclusion Molecular type is associated with sentinel lymph node positivity. The risk of sentinel lymph node positivity in Luminal A patients is lower than that in Luminal B patients. But there is no significant relationship between molecular typing and non-sentinel lymph node metastasis.