双色FISH分析浸润性乳腺癌HER-2基因扩增模式

[目的]应用荧光原位杂交技术(FISH)分析乳腺癌HER-2基因状态。[方法]采用双色FISH技术检测100例浸润性乳腺癌HER-2基因,分析FISH和免疫组织化学(IHC)检测结果,分析17号染色体多倍体比率及其与HER-2基因扩增的关系。[结果]100例浸润性乳腺癌标本中,HER-2蛋白IHC3+21例者中FISH检测均为阳性;IHC2+69例者中FISH检测为阳性的占72%,IHC1+10例者FISH检测为阳性的占20%。17号染色体多倍体的比率为51%。17号染色体二倍体与多倍体标本中,HER-2基因扩增的比率分别是76%和69%,差异无统计学意义(P=0.330)。[结论]乳腺癌IHC检测HER-2为1+~2+者需进一步行FISH检测确定HER-2基因状态;应用双色FISH方法能准确、全面评估HER-2基因状态。     

乳腺癌17号染色体多体对HER2检测的影响及其临床病理学意义

目的:探讨乳腺癌17号染色体多体对人类表皮生长因子受体2(epidermal growth factor receptor 2,HER2)检测结果的影响及其临床病理学意义.方法:采用荧光原位杂交(fluorescence in situ hybridization, FISH)双色法检测71例原发性浸润性乳腺癌中HER2基因和17号染色体拷贝数目情况.采用HER2绝对拷贝数标准和HER2/chromosome 17 比值标准,判定HER2的FISH检测结果;基于FISH检测结果,结合免疫组织化学法(immunohistochemistry, IHC)检测的HER2蛋白表达情况及相关临床病理参数进行分组对比分析.结果: 无论按照HER2绝对拷贝数标准(14/71,19.7%)或HER2/chromosome17 比值标准(2/71, 2.8%),所有FISH检测结果示HER2基因扩展可疑的病例都为17号染色体多体;与HER2基因扩增阴性者相比,单纯17号染色体多体组在肿瘤分级、淋巴结转移以及激素受体表达上差异无统计学意义(P均>0.05);而与HER2基因扩增阳性组相比,单纯17号染色体多体组表现出更低的肿瘤分级(50.0% vs 81.5%, P=0.025)、更高的淋巴结阴性率(55.6% vs 25.9%, P=0.045)以及更高的雌激素受体(estrogen receptor,ER)阳性率(83.3% vs 41.7%, P=0.005)和孕激素受体(progestogen receptor,PR)阳性率(87.5% vs 44.4%, P=0.003).结论:相比于HER2基因扩增组,单纯17号染色体多体组更倾向于HER2基因扩增阴性;17号染色体多体会影响HER2检测结果,是FISH检测中导致可疑结果产生的主要原因.     

荧光原位杂交与免疫组化检测乳腺癌组织HER-2基因扩增或蛋白表达情况的比较分析

目的 评估免疫组织化学(IHC)法检测乳腺癌组织中HER-2蛋白表达和荧光原位杂交(FISH)法检测其HER-2基因扩增在乳腺癌分子靶向治疗中的临床意义.方法 采用IHC法及FISH法分别检测47例乳腺癌组织中HER-2蛋白表达及HER-2基因扩增情况.结果 47例乳腺癌石蜡标本中,HER-2蛋白表达(+++)20例(42.55%),(++)10例(21.28%),(+)17例(36.17%);HER-2基因扩增22例(46.81%),无扩增25例(53.19%),其中17号染色体多体5例(10.64%).两种检测结果呈正相关(rs=0.415,P<0.05).结论 IHC法检测乳腺癌组织中HER-2蛋白表达町以作为是否应用赫赛汀的初筛;HER-2蛋白表达阳性的病例有必要进一步进行HER-2基凶扩增检测,来确定临床治疗是否应用赫赛汀.     

IHC和FISH检测乳腺癌HER-2表达的对比研究

目的:比较免疫组化(IHC)和荧光原位杂交(FISH)技术在检测乳腺浸润性癌患者中HER-2蛋白表达和基因扩增的一致性。方法:分别选用IHC和FISH技术对102例乳腺浸润性癌HER-2进行蛋白表达和基因扩增检测,比较两者检测的结果和相关性。结果:102例浸润性乳腺癌标本中FISH阳性55例,阴性47例。IHC检测0、1+、2+和3+的FISH阳性符合率分别为0(0/6)、9.52%(2/21)、65.00%(39/60)和93.33%(14/15)。IHC检测HER-2为2+/3+的标本中70.67%(53/75)显示HER-2基因扩增,1+/0患者中7.50%(2/27)显示HER-2基因扩增,Kappa系数为0.511,P<0.01。FISH检测结果显示,17号染色体多体总发生率为11.76%(12/102),在HER-2高表达的患者中发生率为9.33%(7/75),无或低表达发生率为18.52%(5/27),χ2=1.614,P=0.204。结论:HER-2蛋白表达和基因扩增IHC和FISH检测方法有较高的符合率,一致性较好。17号染色体多体可能是造成2种方法结果差异原因之一。     

应用荧光原位杂交法检测乳腺癌石腊样本中HER-2 基因的扩增

 目的 探讨荧光原位杂交法（Fluorescence in situ hybridization，FISH）检测乳腺癌HER-2基因扩增在临床病理诊断及分子靶向治疗中应用的可能性。方法 用FISH技术和免疫组化（Immunohisto—chemistry，IHC）技术检测50例乳腺导管癌石蜡包埋标本并比较两种方法的结果以及与临床病理的关系。结果 16／50例HER-2蛋白表达阳性，其中强阳性5例，中度阳性9例，弱阳性2例；11／50（22％）例乳腺癌标本FISH技术检测HER-2基因扩增阳性，其中5／5为免疫组化HER-2蛋白强阳性病例；6／9为中度阳性病例，其中1例为17号染色体多倍体与HER-2基因扩增。HER-2基因扩增与蛋白表达与乳腺癌转移有关（P〈0．05）。结论 FISH技术可稳定地检测用IHC确定的HER-2蛋白阳性乳腺癌中HER-2基因的扩增状况，并用于临床赫赛汀分子靶向治疗病例的筛选。     

乳腺浸润性导管癌17号染色体拷贝数变异与临床病理特征相关性分析

目的 乳腺癌是影响妇女健康的主要癌症之一,且发病率呈现明显上升趋势.DNA拷贝数变化(copy number variation,CNV) 能够影响基因表达,从而引起肿瘤发生,研究CNV对探索肿瘤的发病机制有很大帮助.本研究探讨乳腺癌17号染色体拷贝数变异和临床病理特征关系.方法 应用荧光原位杂交(fluorescence in situ hybridization,FISH) 法检测2010-01-01-2011-01-01新疆医科大学附属肿瘤医院乳腺润性导管癌标本283例,观察17号染色体拷贝数情况及人表皮生长因子受体2(human epidermal growth factor receptor 2,HER2) 基因扩增情况,并用免疫组织化学法检测HER2受体蛋白的表达水平.结果 283例乳腺癌中17号染色体拷贝数多倍体为43例(15.19%),双倍体为226例(79.86%),单倍体为 14例(4.95%),乳腺癌17号染色体多倍体HER2基因阳性率为53.49%(23/43).283例乳腺癌中HER2基因表达阳性为84例,阳性率为29.68%(84/283);17号染色体拷贝数不同在HER2基因是否扩增方面差异有统计学意义,χ2=9.564,P=0.007;乳腺癌17号染色体拷贝数变异在p53基因表达(χ2=8.181,P=0.017)、病理组织学分级(χ2=11.203,P=0.019)方面差异有统计学意义,与年龄、肿瘤大小和淋巴结转移等指标差异无统计学意义.17号染色体拷贝数不同组中预后存在差异,差异有统计学意义,χ2=241.363,P=0.001.结论 17号染色体拷贝数变异和乳腺癌病理特征及预后相关,检测乳腺癌中17号染色体拷贝数变异可作为指导临床治疗和判断预后的参考指标.     

微阵列技术用于检测乳腺癌人表皮生长因子受体2基因状态

目的探讨细胞核微阵列技术及组织微阵列技术用于检测乳腺癌组织中HER-2基因扩增和蛋白表达状态。方法将248例乳腺癌普通组织蜡块制成组织微阵列组,应用免疫组织化学法（IHC）和荧光原位杂交法（FISH）分别检测HER-2基因和蛋白表达。两种检测方法的-致性采用检验,并以FISH检测结果为金标准,绘制IHC检测乳腺癌HER-2表达的ROC曲线图。结果248例乳腺癌FISH与IHC检测结果-致性分析显示：Kappa=0．711,P=0．000,两种检测方法的-致性尚可。IHC检测乳腺癌HER-2ROC曲线下面积为0．888,P=0．000,约登指数为0．700,准确率为87．9％。IHC（＋＋）中4例为17号染色体单体型,占FISH阳性病例总数的5．26％（4／76）。IHC（＋＋＋）中5例为17号染色体多倍体型,FISH检测均为阴性,占FISH阴性总例数的2．9％（5／172）。IHC的检测可以较好地反映出FISH的结果。结论细胞核微阵列及组织微阵列技术用于检测乳腺癌HER．2基因状态有着节约实验成本、同一性好、结果可靠的优点。     

荧光原位杂交与免疫组化法检测乳腺癌HER-2表达的临床意义

[目的]探讨乳腺癌中荧光原位杂交(FISH)检测HER-2基因的扩增和免疫组织化学(IHC)检测HER-2蛋白表达在临床诊断及分子靶向治疗中的应用。[方法]采用FISH与IHC检测50例乳腺癌组织中HER-2基因的扩增与HER-2蛋白表达。[结果]50例浸润性乳腺癌中,FISH检测HER-2基因扩增阳性15例(30%),IHC检测HER-2蛋白表达(-～+)40例,HER-2蛋白表达(++)的2例,HER-2蛋白表达(+++)的8例。[结论]FISH检测HER-2基因的扩增与IHC检测HER-2蛋白表达(++～+++)有较高的一致性。对于IHC检测HER-2(-～++)表达时,必须进一步FISH检测。     

IHC、FISH与CISH检测乳腺癌Her-2基因状态的对比研究

目的 比较免疫组织化学法(IHC)、荧光原位杂交法(FISH)与显色原位杂交法(CISH)检测乳腺癌HER2基因状态的一致性,探讨FISH法与CISH法榆测乳腺癌HER2基因状态的临床意义.方法 对64例乳腺浸润性导管癌石蜡标本分别应用IHC法、CISH法与FISH法检测HER2蛋白、HER2基因状态及17号染色体多体的发生率.结果 HER2蛋白表达(+++)组,IHC与CISH、FISH法检测HER2基因扩增阳性的符合率均为100%;HER2蛋白表达(++)组,IHC与CISH、FISH法检测的符合率分别为95.83%与91.67%;HER2蛋白表达(+/-)组,IHC与CISH、FISH法检测的符合率亦均为100%.FISH法与CISH法的检测结果1例存在差异,FISH法与CISH法检测HER2基凶状态总的符合率为98.41%.17号染色体多体的发生率在IHC(+++、++、+/-)三组中分别为45.16%、45.83%和11.11%,其总的发生率为40.62%.结论 IHC法柃测HER2蛋白仅作为初筛方法;FISH法与CISH法检测HER2基因状态存在较高程度的符合率,CISH法可作为一种更加方便可行的方法检测HER2基凶状态;在疑有17号染色体多体干扰时,应进一步行FISH法检测.     

乳腺髓样癌HER．2基因扩增与临床病理因素相关性分析

目的：总结分析荧光原位杂交（fluorescenceinsituhybridization,FISH）技术检测乳腺髓样癌HER-2基因扩增的经验和临床病理学意义。方法：用FISH和免疫组化技术诊断32例乳腺髓样癌患者HER-2基因状态,并分析典型髓样癌和非典型髓样癌HER-2基因扩增的关系。结果：乳腺髓样癌HER-2基因扩增阳性率为37．5％（12／32）,其中典型髓样癌为7．7％（1／13）,非典型髓样癌为57．9％（1l／19）。HERu2基因扩增与髓样癌肿瘤类型（P=0．008）、肿瘤大小（P=0．040）、淋巴结转移（P=0．006）、临床分期（P=0．037）、HER-2蛋白表达（P=0．0001）和p53蛋白表达（P=0．015）有关,与患者年龄（．P=0．438）、ER（P=0．081）和PR（P=0．517）无关。乳腺髓样癌类型与HER-2蛋白表达有关（P=0．010）,与患者年龄（P=0．426）、肿瘤大小（P=0．786）、淋巴结转移（P=0．115）、临床分期（P=0．129）、ER（P=0．116）、PR（P=0．773）和p53（P=0．280）无关。结论：HER-2基因扩增可能参与乳腺髓样癌的演化与进展,乳腺典型髓样癌与非典型髓样癌的HER-2基因扩增有显著性差异,临床应用FISH技术诊断HER-2基因扩增靶标有助于指导乳腺非典型髓样癌-妁分子靶向治疗。     

Efficacy of primed in situ labelling in determination of HER-2 gene amplification and CEN-17 status in breast cancer tissue

Considerable attention has been given to the accuracy of HER-2 testing and the correlation between the results of different testing methods. This interest reflects the growing importance of HER-2 status in the management of patients with breast cancer. In this study the detection of HER-2 gene and centromere 17 status was evaluated using dual-colour primed in situ labelling (PRINS) in comparison with fluorescence in situ hybridization (FISH). These two methods were evaluated on a series of 27 formalin fixed paraffin embedded breast carcinoma tumours, previously tested for protein overexpression by HercepTest (grouped into Hercep 1+/0, 2+ and 3+). HER-2 gene amplification (ratio ≥ 2.2) by PRINS was found in 3:3, 6:21 and 0:3 in IHC 3+, 2+ and 1+/0 cases, respectively. Comparing FISH and IHC (immunohistochemistry), showed the same results as for PRINS and IHC. Chromosome 17 aneusomy was found in 10 of 21 IHC 2+ cases (47.6%), of which 1 (10%) showed hypodisomy (chromosome 17 copy number per cell ≤ 1.75), 7 (70%) showed low polysomy (chromosome 17 copy number per cell=2.26 - 3.75) and 2 (20%) showed high polysomy (chromosome 17 copy number per cell ≥ 3.76). The overall concordance of detection of HER-2 gene amplification by FISH and PRINS was 100% (27:27). Furthermore, both the level of HER-2 amplification and copy number of CEN17 analysis results correlated well between the two methods. In conclusion, PRINS is a reliable, reproducible technique and in our opinion can be used as an additional test to determine HER-2 status in breast tumours.     

Analysis of aneusomy level and HER-2 gene copy number and their effect on amplification rate in breast cancer specimens read as 2+ in immunohistochemical analysis

Our aim was to determine the aneusomy level and the HER-2 gene copy numbers, by fluorescence in situ hybridization (FISH) and to analyze their impact on the amplification rate in breast carcinomas considered HER-2 weakly positive cases by immunohistochemistry. We evaluated 343 breast carcinomas using double colour FISH (LSI Her-2/neu gene and CEP 17). Monosomy and polysomy were demonstrated in 24.2% and 46.1% respectively and 101/343 (29.6%) of the specimens were amplified by FISH. A statistically significant difference was observed, when we compared the amplification percentage in polysomic and monosomic specimens (P<0.0001) and, among polysomic specimens, when tumours were compared with HER-2 gene signals number per cell between 3 and 10 and >10 respectively (P<0.0001). Logistic regression analysis showed that HER-2 signals >10 and polysomy absence were independently associated with amplification. Our results confirm that the majority of 2+ IHC cases express the HER-2 protein without gene amplification and highlight the effect of chromosome 17 aneusomy and the HER-2 gene copy number on amplification.     

Bevacizumab in metastatic breast cancer: a meta-analysis of randomized controlled trials

Amplification of the HER2 gene, present in 15–30% of breast carcinomas, correlates with poor outcome and is an indication for treatment with trastuzumab. Standard testing methods for HER2 amplification are fluorescence (FISH) or chromogenic in situ hybridization (CISH). In FISH/CISH scoring, correction for chromosome 17 polysomy is believed to be critical for determination of true HER2 amplification as opposed to increased chromosome 17 copy number. The term “polysomy 17” is widely used and defined as ≥3 copies of the chromosome 17 centromere (probe CEP17, D17Z1). Thus, the centromere is assumed to be representative for the entire chromosome. This study aimed to investigate the frequency of polysomy 17 and its association with HER2 amplification in 111 invasive breast cancer patients by CEP17 CISH and by copy number analysis of a set of 17 genes along chromosome 17 using multiplex ligation-dependent probe amplification (MLPA). Chromosome 17 usually showed a complex pattern of gains and losses by MLPA, unrelated to the copy number status of the centromere. Increase in centromere 17 copy number (denoted “polysomy 17”), as assessed by CEP17 CISH, was found in 19% of the patients. Of these patients, 60% also showed amplification of HER2 measured by MLPA. However, none of the 111 patients showed a true polysomy of chromosome 17 by MLPA. Only two patients (1.8%) had a possible gain of 17q. Amplification of 17p was not found in any of the patients, although a possible loss of 17p was found in one patient. In conclusion, this extensive analysis of amplicons along chromosome 17 shows that true polysomy of chromosome 17, either of the whole chromosome or of the short or the long arm, is very rare in invasive breast cancer. Abnormal CEP17 copy numbers may therefore actually stem from high level gains or amplification of CEP17 regardless of copy number gains of the short and long arms of chromosome 17 and, at least in some cases, correction with CEP17 probes may provide misleading HER2 gene status assessment results.     

Polysomy 17 in HER-2/neu status elaboration in breast cancer: effect on daily practice.

PURPOSE: To assess the effect of chromosome 17 copy number on HER-2/neu status determination in breast cancers. EXPERIMENTAL DESIGN: HER-2/neu gene copy and chromosome 17 centromere numbers were evaluated on 893 breast carcinomas using double color fluorescence in situ hybridization (FISH). The net and chromosome 17 corrected (ratio) HER-2/neu copy numbers were compared and related to immunohistochemistry done according to the Food and Drug Administration (FDA)-approved scoring system (0, 1+, 2+, and 3+) as a first screening step in 584 cases. RESULTS: When a ratio > or = 2 was considered as criterion for FISH positivity, 49.3% (440 of 893) of cases showed amplification versus 56.2% (502 of 893) by using a net HER-2/neu gene copy number >4 as a alternative criterion; 14.8% (67 of 453) of cases having a ratio <2 had a net HER-2/neu gene copy number >4 and 1.1% (5 of 440) with a ratio > or = 2 had a net HER-2/neu gene copy number <4. Among discordant cases, 88.8% (64 of 72) were polysomic (>2.25 chromosomes 17/cell) and among polysomic cases, 12.8% (40 of 312) of the low polysomic (2.26-3.75 chromosomes 17/cell) and 36.9% (24 of 65) of the highly polysomic (>3.75 chromosomes 17/cell) cases showed discordance. In cases with a ratio <2, polysomy 17 incidences were 85.7% (6 of 7) in IHC 3+, 42.4% (79 of 186) in IHC 2+, 33.3% (15 of 45) in IHC 1+, and 29.1% (16 of 55) in IHC 0. CONCLUSION: A net increase in HER-2/neu gene copy number consecutive to polysomy 17 in the absence of specific gene amplification might lead to a strong protein overexpression in a small subset of breast carcinomas. HER-2/neu status determination by FISH is dependent on the criterion considered for positivity in clinical practice.     

No Strong Association Between HER-2/neu Protein Overexpression and Gene Amplification in High-grade Invasive Urothelial Carcinomas

The generation of urothelial carcinoma is caused by the accumulation of various molecular changes, as in most malignancies. There are conflicting data about the status of HER-2/neu oncogene in urothelial carcinomas. The aim of this study was to determine the status of HER-2/neu oncogene in high-grade invasive urothelial carcinoma of urinary bladder both in protein and DNA level. We evaluated HER-2/neu protein overexpression by immunohistochemistry (IHC) and gene amplification by fluorescent in situ hybridization (FISH) and real-time quantitative PCR in paraffin-embedded samples of high-grade invasive urothelial carcinoma obtained from 36 patients. Polysomy 17 was also assessed by FISH. Immunohistochemically, HER-2/neu protein overexpression was observed in 22 (61.1%) tumors (ten tumors with score 3+ and 12 with score 2+). Fourteen of 36 tumors (38.9%) were evaluated as negative (score 0 or 1+). Complete concordance between FISH and the PCR was seen in all of the samples scored as 0 and 1+ by IHC. HER-2/neu gene amplification was observed in three of 27 (11.1%) tumors by FISH (nine samples were non-informative) and in eight of 36 (22.2%) tumors by the PCR. The complete concordance between HER2-2/neu protein overexpression and gene amplification was seen only in three of 27 tumors. Polysomy 17 was seen in nine tumors (33.3%). The results indicated that, in contrast to breast cancer, there was no strong association between HER-2/neu overexpression and gene amplification in invasive urothelial carcinomas, and polysomy 17 was higher in tumors showing HER-2/neu overexpression.     

Interlaboratory comparison of HER-2 oncogene amplification as detected by chromogenic and fluorescence in situ hybridization.

PURPOSE: Chromogenic in situ hybridization (CISH) is a new modification of the fluorescence in situ hybridization (FISH) technique for detection of oncogene amplification in archival tumor samples. In CISH, the oncogene probe is detected using a peroxidase reaction, allowing use of transmitted light microscopy. We compared detection of HER-2/neu amplification by CISH with a Food and Drug Administration-approved two-color FISH test in an interlaboratory setting. EXPERIMENTAL DESIGN: Formalin-fixed paraffin-embedded tumor samples from 197 breast cancers were analyzed for HER-2 amplification by CISH. Two-color FISH (PathVysion) CISH of 17 centromere was done if the observer considered it necessary to ascertain amplification status in tumors with borderline HER-2 CISH copy numbers. RESULTS: Paired CISH/FISH results were available from 192 (97%) of 197 cases, no clear difference in success rates of either method was observed. Centromere 17 CISH was considered necessary in seven tumors. CISH and two-color FISH results were concordant in 180 cases (93.8%). There were 92 and 88 tumors found HER-2 amplified and nonamplified, respectively, by both methods. Eight tumors were amplified by CISH but not by FISH, and four tumors exhibited the opposite condition (kappa coefficient 0.875). In 7 of 12 cases differences between the two methods could have related to a lack of CISH chromosome 17 information. The remaining cases were explained by difficult histology (ductal carcinoma in situ, poor representativity, dense lymphocytic infiltration, or intratumoral heterogeneity). CONCLUSIONS: These results indicate that CISH could provide an accurate and practical alternative to FISH for clinical diagnosis of HER-2/neu oncogene amplification in archival formalin-fixed breast cancer samples.     

Prognostic Value of TOP2A Gene Amplification and Chromosome 17 Polysomy in Early Breast Cancer

The aim of this study was to analyze the occurrence of TOP2A gene amplification and chromosome 17 polysomy in patients with early breast cancer and to correlate the status of these alterations with the prognostic significance expressed as patients' clinical features and survival. Such concurrent analyses of TOP2A gene status and chromosome 17 polysomy have not been performed before. Study group included 149 consecutive stage I-III patients administered standard multimodality treatment. TOP2A abnormalities were examined by standard fluorescence in situ hybridization (FISH) and developed by our group quantitative real-time PCR (qPCR). TOP2A amplification and deletion assessed by FISH were found in 23% and 7% of the tumours, respectively, and by qPCR in 31% and 11% of the tumours, respectively. Chromosome 17 polysomy was detected in 40% of the cases. TOP2A amplification (by qPCR) correlated with shorter disease-free survival (p?=?0.03) and overall survival (p?=?0.047), and the prognostic value of TOP2A was confirmed in the multivariate analysis (HR?=?3.22, 95% CI 1.09-9.56, p?=?0.03). TOP2A gene amplification, but not chromosome 17 polysomy, carries negative prognostic information in early breast cancer. Given the aforementioned results, qPCR might serve as a prognostic tool in determining the patient's prognosis.     

Caveolin-1在乳腺浸润性导管癌间质内癌相关成纤维细胞中的表达水平与乳腺癌分子亚型的相关性

目的 检测Caveolin-1（Cav-1）在乳腺浸润性导管癌间质内癌相关成纤维细胞（CAFs）中的表达,分析Cav-1与乳腺癌分子亚型、HER-2基因状态的相关性及其与预后的关系。方法应用免疫组织化学法检测168例乳腺癌组织Cav-1在CAFs中的表达情况。用荧光原位杂交（FISH）方法检测乳腺癌组织中HER-2基因的扩增状态。结果 Cav-1在HER-2过表达型和Luminal B型的阳性表达率均为83.3％,显著高于Luminal A型（58.1％）和Basal like型（35.3％）,差异有统计学意义（P＜0.05）。乳腺癌HER 2基因扩增占39.3％（66／168）,与HER-2蛋白表达呈正相关（r=0.625,P＜0.05）。HER-2基因扩增组的Cav-1阳性表达率为83.3％,显著高于未扩增组的55.9％（P＜0.05）。Cav-1表达水平与HER-2蛋白（r=0.253）及基因（r=0.305）表达均呈正相关（P＜005）,与预后亦明显相关（P=0.041）。结论 乳腺癌间质内Cav-1表达与分子分型相关,HER 2蛋白表达水平增高及基因扩增与间质Cav-1表达水平增高呈正相关（P＜0.05）,乳腺癌间质CAFs中Cav-1高表达提示患者预后较好。