人源性乳腺癌骨转移小鼠模型的建立

目的 建立人乳腺癌细胞转移到人骨的"人源性"乳腺癌骨转移小鼠模型.方法 严重联合免疫缺陷(SCID/berg)雌小鼠50只,随机分为实验组(n=30)和对照组(n=20),其中实验组植入人骨后随机均分3组:A组(MDA-MB-231干细胞亚群,1×105个/只)、B组(同A组细胞,1 × 106个/只)和C组(MDA-MB-231亲代细胞,1×106个/只);对照组鼠随机均分2组:D组(阳性对照组,未植入人骨,MDA-MB-231亲代细胞,1×105个/只)、E组(阴性对照组,植入人骨,生理盐水).第4、7周行骨扫描,8周取人骨、鼠骨、肺等行HE染色及CK、CD34、CD105、SMA免疫组织化学检查.结果 骨扫描:第4周鼠植入的人骨均成活,第7周部分模型鼠出现可疑骨转移灶.HE染色及CK检查:B组人骨转移率最高77.8%(7/9),与C组人骨(20.0%)、D组鼠骨(20.0%)、E组鼠骨的骨转移率差异均有统计学意义(P《0.05);B组内人骨(77.8%)、鼠骨(0)、鼠肺(11.1%)转移差异有统计学意义(P《0.01).人骨表面结缔组织生长,骨内CD105、SMA、CD34均阳性的血管长入.结论 "人源性"乳腺癌骨转移小鼠模型骨转移发生率优于"非人源性"骨转移小鼠模型,能较好模拟人骨转移的血循环过程.     

Osteopontin RNAi对人乳腺癌细胞MDA-MB-231生物学行为的影响

目的 观察乳腺癌细胞MDA-MB-231 osteopontin (OPN) RNA靶向干扰效果.方法 采用OPN mRNA干扰质粒转染MDA-MB-231细胞,建立OPN基因沉默细胞株,采用RT-PCR、蛋白质印迹法从mRNA和蛋白水平检测乳腺癌细胞OPN表达量的变化,侵袭试验检测OPN下调对细胞侵袭能力的影响,MTT法测细胞增殖能力的改变,裸鼠成瘤后观察OPN RNA干扰对肿瘤细胞生长的影响及对移植瘤乏氧程度的影响.结果 与MDA-MB-231细胞相比,OPN沉默细胞在常氧和乏氧状态下OPN表达均显著下调(均P＜0.05),OPN稳定沉默细胞侵袭力和增殖能力下降(均P＜0.01),OPN RNAi能明显抑制裸鼠移植瘤的生长(P＜0.05),且移植瘤内乏氧程度降低(P＜0.05).结论 OPN RNA干扰可抑制乳腺癌细胞MDA-MB-231细胞侵袭力和增殖能力,降低移植瘤的乏氧程度.     

利用RNA干扰抑制CXCR4基因表达对乳腺癌细胞转移和侵袭能力的影响

目的探讨抑制趋化因子受体CXCR4基因对乳腺癌细胞转移和侵袭能力的影响。方法将人乳腺癌细胞株MDA-MB-31分为未干扰组、CXCR4干扰组、B-actin干扰组和空白载体干扰组。设计并合成了针对CXCR4基因的发夹式siRNA模板,体外合成siRNA表达框架（siRNA expression cassettes,SECs）,经脂质体转染CXCR4干扰组细胞,采用Western blot免疫印迹法和逆转录聚合酶链反应检测各组的抑制效果,用Biocdat Mamgel侵袭能力检测仪检测MDA-MB-231细胞的转移侵袭能力。结果SECs在mRNA水平和蛋白水平均明显抑制CXCR4基因的表达。CXCR4表达被抑制后,癌细胞侵袭能力受到明显抑制,与未干扰组相比,差异有统计学意义（P〈0．05）。结论SECs可以高效特异地抑制人乳腺癌细胞中CXCR4基因的表达。CXCR4基因高表达与乳腺癌细胞的转移密切相关,抑制细胞中CXCR4的表达可以抑制乳腺癌细胞转移和侵袭能力。     

不同浓度七氟醚对人肺腺癌细胞株A549黏附能力、CD24和CD44v6表达的影响

目的 观察不同浓度七氟醚对人肺腺癌细胞株A549黏附能力、CD24和CD44v6表达的影响.方法 人肺腺癌细胞株A549用含10％胎牛血清的RPMI 1640培养基于37℃、5％CO2、饱和湿度培养箱中培养.取对数生长期的人肺腺癌A549细胞,接种于24孔培养板中,采用随机数字表法,将其随机分为4组:对照组(C组)、1.7％七氟醚组(S1组)、3.4％七氟醚组(S2组)和5.1％七氟醚组(S3组).S1组、S2组和S组人肺腺癌A549细胞通入95％ O2-5％CO2混合气体6 L/min,经1.7％、3.4％、5.1％七氟醚作用6h,C组通入95％ O2-5％ CO2混合气体2 L/min 6 h.各组处理完成后,置于37℃、5％CO2培养箱中继续培养24h.分别于处理前、处理2、4和6 h(T4)时,每组取6个复孔的细胞,再培养24h后,检测细胞黏附率;分别采用RT-PCR法和流式细胞仪检测CD24和CD44v6的mRNA及其蛋白表达.结果 与处理前比较,S1组、S2组和S3组处理2、4和6h时细胞黏附率降低,CD24和CD44v6的mRNA及其蛋白表达下调(P＜0.05);与处理2h时比较,S2组和S3组处理4和6h时细胞黏附率降低,CD24和CD44v6的mRNA及其蛋白表达下调(P＜0.05);与处理4h时比较,S2组和S3组处理6h时细胞黏附率降低,CD24和CD44v6的mRNA及其蛋白表达下调(P＜0.05);与C组比较,S1组、S2组和S组处理2、4和6h时细胞黏附率降低,CD24和CD44v6的mRNA及其蛋白表达下调(P＜0.05);与S1组比较,S2组和S3组处理2、4和6h时细胞黏附率降低,CD24和CD44v6的mRNA及其蛋白表达下调(P＜0.05);与S2组比较,S3组处理2、4和6h时细胞黏附率降低,CD24和CD44v6的mRNA及其蛋白表达下调(P＜0.05).结论 七氟醚可降低人肺腺癌细胞株A549的黏附能力,且呈浓度和时间依赖性,其机制可能与下调CD24和CD44v6的表达有关.     

5-杂氮-2′-脱氧胞苷对实验性乳腺癌肺转移的影响

目的探讨5-杂氮-2′-脱氧胞苷(5-Aza-CdR)对乳腺癌MDA-MB-231细胞实验性肺转移的影响及可能的机制。方法将MDA-MB-231细胞分为对照组与5-Aza-CdR处理组,通过半定量RT-PCR(SqRT-PCR)与甲基化特异性PCR(MSP)方法检测两组细胞的乳腺癌转移抑制基因-1(BRMS1),CXC趋化因子受体-4(CXCR4)基因的mRNA表达及启动子区甲基化的状况。分别将两组细胞通过边缘尾静脉注射至BALB/c nu/nu裸鼠体内(每组5只)。5周后,用荧光定量RT-PCR(FqRT-PCR)检测裸鼠肺组织内的目的基因HPRT及内参GAPDH的mRNA丰度。结果对照组和处理组细胞的BRMS1相对灰度值(IDV)分别为0与0.39±0.001,处理组BRMS1 mRNA表达较对照组明显上调(P0.05),5-Aza-CdR使BRMS1启动子区甲基化的CpG岛B完全去甲基化;CXCR4相对IDV分别为0.58±0.003与0.58±0.01,两组间差异无统计学意义(P0.05),CXCR4启动子区CpG岛1的非甲基化状态亦无明显改变。对照组与处理组细胞的裸鼠肺脏HPRT和GAPDH的Ct值分别为:24.75±1.55,16.19±0.69与27.61±1.67,17.48±0.96,2-ΔΔCt=0.34,处理组裸鼠肺脏HPRTmRNA丰度明显低于对照组,肺组织内转移癌较少。结论 5-Aza-CdR通过去甲基化机制重新激活肿瘤转移抑制基因BRMS1的表达,从而降低了MDA-MB-231细胞实验性肺转移能力。     

单抗CD44-生物素-亲和素系统提高软骨细胞与支架黏附能力的研究

目的 观察单抗CD44-生物素(Biotin) -亲和素(Avidin)绑定系统在构建组织工程软骨中能否提高软骨细胞与支架的黏附能力.方法 分别制备软骨细胞二维和三维培养体系,分3组:A:壳聚糖+软骨细胞;B:生物素+亲和素化壳聚糖+软骨细胞;C:生物素化单抗CD44+亲和素化壳聚糖+软骨细胞.分别测定细胞展平面积、细胞接种脱落率、细胞增殖率,逆转录-聚合酶链反应(RT-PCR)法检测Ⅱ型胶原(ColⅡ)、聚集蛋白聚糖(aggrecan )、sox9的mRNA表达,组织学切片观察壳聚糖支架内细胞黏附生长情况.结果 细胞展平面积、细胞增殖率及ColⅡ、aggrecan、sox9的mRNA表达量皆为:C组＞B组＞A组(P＜0.05).细胞接种脱落率:A组为C组的3.71倍、为B组的2.17倍,而B组为C组的1.71倍,A组＞B组＞C组(P＜0.05).组织切片显示细胞在支架内C组增殖旺盛、胞外基质表达较丰富,A组增殖较弱、胞外基质表达较弱,B组介于C与A组间.结论 单抗CD44-Biotin-Avidin绑定系统能比Biotin-Avidin绑定系统更显著的提高软骨细胞与支架的黏附能力,促进组织工程软骨种子细胞的增殖和软骨细胞表型的表达.     

骨形态发生蛋白7在前列腺癌骨转移中的意义

目的 研究骨形态发生蛋白7(BMP7)与前列腺癌骨转移的关系.方法 采用逆转录-聚合酶链反应(RT-PCR)法检测人前列腺癌PC-3、乳腺癌细胞MDA-MB-231、肾癌细胞KETR-3、膀胱癌细胞T24、胃癌细胞MGC-803中BMP7 mRNA表达.免疫组织化学PV法检测45例有骨转移,42例无骨转移前列腺癌患者前列腺癌组织的BMP7蛋白表达.结果 RT-PCR结果显示,BMP7相对吸光度均值在前列腺癌PC-3细胞(9.59×10-1±1.67×10-2)和乳腺癌细胞(9.50×10-1±3.89×10-2)显著增高;与胃癌细胞MGC-803(2.93×10-1±1.33×10-2)、膀胱癌细胞T24(2.96×10-1±1.21×10-2)、肾癌细胞KETR-3(3.26×10-1±1.53×10-2)比较,差异有统计学意义(P＜0.05).免疫组织化学结果显示,骨转移前列腺癌组BMP7表达吸光度均值(74.80±5.76)明显高于无骨转移前列腺癌组(65.94±1.76),两组差异有统计学意义(P＜0.05).结论 BMP7在嗜骨性转移的前列腺癌细胞中,以及有转移的前列腺癌组织中的高表达,表明BMP7与前列腺癌骨转移有关.     

乳腺癌中CD44v6与CXCR4 mRNA表达及临床意义

目的:研究乳腺癌组织中细胞表面黏附分子拼接变异体-6(CD44v6)和趋化因子受体4(CXCR4)m RNA的表达,探讨其表达相关性及与临床病理之间的关系。方法:应用q RT-PCR检测60例乳腺癌组织及癌旁正常乳腺组织中CD44v6和CXCR4 m RNA的表达,分析两者表达、相关性及其与临床病理学特征的关系。结果:乳腺癌癌组织CD44v6和CXCR4 m RNA表达水平高于癌旁正常乳腺组织(P0.05);CD44v6和CXCR4的m RNA阳性表达率分别为56.67%(34/60)和61.67%(37/60),均明显高于癌旁正常乳腺组织(P0.01),且两者表达具有正相关性(r=0.399,P0.05);CD44v6与CXCR4 m RNA表达与乳腺癌的临床TNM分期及淋巴结转移有关(P0.01,P0.05),与患者的年龄、肿瘤大小及病理类型无关(P0.05)。结论:CD44v6和CXCR与乳腺癌发展和转移密有关,可作为乳腺癌的重要分子标志物和治疗靶点,联合检测两者的m RNA表达对乳腺癌的临床诊断及预后判断具有一定的指导意义。     

Involvement of cell-cell and cell-matrix interactions in bone destruction induced by metastatic MDA-MB-231 human breast cancer cells in nude mice

To clarify the mechanisms of bone destruction associated with bone metastases, we studied an animal model in which inoculation of MDA-MB-231 human breast cancer cells into the left cardiac ventricle of female nude mice causes osteolytic lesions in bone using morphological techniques. On the bone surfaces facing the metastatic tumor cells, there existed many tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclasts. TRAP-positive mononuclear osteoclast precursor cells were also observed in the tumor nests. Immunohistochemical studies showed that the cancer cells produced parathyroid hormone-related protein (PTHrP) but not receptor activator of NF-κB ligand (RANKL). Histochemical and immunohistochemical examinations demonstrated that alkaline phosphatase and RANKL-positive stromal cells were frequently adjacent to TRAP-positive osteoclast-like cells. Immunoelectron microscopic observation revealed that osteoclast-like cells were in contact with RANKL-positive stromal cells. MDA-MB-231 cells and osteoclastlike cells in the tumor nests showed CD44-positive reactivity on their plasma membranes. Hyaluronan (HA) and osteopontin (OPN), the ligands for CD44, were occasionally colocalized with CD44. These results suggest that tumorproducing osteoclastogenic factors, including PTHrP, upregulate RANKL expression in bone marrow stromal cells, which in turn stimulates the differentiation and activation of osteoclasts, leading to the progression of bone destruction in the bone metastases of MDA-MB-231 cells. Because the interactions between CD44 and its ligands, HA and OPN, have been shown to upregulate osteoclast differentiation and function, in addition to the cell-cell interactions mediated by RANK and RANKL, the cell-matrix interactions mediated by these molecules may also contribute to the progression of osteoclastic bone destruction.     

The ubiquitin E3 ligase WWP1 decreases CXCL12-mediated MDA231 breast cancer cell migration and bone metastasis

Advanced breast cancers preferentially metastasize to bone where cells in the bone microenvironment produce factors that enhance breast cancer cell homing and growth. Expression of the ubiquitin E3 ligase WWP1 is increased in some breast cancers, but its role in bone metastasis has not been investigated. Here, we studied the effects of WWP1 and itch, its closest family member, on breast cancer bone metastasis. First, we immunostained a multi-tumor tissue microarray and a breast cancer tissue microarray and demonstrated that WWP1 and ITCH are expressed in some of breast cancer cases. We then knocked down WWP1 or itch in MDA-MB-231 breast cancer cells using shRNA and inoculated these cells and control cells into the left ventricle of athymic nude mice. Radiographs showed that mice given shWWP1 cells had more osteolytic lesions than mice given control MDA-MB-231 cells. Histologic analysis confirmed osteolysis and showed significantly increased tumor area in bone marrow of the mice. WWP1 knockdown did not affect cell growth, survival or osteoclastogenic potential, but markedly increased cell migration toward a CXCL12 gradient in vitro. Furthermore, WWP1 knockdown significantly reduced CXCL12-induced CXCR4 lysosomal trafficking and degradation. In contrast, itch knockdown had no effect on MDA-MB-231 cell bone metastasis. Taken together, these findings demonstrate that WWP1 negatively regulates cell migration to CXCL12 by limiting CXCR4 degradation to promote breast cancer metastasis to bone and highlight the potential utility of WWP1 as a prognostic indicator for breast cancer bone metastasis.     

放射性核素骨显像支持下建立乳腺癌骨转移裸鼠莫型

目的 建立人乳腺癌骨转移裸小鼠模型。方法 采用人乳腺癌骨高转移细胞株MDA-MB-231BO,运用细胞悬液浓度0.8×107/ml、1.0×107/ml进行左心室注射,放射性核素骨显像和X线分别检测建立的人乳腺癌骨转移裸鼠模型。观察两组裸小鼠造模后的生存时间、体质量下降率,及骨转移程度与各部位转移率。结果 在两组裸小鼠体内均建成了乳腺癌骨转移模型;1.0×107/ml组裸鼠生存时间显著低于0.8×107/ml组(P＜0.01),体质量下降率显著高于0.8×107/ml组(P＜0.05);1.0×107/ml组骨转移程度高于0.8×107/ml组,1.0×107/m1组肿瘤细胞数/细胞总数显著高于0.8×107/ml组(P＜0.05);1.0 × 107/m1组转移部位数高于0.8×107/ml组;放射性核素骨显像的检出率为100％。结论 核素骨显像在裸鼠骨转移方面具有早期诊断意义;浓度为0.8×107/ml人乳腺癌骨高转移细胞株MDA-MB-231BO可以成功的建立乳腺癌骨转移裸鼠模型,完整地模拟了乳腺癌骨转移患者的自然临床病理过程。     

Early detection of bone metastases in a murine model using fluorescent human breast cancer cells: application to the use of the bisphosphonate zoledronic acid in the treatment of osteolytic lesions.

A very common metastatic site for human breast cancer is bone. The traditional bone metastasis model requires human MDA-MB-231 breast carcinoma cell inoculation into the left heart ventricle of nude mice. MDA-MB-231 cells usually develop osteolytic lesions 3-4 weeks after intracardiac inoculation in these animals. Here, we report a new approach to study the formation of bone metastasis in animals using breast carcinoma cells expressing the bioluminescent jellyfish protein (green fluorescent protein [GFP]). We first established a subclone of MDA-MB-231 cells by repeated in vivo passages in bone using the heart injection model. On stable transfection of this subclone with an expression vector for GFP and subsequent inoculation of GFP-expressing tumor cells (B02/GFP.2) in the mouse tail vein, B02/GFP.2 cells displayed a unique predilection for dissemination to bone. Externally fluorescence imaging of live animals allowed the detection of fluorescent bone metastases approximately 1 week before the occurrence of radiologically distinctive osteolytic lesions. The number, size, and intensity of fluorescent bone metastases increased progressively with time and was indicative of breast cancer cell progression within bone. Histological examination of fluorescent long bones from B02/GFP.2-bearing mice revealed the occurrence of profound bone destruction. Treatment of B02/GFP.2-bearing mice with the bisphosphonate zoledronic acid markedly inhibited the progression of established osteolytic lesions and the expansion of breast cancer cells within bone. Overall, this new bone metastasis model of breast cancer combining both fluorescence imaging and radiography should provide an invaluable tool to study the effectiveness of pharmaceutical agents that could suppress cancer colonization in bone.     

High TFAP2C/low CD44 expression is associated with an increased rate of pathologic complete response following neoadjuvant chemotherapy in breast cancer

Background

In luminal breast cancer cell lines, TFAP2C regulates expression of key genes in the estrogen receptor–associated cluster and represses basal-associated genes including CD44. We examined the effect of TFAP2C overexpression in a basal cell line and characterized the expression of TFAP2C and CD44 in breast cancer specimens to determine if expression was associated with clinical response.

Methods

MDA-MB-231 breast cancer cells were treated with a TFAP2C-containing plasmid and evaluated for effects on CD44 expression. Pretreatment biopsy cores from patients receiving neoadjuvant chemotherapy for breast cancer were evaluated for TFAP2A, p53, TFAP2C, and CD44 expression by immunohistochemistry.

Results

Overexpression of TFAP2C in MDA-MB-231 cells resulted in decreased expression of CD44 mRNA and protein, P < 0.05. A pathologic complete response (pCR) following neoadjuvant chemotherapy was achieved in 17% of patients (4/23). Average expression for TFAP2C by immunohistochemistry in patients with a pCR was 93%, compared with 46% in patients with residual disease, P = 0.016; and in tumors that stained at ≥80% for TFAP2C, 4 of 9 (44%) achieved pCR, compared with 0 of 14 below 80%, P = 0.01. Additionally, in tumors that stained ≤80% for CD44, 4 of 10 (40%) achieved pCR, compared with 0 of 13 >80%, P = 0.02. In tumors that stained high for TFAP2C (≥80%) and low for CD44 (≤80%), 4 of 7 (57%) achieved pCR, compared with 0 of 16 in all other groups (P = 0.004).

Conclusions

TFAP2C repressed CD44 expression in basal-derived breast cancer. In primary breast cancer specimens, high TFAP2C and low CD44 expression were associated with pCR after neoadjuvant chemotherapy and could be predictive of tumors that have improved response to neoadjuvant chemotherapy.     

Genistein对乳腺癌细胞致成骨细胞生物学功能改变的影响

目的 探讨Genistein对乳腺癌细胞致成骨细胞(osteoblast, OB)增殖、分化和矿化功能的影响,观察Genistein在乳腺癌骨转移的病理条件下是否能调节OB生物学功能.方法 源于大鼠颅盖骨的原代OB与50%来自人源性乳腺癌细胞系MDA-MB-231或MCF-7的条件培养基(conditioned medium,CM)共同培养,并加入5×10-7 mol/L (G7)、5×10-8 mol/L (G8)或5×10-9mol/L (G9) 的Genistein进行干预.MTT法观察其对OB增殖的影响;PNPP偶氮法观察其对OB碱性磷酸酶(alkaline phosphatase, ALP)活性的影响;茜素红S(ARS)进行矿化结节染色并计算面积以观察其对OB矿化能力的影响.结果 MDA-MB-231和MCF-7细胞条件培养基可显著抑制OB的增殖.用Genistein干预1 d、3 d和5 d后,OB增值率可有不同程度的提高,差异有统计学意义(P<0.05).此外,乳腺癌细胞条件培养基可明显下调OB的ALP活性,而用不同浓度的Genistein干预后,OB的ALP活性分别较MDA-MB-231和MCF-7细胞条件培养基组增加22.7%、32.4%、63.5%和27.7%、32.0%、58.3%(P<0.05).Genistein还可改善乳腺癌细胞条件培养基对OB矿化能力的抑制,增加OB形成的矿化结节面积.结论 在乳腺癌骨转移的病理条件下,Genistein可促进OB的增殖、分化和矿化能力,改善乳腺癌细胞对OB生物学功能的抑制作用.     

CD44+/CD24-/low在乳腺癌中表达及其临床意义

目的 观察乳腺癌中CD44+/CD24-/low的表达与临床病理特征的关系及其对预后的影响.方法 应用双染免疫组织化学检测144例乳腺癌与30例乳腺良性肿瘤或正常乳腺组织中CD44+/CD24-/low的表达,收集并分析患者的临床病理和随访资料.结果 CD44+/CD24-/low在乳腺良性肿瘤或正常乳腺中表达率为0%～8%,乳腺癌中表达率为0%～75%.67例(46.5%)乳腺癌患者CD44+/CD24-/low表型的细胞>10%,余77例(53.5%)≤10%.CD44+/CD24-/low的表达高低在淋巴结转移(P<0.01)、病理分期(P<0.01)、HER-2表达(P<0.01)以及复发(P<0.01)上差异有统计学意义.CD44+/CD24-/low高表达的肿瘤复发时主要表现为远处转移,尤其是骨转移.CD44+/CD24-/low高表达和低表达的5年无病生存率为65%和82%(P<0.01),5年总生存率为68%和86%(P<0.05),差异有统计学意义.结论 CD44+/CD24-/low的表达可能与乳腺癌的转移有关,有可能作为评估乳腺癌患者预后的参考指标.     

乳腺癌组织CD44+CD24-/low细胞含量检测及其临床意义

目的 探讨乳腺癌组织中CD44+CD24-/low干细胞比例与各项临床指标的相关性.方法 新鲜乳腺癌组织标本68例.机械-酶法制成细胞悬液,流式细胞术检测CD44+CD24-/loe细胞的含量,探讨其含量与肿瘤分期、免疫组织化学、远处转移等的相关性.结果 (1)68例乳腺癌组织中的CD44+CD24-/low腺癌干细胞比例为0.1%～15.2%.(2)除ER组和远处转移组CD44+CD24-/low细胞的含量差异有统计学意义(P<0.05)外,年龄、肿瘤分期、腋窝淋巴结转移等组别,CD44+CD24-/low细胞的含量差异均无统计学意义(P>0.05).结论 CD44+CD24-/low乳腺癌干细胞比例与ER阴性表达、癌肿侵袭性和预后等临床指标明显相关.     

乳腺癌组织CD44+CD24-/low细胞含量检测及其临床意义

目的 探讨乳腺癌组织中CD44+CD24-/low干细胞比例与各项临床指标的相关性.方法 新鲜乳腺癌组织标本68例.机械-酶法制成细胞悬液,流式细胞术检测CD44+CD24-/loe细胞的含量,探讨其含量与肿瘤分期、免疫组织化学、远处转移等的相关性.结果 (1)68例乳腺癌组织中的CD44+CD24-/low腺癌干细胞比例为0.1%～15.2%.(2)除ER组和远处转移组CD44+CD24-/low细胞的含量差异有统计学意义(P<0.05)外,年龄、肿瘤分期、腋窝淋巴结转移等组别,CD44+CD24-/low细胞的含量差异均无统计学意义(P>0.05).结论 CD44+CD24-/low乳腺癌干细胞比例与ER阴性表达、癌肿侵袭性和预后等临床指标明显相关.