CD105在乳腺癌发生发展过程中表达的研究

目的:用CD105单克隆抗体(mAb)检测乳腺癌演变中微血管密度(MVD)变化,旨在探讨CD105在乳腺癌发生发展过程中的表达及分析其临床相关因素.方法:采用免疫组织化学(SP法)检测20例导管上皮不典型增生(ADH)、20例导管内癌(DCIS)和20例微浸润性癌(MDC)和60例浸润性导管癌[IDC(NOS)]的CD105表达,进行MVD计数.结果:用CD105标记乳腺ADH、DCIS、MDC和IDC(NOS)的MVD分别是8.25±5.78、10.05±4.23、25.35±7.62和36.82±7.11,4组两两组间差异有统计学意义,P《0.05,P值分别为0.035、0.001和0.001.在IDC(NOS)中,CD105标记的MVD与腋淋巴结转移有关,P《0.05;而与年龄、组织学分级、肿瘤直径及临床分期无关,P》0.05.结论:CD105标记的MVD可能与乳腺癌的预后有关,CD105可能会成为鉴别乳腺良恶性病变和靶向治疗及化学预防的标志之一.     

D2-40与乳腺浸润性导管癌临床病理分析

目的:观察淋巴管密度与乳腺非特殊类型浸润性导管癌(IDC,NOS)临床病理关系。方法:用淋巴管内皮细胞抗体D2-40单克隆抗体标记70例乳腺IDC(NOS)淋巴管表达,计算淋巴管密度,并同时进行ER、PR、HER-2、p53、VEGF和CD44V6检测,分析LVD与各临床病理指标的关系。结果:在IDC(NOS)中,D2-40标记的LVD与临床分期和腋淋巴结转移有关(P<0.05),而与年龄、组织学分级、及肿瘤直径无关(P>0.05)。进一步对临床分期行L-S-D检验,发现临床分期I期中的LVD与临床分期II、III期中的LVD有显著性差异,而临床分期II、III期间的LVD并无显著性差异。在IDC(NOS)中,D2-40标记的LVD与CD44V6表达相关(P<0.05),与ER、PR、HER-2、p53及VEGF的表达无关(P>0.05)。多因素分析显示,在IDC(NOS)中,D2-40标记的LVD与腋淋巴结转移和CD44V6有关(P<0.05),而与年龄、组织学分级、肿瘤直径、临床分期、ER、PR、HER-2、p53及VEGF无关(P>0.05)。结论:在IDC(NOS)中,D2-40标记的LVD与淋巴结状态相关,提示LVD可能与乳腺癌的预后有关,可能成为乳腺癌预后的独立指标。在IDC(NOS)中,D2-40标记的LVD与CD44V6表达呈正相关,并具有统计学意义,提示在肿瘤的生长过程中,CD44V6可能通过裂解细胞间质,促进肿瘤生长,导致间质中淋巴管密度增加,提高了肿瘤转移的机率。     

VEGF-C阳性肥大细胞与乳腺癌淋巴管生成及淋巴结转移的关系

目的 研究乳腺浸润性导管癌中肥大细胞内VEGF-C的表达以探讨MC影响乳腺癌淋巴管生成及淋巴结转移的机制.方法 用免疫组织化学双重染色检查乳腺良性病变和乳腺浸润性导管癌间质中肥大细胞内VEGF-C,用VEGF-C经SP法标记乳腺良性病变和癌组织,用D2-40标记淋巴管并计数.结果乳腺良性病变MC中极少或无蓝黑色VEGF-C颗粒,而乳腺浸润性导管癌MC中均含有较明显,并且前者MC数量(7.80±1.22),明显低于后者MC数量(15.44±2.39),差异有统计学意义(P＜0.01).在浸润性导管癌中,Ⅰ、Ⅱ、Ⅲ级MC数量分别为(10.75±2.61)、(13.70±1.92)、(15.33±0.62),差异亦有统计学意义(P＜0.01).浸润性导管癌有淋巴结转移组的MC数量及癌周边LVD(14.03±2.01,11.21±4.60)明显高于无淋巴结转移组(11.22±0.55,5.78±3.02),差异均有统计学意义(P＜0.01);MC数量与乳腺癌淋巴管数量呈正相关(r=0.18).结论 乳腺癌可诱导MC表达VEGF-C,MC数量与乳腺癌淋巴结转移及淋巴管生成呈正相关性.     

人乳腺癌中D2-40标记的微淋巴管密度与淋巴结转移关系的研究

目的:探讨人类乳腺癌组织中D2-40标记的微淋巴管的形态特征及微淋巴管密度(Lymphatic mlcroves-sel density,LMVD)与乳腺癌淋巴结转移的关系.方法:收集沈阳军区总医院2003年1月～2006年10月手术切除的乳腺癌术后组织石蜡标本102例,另选取乳腺纤维腺瘤标本25例为对照组.采用单标及双标免疫组织化学法分别检测D2-40和CD31的表达,计数D2-40阳性微淋巴管密度(LMVD),分析其与乳腺癌淋巴结转移的关系.结果:102例乳腺癌组织中D2-40阳性率为76.5%(78/102),25例对照组D2-40阳性表达率为24.0%(6/25),显著低于乳腺癌组织(X2=24.685,P=0.000).102例浸润性乳腺癌组织中D2-40阳性的微淋巴管中位LMVD为21.61(19.72±5.11)个微淋巴管/100倍视野,且癌周组织中位LMVD显著高于瘤内(P<0.05).单因素方差分析和Pearson相关性分析显示腋淋巴结转移数目和乳腺癌瘤周D2-40标记淋巴管密度有关(P＜0.01.r=0.964).而与瘤内D2-40标记的淋巴管密度无统计学相关(P>0.05).结论:D2-40可以特异性标记乳腺癌组织中微淋巴管内皮细胞,其标记的癌周微淋巴管密度与乳腺癌的淋巴结转移数目密切相关,因此抑制癌周微淋巴管生成有望成为抗肿瘤治疗新的靶点.     

乳腺癌和乳腺导管内增生性病变JAG1基因甲基化的检测及临床意义

目的:探讨JAG1基因甲基化在乳腺浸润性导管癌发病中的作用。方法:采用MassARRAY方法对乳腺浸润性导管癌(IDC;n=75)、乳腺导管原位癌(DCIS;n=23)、乳腺非典型性导管增生症(ADH;n=20)以及乳腺普通型导管增生症(UDH;n=27)进行JAG1基因甲基化的定量检测。结果:JAG1基因启动区CpG_13、CpG_20.21.22、CpG_26位点在UDH组中的平均甲基化率高于ADH、DCIS、IDC组（P<0.05）。结论:在乳腺癌患者中JAG1(该基因的表达与乳腺癌细胞的生长、浸润、转移、预后有关)基因的部分位点呈现低甲基化改变。CpG_13、CpG_20.21.22、CpG_26位点的低甲基化改变与乳腺癌的形成具有相关性,可能该基因特异性CpG位点的低甲基化参与了乳腺良性病变向乳腺癌的发展演进过程。     

早期胃癌淋巴管密度预测淋巴结转移的研究

目的:检测淋巴管内皮标志物D2-40计算早期胃癌淋巴管密度(LVD),探讨LVD与早期胃癌有无淋巴结转移之间的关系.方法:用免疫组化SP染色法,对80例早期胃癌淋巴结未发生转移与20例早期胃癌淋巴结发生转移的癌周检测D2-40标记阳性LVD的表达水平,并进行统计学分析.结果:D2-40标记阳性LVD在早期胃癌伴有淋巴结转移癌周高于早期胃癌不伴有淋巴结转移癌周(P＜0.05),光镜下LVD的截断(cut-off)值为18.50个.结论:早期胃癌伴有淋巴结转移癌周的LVD高于早期胃癌不伴有淋巴结转移癌周,D2-40阳性LVD可用来判断有无淋巴结转移.     

人乳腺癌组织中D2-40标记的微淋巴管密度与血管内皮生长因子C表达的关系

目的 探讨人乳腺癌组织中D2-40标记的微淋巴管密度(LMVD)与血管内皮生长因子C(VEGF-C)表达的关系.方法 收集102例乳腺癌、25例乳腺纤维腺瘤和10例正常乳腺组织标本,采用免疫组化SP法检测D2-40单抗标记的LMVD和VEGF-C蛋白的表达水平,采用原位杂交法检测VEGF-C mRNA的转录水平. 结果 102例人乳腺癌组织中,D2-40标记微淋巴管的阳性率为76.5%,高于乳腺纤维腺瘤组织.癌周组织的LMVD为30.1个微淋巴管/100倍视野,显著高于癌中心区、正常乳腺组织和乳腺纤维腺瘤组织的LMVD (均P＜0.01),且与乳腺癌腋窝淋巴结转移数目明显相关(r=0.964,P<0.01).102例乳腺癌组织中,VEGF-C蛋白和mRNA的阳性表达率分别为55.9%和59.8%,均高于乳腺纤维腺瘤组织(χ2=11.653,P=0.003;χ2=10.345,P=0.006),且与淋巴结转移数目、临床分期、c-erbB-2和p53基因的表达相关(均P<0.05).VEGF-C蛋白和mRNA的表达水平均与D2-40标记的LMVD相关(P<0.05),尤其见于癌周组织中(P<0.01).结论 D2-40单抗标记的LMVD与VEGF-C的表达有密切关系,VEGF-C参与的乳腺癌微淋巴管的生成在乳腺癌淋巴转移中有重要意义.     

乳腺癌组织VEGF-D表达及淋巴管生成的临床意义探讨

目的:探讨乳腺癌组织中血管内皮生长因子-D(VEGF-D)、淋巴管密度(LVD)的表达及其与临床病理参数的关系.方法:应用Envision免疫组化技术对100例乳腺癌组织和20例乳腺纤维腺瘤组织中淋巴管内皮细胞透明质酸受体-1(LYVE-1)和VEGF-D的表达进行检测;计数LVD;并分析VEGF-D表达与LVD、乳腺癌临床病理参数的相关性.结果:乳腺癌癌旁组织中淋巴管密度显著高于乳腺纤维腺瘤组织(9.52±3.47 vs 1.31±1.02,P＜0.01);乳腺癌癌旁组织LVD与病理分期和淋巴结转移显著相关,P均＜0.01;乳腺癌组织VEGF-D蛋白表达的阳性率(76%)显著高于乳腺纤维腺瘤组织(10%),P＜0.0001;乳腺癌VEGF-D表达与淋巴结转移(P＜0.01)显著相关;乳腺癌VEGF-D蛋白表达阳性者的癌旁LVD(11.39±2.72 vs 3.81±1.71,P＜0.01)显著高于VEGF-D蛋白表达阴性者的癌旁LVD;乳腺癌VEGF-D表达与癌旁组织LVD存在明显的相关性.结论:乳腺癌组织VEGF-D与LVD的表达呈正相关,VEGF-D的表达与淋巴转移相关,VEGF-D的过表达可促进淋巴管生成,导致LMD的升高,进而促进乳腺癌淋巴转移,LVD与VEGF-D可作为乳腺癌淋巴转移的预测因子.     

VEGF-C D2-40 E-Cad在乳腺癌中的表达及意义

目的:探讨VEGF-C、D2-40、E-Cad在乳腺癌中的表达及意义.方法:采用免疫组织化学方法,检测临床病理及随访资料完整的88例乳腺浸润性导管癌及54例导管内增生性病变组织中VEGF-C的表达情况,分析其与D2-40、E-Cad表达的关系及其临床病理意义.结果:VEGF-C在浸润癌组的阳性表达率显著性强于不典型增生组和普通型增生组;同时淋巴结转移组显著性强于无淋巴结转移组:乳腺癌变组LVD明显高于乳腺不典型增生组和普通型增生组,淋巴结转移阳性组LVD计数明显高于淋巴结转移阴性组;E-Cad在浸润癌组中的阳性表达率明显低于不典型增生组及普通型增生组,淋巴结转移组显著性低于无淋巴结转移组,VEGF-C与D2-40呈正相关,与E-Cad呈负相关.结论:VEGF-C与D2-40的联合检测可以作为临床评价肿瘤早期淋巴道转移的重要指标;VEGF-C与E-Cad的联合使用可作为乳腺癌预后的重要指标.     

乳腺浸润性导管癌癌周淋巴管密度及其临床意义

目的探讨乳腺浸润性导管癌(IDC)癌周淋巴管密度(LMVD)与其临床病理特征及预后的关系.方法选取65例临床病理资料完整的乳腺IDC组织,用免疫组化二步法以单克隆抗体D2-40标记淋巴管内皮细胞,光镜下观察癌周LMVD.结果乳腺IDC LMVD为13.17±2.89,明显高于乳腺纤维腺瘤组织(4.21±2.76),两者差异有统计学意义,P=0.000.LMVD与年龄、组织学分级、绝经状态以及雌激素受体状况之间差异无统计学意义,P均＞0.05;与肿瘤最大直径、腋窝淋巴结转移数目和pTNM分期之间差异有统计学意义,P均＜0.05.高LMVD组的5年DFS明显低于低LMVD组,乳腺癌LMVD与患者5年DFS呈负相关.结论MVD在乳腺IDC的扩散转移中起重要作用,可作为选择乳腺IDC治疗方式及预测其淋巴结转移及预后的重要指标.     

PTEN在乳腺癌及癌前病变中的表达及意义

目的：探讨人第10号染色体缺失的磷酸酶（phosphatase and tensin homolog deleted on chromosometen, PTEN）在乳腺导管上皮不典型增生（ atypical ductal hyperplasia,ADH）、导管内癌（ ductal carcinoma in situ, DCIS）、浸润性导管癌（invasiveductal carcinoma,IDC）三组病变组织中的表达及意义。方法：收集 ADH 60例、DCIS 100例、IDC 165例,利用 Real - time RT - PCR 检测 ADH、DCIS、IDC 病变组织中 PTEN 基因在 mRNA 水平的表达情况;利用 Western - Blot 方法和免疫组织化学技术检测 ADH、DCIS、IDC 病变组织中 PTEN 蛋白的表达情况。结果：Real - time RT - PCR 技术结果显示,ADH 组 PTEN mRNA 表达水平最高,DCIS 组次之,IDC组最低差异具有统计学意义（t =26.661,P <0.05）。Western - Blot 技术检测 PTEN 蛋白在 ADH、DCIS、IDC 三组病变组织中的表达呈逐渐下降趋势,差异具有统计学意义（t =9.355,P <0.05）。免疫组织化学检测 PTEN蛋白在 ADH、DCIS、IDC 三组病变组织中的阳性表达率分别为91.9%、51.0%、36.9%,差异有统计学意义（χ2=54.734,P <0.05）。分析 PTEN 蛋白表达水平与乳腺癌患者临床资料的相关性,结果显示其与患者年龄无相关性（P >0.05）,而与患者的肿瘤分化程度、临床分级及转移有相关性,且差异有统计学意义（χ2=15.8,P <0.05）。结论：无论是在蛋白水平还是 mRNA 水平,PTEN 基因的表达从 ADH 到 DCIS 再到 IDC 呈下降趋势,提示 PTEN 可能参与了乳腺癌发生发展的过程,为日后治疗提供靶点理论依据。     

Chalkley Microvessel but not Lymphatic Vessel DensityCorrelates with Axillary Lymph Node Metastasis in PrimaryBreast Cancers

This study aimed to investigate tumor microvessel density (MVD) and lymphatic vessel density (LVD) usingthe Chalkley method as predictive markers for the risk of axillary lymph node metastasis and their relationshipto other clinicopathological parameters in primary breast cancer cases. Forty two node-positive and eightynode-negative breast cancers were immunostained for CD34 and D2-40. MVD and LVD were counted by theChalkley method at x400 magnification. There was a positive significant correlation of the MVD with the tumorsize, coexisting ductal carcinoma in situ (DCIS) and lymph node metastases (P<0.05). In multivariate analysis,the MVD (2.86-4: OR 5.87 95%CI 1.05-32; >4: OR 20.03 95%CI 3.47-115.55), lymphovascular invasion (OR3.46, 95% CI 1.13-10.58), and associated DCIS (OR 3.1, 95%CI 1.04-9.23) independently predicted axillarylymph node metastasis. There was no significant relationship between LVD and axillary lymph node metastasis.However, D2-40 was a good lymphatic vessel marker to enhance the detection of lymphatic invasion compared toH and E staining. In conclusion, MVD by the Chalkley method, lymphovascular invasion and associated DCIScan be additional predictive factors for axillary lymph node metastases in breast cancer. No relationship wasidentified between LVD and clinicopathological variables, including axillary lymph node metastasis.     

淋巴管密度在甲状腺乳头状癌和滤泡癌的表达及意义

[目的]探讨淋巴管密度（LVD）在甲状腺乳头状癌（PTC）和滤泡癌的表达及意义。[方法]采用免疫组化技术,以D2-40标记淋巴管内皮,CD31标记血管内皮,对105例PTC、18例甲状腺滤泡癌和21例滤泡性腺瘤进行LVD和微血管密度（MVD）的检测。对LVD与乳头状癌的临床病理资料的关系,及乳头状癌和滤泡癌中MVD和LVD的表达差异进行了统计分析。[结果]（1）PTC中均可见D2-40阳性淋巴管,其瘤周LVD较瘤内为高,淋巴结转移组（瘤内6.80±4.40;瘤周13.63±5.09）较无转移组（瘤内4.30±3.06;瘤周10.17±4.53）为高,两组比较有统计学差异（P〈0.01）。（2）甲状腺乳头状癌的瘤内LVD与TNM分期有关,高分期组（Ⅲ期/Ⅳ期）的瘤内LVD（7.33±4.79）较低分期组（Ⅰ期/Ⅱ期,5.16±3.71）为高,两者相比有统计学差异（P〈0.05）。（3）甲状腺乳头状癌的瘤内LVD（5.47±3.93）较滤泡癌的瘤内LVD（1.56±1.92）为高,两者相比,差异具有统计学意义（P〈0.05）。[结论]甲状腺乳头状癌LVD与淋巴结转移密切相关,瘤周淋巴管的扩张形态和相对较高的LVD在甲状腺乳头状癌淋巴道转移中可能发挥了重要的作用。     

基于D2-40检测胰腺癌组织中淋巴管密度的价值

[目的]探讨胰腺癌组织中淋巴管密度与肿瘤恶性程度、淋巴转移的相关性。[方法]应用免疫组化方法,采用单克隆抗体D2-40检测经手术切除的33例胰腺癌组织的瘤周淋巴管密度（pLVD）和瘤内淋巴管密度（iLVD）,分析胰腺癌组织pLVD、iLVD与患者临床病理参数之间的关系。[结果]胰腺癌的pLVD明显高于iLVD。胰腺癌的pLVD与肿瘤的分化程度、淋巴结转移及淋巴管累及明显相关,与年龄、性别、肿块大小、发生部位、浸润侵犯无关。[结论]胰腺癌中检测pLVD较iLVD更有价值;上述pLVD可以预测淋巴结转移,有助于判断预后。     

Evidence of chromosomal alterations in pure usual ductal hyperplasia as a breast carcinoma precursor

Previous studies have shown the chromosomal alterations in usual ductal hyperplasia (UDH), atypical ductal hyperplasia (ADH), and ductal carcinoma in situ (DCIS) in the breast with bilateral ductal hyperplasia or adjacent to invasive ductal carcinoma (IDC). However, the role of UDH as a putative precursor of breast IDC is not clear and has not been fully addressed. The aim of this study was to clarify the role of UDH in breast carcinoma pathogenesis. To investigate chromosomal imbalances and commonality, samples of pure unilateral UDH (n=20) were obtained by laser capture microdissection and analyzed by comparative genomic hybridization. Other ductal lesions, including ADH (n=2), high-grade DCIS (n=3), and grade III IDC (n=5), were assessed at the same time for comparison. The mean values of alteration were 1.95 (39/20) in UDH, 9.5 (19/2) in ADH, 11.0 (33/3) in DCIS and 18.2 (89/5) in IDC, respectively. Some common predisposition regions for the deletions were at chromosomes 1p36-pter, 13q11-14, and 16q11-23, while the high frequency amplification regions were 1q31-qter, 3p21-pter, 6p21-pter, 11q11-14, 12q11-qter, 13q21-qter, 16p12-pter, 17q12-22, and 20q. The genetic abnormalities in the spectrum of breast ductal hyperplasia revealed that the deletion of DNA copy in UDH was the lowest, and gradually increased in the lineages of ADH, DCIS and IDC. Results showed that a significant portion of UDH shares common genetic alterations with ADH, DCIS and IDC, indicating UDH as a precursor of invasive breast ductal carcinoma.     

Upregulation of focal adhesion kinase (FAK) expression in ductal carcinoma <Emphasis Type="Italic">in situ</Emphasis> (DCIS) is an early event in breast tumorigenesis

Focal adhesion kinase (FAK) is a protein tyrosine kinase that is overexpressed in a subset of invasive breast cancers. FAK transmits signals that mediate several functions including tumor cell proliferation, migration, adhesion and survival. We used immunohistochemical techniques to assess FAK expression in patients with fibrocystic disease (FCD), atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC). Formalin-fixed, paraffin-embedded (FFPE) tissue sections were obtained from 119 patients (12 FCD, 38 ADH, 51 DCIS and 18 IDC). The anti-FAK 4.47 monoclonal antibody was used to detect FAK expression. FAK expression was scored as high (3 or 4 intensity and 90 positive cells) or low. The DCIS tissue sections demonstrated high FAK expression in 34/51 (66) of the sections. High FAK expression was demonstrated in 6/18 (33) of the IDC tissue sections and 8/38 (21)of the ADH tissue sections. None (0/12) of the FCD tissues sections stained high for FAK. The pattern of FAK expression in DCIS was significantly higher than ADH (p < 0.0001) and IDC (p =0.02). We conclude that FAK overexpression in preinvasive, DCIS tumors precedes tumor cell invasion or metastasis, suggesting that FAK may function as a survival signal and be an early event in breast tumorigenesis.     

乳腺导管原位癌与浸润性导管癌染色体微卫星杂合性缺失的比较

目的:研究乳腺导管原位癌与浸润性导管癌染色体3p区域微卫星杂合性缺失(loss of heterozygosity,LOH)的发生情况.方法:选取本院2005年9月至2009年2月手术切除石蜡包埋的乳腺癌组织切块43例,应用激光显微切割技术留取组织中乳腺浸润性导管癌(invasive ductal type carci...     

Lymphatic vessel density as prognostic factor in breast carcinoma: relation to clinicopathologic parameters

Angiogenesis and lymphangiogenesis are essential for breast cancer growth and progression. This study aimed at investigating lymphatic microvessel density (LVD) and microvessel density (MVD) as prognostic markers in breast carcinoma. Forty breast carcinomas were immunostained for D2-40, CD31 and VEGF. Median lymphatic and blood microvessel densities, as well as VEGF expression, were related to each other and to clinicopathologic parameters including lymph node (LN) status. The efficacy of haematoxylin and eosin (H&E) in detecting lymphatic vessel invasion (LVI) compared to D2-40 immunostaining was also investigated. D2-40 stained normal lymphatic endothelium and myoepithelial cells, but with different staining patterns. D2-40 LVD related significantly to CD31 counts (r=0.470; p=0.002), and LN metastasis (Mann-Whitney U=101.500; p=0.043); however, it did not relate to age, tumor grade, tumor size or LVI. D2-40 identified LVI in 3 more cases (7.5%) than those detected by H&E. VEGF was expressed in 85%of cases, and was significantly related to CD31 and D2-40 counts (p=0.033 and 0.007, respectively). In conclusion, D2-40 LVD showed a significant association with LN metastasis, and can be considered to segregate patients with positive from those with negative LNs. D2-40 enhances the detection of LVI relative to H&E staining reflecting a potential for lymphatic metastatic spread and possible poor prognosis.     

Can Lymphatic Vascular Density Be Used in Determining Metastatic Spreading Potential of Tumor in Invasive Ductal Carcinomas?

Regional lymph node status is the primary parameter determining treatment strategies and prognoses in breast cancer. Lymphatic vessels in primary tumor tissue play a significant role in lymphatic metastasis. The aim of this study was to investigate the correlation of intra- and peritumoral lymphatic microvessel densities (LVD) with prognostic parameters in breast cancer, including lymphatic invasion (LI). Lymphangiogenesis was investigated using D2-40 monoclonal antibody in 69 invasive ductal carcinoma cases who underwent mastectomy and axillary lymph node dissection. Positively stained microvessels were counted at 400× in dense lymphatic vascular foci (hotspots). Tumor LI was established when at least one neoplastic cell cluster was clearly visible inside a D2-40-positive lymph vessel. Relationships were sought between clinicopathological parameters and mean LVD and LI in primary tumor tissue. Peritumoral LVD was markedly higher than intratumoral LVD (p < 0.001). No significant relationship was found between intratumoral LVD and clinicopathological parameters (p > 0.05). However, significant relationships were detected between peritumoral LVD and LVI [H&E] (p = 0.04), number of lymphatic invasion [n/mm2, D2-40] (p = 0.001), tumor size (p = 0.01), lymph node status (p = 0.03), and tumor stage (p = 0.04). The immunohistochemical determination of LI and LVD can contribute to the prediction of a tumor’s biological behavior in invasive ductal carcinomas. Peritumoral LVD in primary tumor tissue is closely related to parameters influencing the prognosis of a tumor.