肿瘤细胞治疗研究
英文原题：Molecular subtyping and target identification in triple negative breast cancer through immunohistochemistry biomarkers.
Molecular subtyping and target identification in triple negative breast cancer through immunohistochemistry biomarkers.
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患者年龄为 50.11 ± 12.13 岁（76.56% 的患者超过 40 岁），23.44% 有 BC 家族史。他们处于非晚期阶段：51.6% 为 T2 期，56.2% 淋巴结受累阴性，76.6% 无转移，64.1% 为 II 级 Scarff-Bloom-Richardson 分类（SBR）。IHC 亚型为：53.1% 基底样 1（BL1），6.3% 基底样 2（BL2），17.2% 间充质（MES），9.4% 管腔雄激素受体（LAR），4.7% 混合亚型，9.4%“未分类”型。LAR 亚型涉及最年轻的患者（40.17 ± 8.68 岁，p = 0.02）。“未分类”亚型更频繁地表达 p53 突变型模式（100%，p = 0.07）。
基于免疫组织化学（IHC）的三阴性乳腺癌（TNBC）分子分型和靶点识别对于常规应用具有相当大的价值。然而，全球范围内关于该主题的文献有限，需要来自不同人群的数据加以丰富。
我们评估了TNBC患者队列中分型生物标志物（细胞角蛋白5、14和17，表皮生长因子受体，Claudins 3和7，E-cadherin，Vimentin和雄激素受体）和预测生物标志物（TIL（肿瘤浸润淋巴细胞）（TILs）密度，乳腺癌抗原1（BRCA1）和P53）的IHC表达。同时研究了临床病理参数和总生存期（OS）。
患者年龄为50.11 ± 12.13岁（76.56%的患者超过40岁），23.44%有BC家族史。他们处于非晚期阶段：51.6%为T2期，56.2%淋巴结受累阴性，76.6%无转移，64.1%为II级Scarff-Bloom-Richardson分类（SBR）。IHC亚型为：53.1%基底样1（BL1），6.3%基底样2（BL2），17.2%间充质（MES），9.4%管腔雄激素受体（LAR），4.7%混合亚型，9.4%“未分类”型。LAR亚型涉及最年轻的患者（40.17 ± 8.68岁，p = 0.02）。“未分类”亚型更频繁地表达p53突变型模式（100%，p = 0.07）。BRCA1突变模式和TILs浸润分别存在于23.44%和37.5%的患者中。各亚型的OS差异显著（p = 0.007，log-rank检验）。各亚型的中位OS分别为15.47个月（未分类）、18.94个月（BL2）、27.23个月（MES）、27.28个月（混合）、30.88个月（BL1）和45.07个月（LAR）。按年龄、BRCA1表达、p53模式和TILs密度分层的OS无差异。然而，按TNM分期的OS不同（p = 0.001）。多变量Cox比例风险回归分析显示，TNM分期和TNBC亚型独立影响OS（分别为p < 0.001和p = 0.017）。因此，IHC在TNBC亚型分型中对于预后目的和治疗生物标志物的识别是有用的。需要进一步研究以确认我们的结果，并将IHC作为常规工具来改善患者的护理。
The Triple-Negative Breast Cancer (TNBC) molecular subtyping and target identification based on Immunohistochemistry (IHC) is of considerable worth for routine use. Yet, literature on this topic is limited worldwide and needs to be enriched with data from different populations.
We assessed the IHC expression of subtyping biomarkers (Cytokeratins 5, 14 and 17, Epidermal Growth Factor Receptor, Claudins 3 and 7, E-cadherin, Vimentin and Androgen receptor) and predictive biomarkers (Tumor-infiltrating lymphocytes (TILs) density, Breast Cancer Antigen 1 (BRCA1) and P53) in a cohort of TNBC patients. Clinicopathologic parameters and overall survival (OS) were investigated as well.
The patients were aged 50.11 ± 12.13y (more than 40y in 76.56% of patients), and 23.44% had a BC family history. They were in a non-advanced stage: 51.6% T2 stage, 56.2% negative lymph node involvement, 76.6% without metastasis and 64.1% grade II Scarff-Bloom-Richardson classification (SBR). The IHC subtypes were: 53.1% Basal-like1 (BL1), 6.3% Basal-like2 (BL2), 17.2% Mesenchymal (MES), 9.4% Luminal Androgen Receptor (LAR), 4.7% Mixed subtype and 9.4% "Unclassified" type. The LAR subtype involved the youngest patients (40.17 ± 8.68y, p = 0.02). The "Unclassified" subtype expressed the p53 mutated-type pattern more frequently (100%, p = 0.07). The BRCA1 mutated pattern and TILs infiltration were present in (23.44% and 37.5% of patients, respectively). The OS of the subtypes differed significantly (p = 0.007, log-rank test). The subtypes median OS were, respectively, 15.47 mo. (Unclassified), 18.94 mo. (BL2), 27.23 mo. (MES), 27.28 mo. (Mixed), 30.88 mo. (BL1), and 45.07 mo. (LAR). There was no difference in the OS following age, BRCA1 expression, p53 pattern and TILs density. Though, the OS following the TNM stage was different (p = 0.001). A multivariable Cox proportional hazards regression analysis showed that TNM staging and TNBC subtypes, independently influence the OS (p < 0.001 and p = 0.017, respectively). Hence, IHC is useful in TNBC subtyping for prognostic purposes and in the identification of therapeutic biomarkers. Further investigation is required to confirm our results and to implement IHC as a routine tool to improve patient's care.
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