乳腺癌组织蛋白酶D和PSA表达与同侧腋淋巴结转移的关系

目的：探讨乳腺癌中组织蛋白酶Ｄ（ｃａｔｈｅｐｓｉｎＤ，ＣＤ）和前列腺特异性抗原（ＰＳＡ）的表达与同侧腋淋巴结转移的关系。方法：应用ＬＳＡＢ免疫组化法检测ＣＤ和ＰＳＡ在７８例乳腺癌中的表达，其中伴同侧腋淋巴结转移者３６例。结果：（１）７８例乳腺癌ＣＤ阳性表达率４１．０３％（３２／７８），ＰＳＡ阳性表达率４３．５％（３４／７８）；（２）同侧腋淋巴结转移组ＣＤ阳性表达率６９．４４％（２５／３６），无同侧腋淋巴结转移组ＣＤ阳性表达率１６．６７％（７／４２），差异有高度显著性（Ｐ＜０．０１）；（３）同侧腋淋巴结转移组ＰＳＡ阳性表达率２５．０％（９／３６），无同侧腋淋巴结转移组ＰＳＡ阳性表达率５９．５２％（２５／４２），差异有高度显著性（Ｐ＜０．０１）。结论：ＣＤ和ＰＳＡ的表达可作为乳腺癌预后检测的参考指标。ＣＤ表达阳性率与同侧腋淋巴结转移呈正相关，与预后负相关；而ＰＳＡ表达阳性率与同侧腋淋巴结转移呈负相关，与预后正相关     

nm23基因产物／NDPK在大肠癌中的表达及其临床意义

应用免疫组化Ｓ－Ｐ方法，研究１０３例大肠癌手术标本中ｎｍ２３基因产物／ＮＤＰＫ的表达及其意义。结果显示：大肠癌原发灶中ＮＤＰＫ表达阳性率７６．７％；其中，无区域淋巴结转移者阳性率为９０．５％，伴区域淋巴结转移者阳性率６７．２％，差异具有显著性意义（Ｐ＜０．０５）；随着大肠癌浸润肠壁深度和Ｄｕｋｅｓ＇分期的进展，原发灶中ｎｍ２３／ＮＤＰＫ表达阳性率逐渐下降，统计学均具有显著性意义（分别Ｐ＜０．０１、Ｐ＜０．０５）；ｎｍ２３／ＮＤＰＫ表达阳性者术后３、５年生存率分别为６５．８％和５４．４％，明显高于ＮＤＰＫ阴性患者术后３年和５年生存率（３７．５％和２０．８％），统计学具有显著性意义（分别Ｐ＜０．０５、Ｐ＜０．００５）。我们认为：ｎｍ２３基因在大肠癌的浸润和淋巴结转移过程中发挥负性调控作用。测定大肠癌组织中ｎｍ２３基因产物／ＮＤＰＫ的表达状况，有助于对大肠癌生物学行为的进一步了解及对患者预后的判断。     

单纯疱疹病毒Ⅱ型和人乳头瘤病毒的感染与人工流产术后不孕症的关系

目的探讨性传播病毒和不孕症的关系。方法应用聚合酶链反应（ＰＣＲ）对６０例人工流产术后不孕症妇女和３９例正常妇女进行了生殖道单纯疱疹病毒Ｉ型（ＨＳＶ２）和人乳头瘤病毒（ＨＰＶ）的检测。结果不孕组和对照组ＨＳＶ２的阳性检出率分别是８０．０％和２５．５％，两组间有极显著性差异（Ｐ＜００１）；ＨＰＶ的阳性率分别是５３３％和３３３％，两组间无显著性差异（Ｐ＜０．０５）；ＨＳＶ和ＨＰＶ在两组中的混合感染的阳性率分别是４３．３％（２６／６０）和２３．１％（９／３９），两者有显著性差异（Ｐ＜０．０５）。表明ＨＳＶ２或ＨＳＶ２和ＨＰＶ的混合感染与人工流产术后不孕症有显著的相关性，很可能是不孕的原因之一。两组９９份标志中，ＨＳＶ２和ＨＰＶ混合感染的阳性率为３５．３５％，统计学分析表明，ＨＳＶ２和ＨＰＶ感染与不孕有极显著的相关性χ＝１２．５，Ｐ＜０．０１。结论ＨＳＶ２和ＨＰＶ的感染和不孕症相关     

p53、p21、p185蛋白表达与横纹肌肉瘤分化及预后的关系

目的研究ｐ５３、ｒａｓ和ｃ－ｅｒｂＢ－２癌基因蛋白产物ｐ２１、ｐ１８５在横纹肌肉瘤（ＲＭＳ）中的表达及其与ＲＭＳ的分型、分级和预后的关系。方法对确诊的５０例中的４１例有随访的ＲＭＳ用免疫组化ＡＢＣ法标记ｐ５３、ｐ２１、ｐ１８５蛋白，结果发现ｐ５３、ｐ２１、ｐ１８５在ＲＭＳ的阳性率分别为７２％、６８％、６０％，其阳性表达与年龄、性别和ＲＭＳ的组织类型差异无显著性（Ｐ＞０．０５）；但与分化程度有关，其中ｐ５３、ｐ２１在低分化ＲＭＳ的阳性率分别为８５％和８０％，显著高于高分化ＲＭＳ的４２．９％和２８．６％（Ｐ＜０．０５）；ｐ５３蛋白在有转移组ＲＭＳ的阳性率为８６．４％，显著高于无转移组６０．７％（Ｐ＜０．０５）；有随访的４１例病例中。存活１年的ｐ５３蛋白阳性率为８６．７％，显著高于３年的４１．７％（Ｐ＜０．０５）。结论ｐ５３、ｐ２１蛋白表达可作为肿瘤分化及恶性程度的评价指标，而ｐ５３更能反映肿瘤预后，是肿瘤预后差的重要指标之一。     

肺癌中MTS1/p16和p53基因产物的表达与细胞增殖的关系

目的：研究肺癌中ＭＴＳ１／ｐ１６和ｐ５３基因产物的表达与细胞增殖的关系。方法：应用Ｓ－Ｐ免疫组织化学方法研究６２例肺癌组织中ｐ１６蛋白和ｐ５３蛋白的表达情况，并进行增殖细胞核抗原（ＰＣＮＡ）检测，计算细胞增殖指数（ｐｒｏｌｉｆｅｒａｔｉｏｎｉｎｄｅｘ，ＰＩ）。结果：６２例肺癌组织中ｐ１６蛋白和ｐ５３蛋白阳性率分别为５８．１％和５９．７％。腺癌ｐ１６蛋白的阳性率明显高于小细胞癌（Ｐ＜０．０５）；淋巴结转移阳性组ｐ１６蛋白的表达显著低于阴性组（Ｐ＜０．０５）；ＰＩ分级为Ⅱ级的ｐ１６蛋白表达显著高于Ⅳ级（Ｐ＜０．０５）。不同组织类型肺癌中ｐ５３蛋白的表达未见明显差异，淋巴结转移阳性组ｐ５３蛋白的表达高于阴性组（Ｐ＜０．０１）；不同ＰＩ分级中ｐ５３蛋白的表达，Ⅳ级明显高于Ⅰ级（Ｐ＜０．０５）和Ⅱ级（Ｐ＜０．０５），Ⅲ级明显高于Ⅰ级（Ｐ＜０．０５）和Ⅱ级（Ｐ＜０．０１）。ｐ１６蛋白低表达和ｐ５３蛋白过表达之间未见明显相关。结论：ｐ１６蛋白低表达和ｐ５３蛋白过表达均有促进肺癌细胞增殖的作用，ｐ１６蛋白的表达与肺癌的细胞分化有关，ｐ５３蛋白过表达对肺癌细胞的转移起重要作用。抑癌基因ｐ５３对ＭＴＳ１／ｐ１６基因无明显调控作     

SLE病人外周血Bcl—2／JH基因重排检测的意义

应用聚合酶链反应（ＰＣＲ）方法检测３１例ＳＬＥ病人外周血单个核细胞（ＰＢＭＣ）Ｂｃｌ－２／ＪＨ基因重排现象和流式细胞仪间接双标记法分析其Ｔ（ＣＤ３）、Ｂ（ＣＤ１９）细胞Ｂｃｌ－２蛋白的表达。结果显示，ＳＬＥ病人Ｔ细胞Ｂｃｌ－２蛋白表达明显高于正常人（４２．９５％±２８．４７％对比９．９４％±４．９６％，Ｐ＝０．０００４），尤其以活动期ＳＬＥ病人为明显，而Ｂ细胞Ｂｃｌ－２蛋白表达与正常人之间并无统计学差异（７９．２１％±１０．６９％对比８１．９６％±６．９７％；Ｐ＝０．４６０２）。７例ＳＬＥ病人具有典型的Ｂｃｌ－２／ＪＨ基因重排（占２２．５８％），且均为ＳＬＥ活动期病人，其Ｔ细胞Ｂｃｌ－２蛋白表达明显高于无基因重排的ＳＬＥ病人，其Ｂ细胞Ｂｃｌ－２表达并无差异（Ｐ＞０．３９０５）。说明Ｂｃｌ－２／ＪＨ基因重排现象可见于ＳＬＥ，并与Ｔ细胞Ｂｃｌ－２蛋白高表达有关，表明细胞凋亡抑制基因Ｂｃｌ－２在ＳＬＥ发病机制中具有重要作用。     

胃癌组织P~（53）蛋白产物的表达与病人预后的关系

采用免疫组化方法对Ｐ￣（５３）蛋白的表达进行观察。结果表明：胃癌组织Ｐ￣（５３）蛋白染色阳性率为３６．５％，肿瘤大于５ｃｍ组、有淋巴结转移和浆膜侵犯及Ⅲ、Ⅳ期胃癌组织Ｐ￣（５３）蛋白染色阳性率分别显著高干肿瘤小于５ｃｍ、无淋巴结转移和浆膜侵犯及Ⅰ、Ⅱ期胃癌组（Ｐ＜０．０１）。Ｐ￣（５３）染色阳性者５年存活率为２１．１％，染色阴性者为５０．０％，两组５年存活率差非常显著（Ｐ＜０．０１）。以上结果提示检测胃癌组织Ｐ￣（５３）蛋白有助于判断胃癌患者预后。     

乳腺癌微血管数与预后因素淋巴结状态,pS2的关系

目的：探讨乳腺癌中微血管数与预后因素淋巴结状态、ｐＳ２的关系。方法：用ＬＳＡＢ法检测浸润性乳腺癌（ＩＢＣ）中的微血管数（ＭＶＣ）和ｐＳ２表达。结果：在７６例ＩＢＣ中ＭＶＣ的均数是５７．８２±２２．２２；淋巴结阳性５２例中有远处转移２３例，无远处转移２９例，ＭＶＣ分别为６８．０２±２０．１２与５５．１８±１９．０８，差异有显著性（Ｐ＜０．０５）。腋淋巴结阴性２４例中，有远处转移９例，无远处转移１５例，ＭＶＣ分别为７０．７７±１１．１１与４２．６２±２３．５４，差异有显著性（Ｐ＜０．０１）。原发癌ｐＳ２阳性与阴性的病例，ＭＶＣ分别为５６．７５±１９．０６与６７．０８±２０．３３，差异有显著性（Ｐ＜０．０５）。结论：ＭＶＣ可作为乳腺癌一项预后指标，无论腋淋巴结阳性或阴性，原发癌ＭＶＣ越高越易形成远处转移；ＭＶＣ与ｐＳ２表达呈负相关     

免疫组化和PCR—SSCP检测p53基因异常的一致性探讨

目的：探讨免疫组化检测ｐ５３蛋白表达和ＰＣＲ－ＳＳＣＰ检测ｐ５３基因突变的一致性。方法：单克隆抗体ＤＯ－７检测８５例非小细胞肺癌（ＮＳＣＬＣ）的ｐ５３蛋白表达，ＰＣＲ－ＳＳＣＰ检测其中３１例腺癌的ｐ５３基因突变。结果：８５例ＮＳＣＬＣ中ｐ５３蛋白表达阳性率为６８％（５８／８５），３１例腺癌中ｐ５３蛋白表达阳性率为６１％（１９／３１），１４例（４６％）出现ｐ５３基因５～８外显子突变，ｐ５３蛋白免疫组化和ＰＣＲ－ＳＳＣＰ检测ｐ５３基因突变无显著相关（χ２＝０．１，Ｐ＝０．７６），其一致率为５２％。结论：ｐ５３蛋白表达并不能很好地反映ｐ５３基因突变。     

层粘连蛋白及其受体在乳腺癌的表达与转移和预后的关系

目的观察层粘连蛋白（ｌａｍｉｎｉｎ,ＬＮ）和层粘连蛋白受体（ｌａｍｉｎｉｎｒｅｃｅｐｔｏｒ,ＬＮ－Ｒ）与乳腺癌转移和预后的关系。方法用ＬＳＡＢ免疫组化法,检测了１０９例乳腺癌原发灶和３７例淋巴结转移灶组织中ＬＮ和ＬＮ－Ｒ在癌细胞内表达的情况。结果有３２例（２９．４％）原发灶浸润性癌细胞内可见ＬＮ表达,５例（１３．７％）腋窝淋巴结转移灶中癌细胞内有ＬＮ表达。乳腺癌原发灶中有ＬＮ－Ｒ表达者占５５．０４％,淋巴结转移灶中ＬＮ－Ｒ表达占８３．７８％,后者明显高于前者（Ｐ＜０．０５）。６４例随访材料中单独ＬＮ表达者无１例死亡,而有ＬＮ－Ｒ表达者生存期明显短于无ＬＮ－Ｒ表达者（Ｐ＜０．００１）。经临床和病理多因素比例风险回归分析,显示淋巴结转移和ＬＮ－Ｒ是影响患者生存的独立因素,ＬＮ－Ｒ的风险度（４．３７５倍）大于淋巴结转移（２．８１０倍）。结论结果提示ＬＮ－Ｒ表达是导致乳腺癌患者死亡的重要生物学因素之一。     

Persistent E-cadherin expression in inflammatory breast cancer.

E-cadherin is a transmembrane glycoprotein that mediates epithelial cell-to-cell adhesion. Because loss of E-cadherin expression results in disruption of cellular clusters, it has been postulated that E-cadherin functions as a tumor suppressor protein. The role of E-cadherin in inflammatory breast cancer (IBC), a distinct and highly aggressive form of breast cancer, is largely unknown. The aim of our study was to elucidate whether E-cadherin expression contributes to the development and progression of the IBC phenotype and to investigate any differences in E-cadherin expression between IBC and stage-matched non-IBC. Forty-two breast cancer cases (20 IBC and 22 non-IBC) were identified. Strict and well-accepted criteria were used for the diagnosis of IBC. Clinical and pathologic features were studied, and formalin-fixed, paraffin-embedded tissue sections were immunostained for E-cadherin, estrogen and progesterone receptors (ER and PR, respectively), and HER2/neu. Statistical analysis was performed using Fisher's exact test. All IBC uniformly expressed E-cadherin, whereas 15 of the 22 (68%) of the non-IBC expressed the protein (P = .006). Intralymphatic tumor emboli in the IBC cases were also all E-cadherin positive. Two IBC tumors demonstrated invasive lobular histology, and both cases were positive for E-cadherin. Of the non-IBC cases, three were invasive lobular carcinomas, and all were positive for E-cadherin. No association was found between E-cadherin expression and ER, PR status, or HER2/neu overexpression. Our study demonstrates that there is a strong association between E-cadherin expression and IBC and suggests that E-cadherin may be involved in the pathogenesis of this form of advanced breast cancer. In our study, we demonstrate that circulating IBC tumor cells strongly express E-cadherin, thereby providing an important exception to the positive association between E-cadherin loss and poor prognosis in breast cancer.     

Correlations of TOP2A gene aberrations and expression of topoisomerase IIα protein and TOP2A mRNA expression in primary breast cancer: a retrospective study of 86 cases using fluorescence in situ hybridization and immunohistochemistry

Our aim in this study was to assess the status of TOP2A gene aberrations (no change/amplification or deletion) and its correlations with topoisomerase IIα (Topo IIα) protein and TOP2A mRNA expression, respectively. TOP2A amplification, Topo IIα protein expression and TOP2A mRNA expression were assessed using samples of 86 cases of breast cancer by fluorescence in fluorescence in situ hybridization, quantitative real-time polymerase chain reaction and immunohistochemistry, respectively. Twenty two (22.57%) had amplification/deletion of TOP2A gene. Twenty eight (32.56%) tumor samples were 17q polysomy or monosomy. Topo IIα protein was expressed in 57 cases (66.27%, 57/86): 22 cases (38.62%, 22/57) and 35 cases (61.40%, 35/57) had amplification/deletion and no change of TOP2A gene, respectively. These three groups showed significant differences by one-way analysis of variance (P < 0.001). The average Ct values of TOP2A mRNA expression in the tumors with deletion, amplification and no change of TOP2A gene were 27.00, 27.33 and 31.66, respectively. We demonstrated that the TOP2A gene was amplified or deleted in breast cancer, with a significant correlation with high expressions of Topo IIα protein and TOP2A mRNA expression. Ki-67 expression index (mean = 14.9) decreased significantly in cases wherein TOP2A gene had no change and Her2/neu protein expression was weakly positive (0-1+, P < 0.001).     

Molecular alterations differentiate microinvasive carcinoma from ductal carcinoma in situ and invasive breast carcinoma: retrospective analysis of a large single-center series

Microinvasive carcinoma (MIC) of the breast is a rare lesion. The clinicopathologic features and biologic behavior of MIC are unclear. Whether MIC is a distinct entity or an interim stage in the progression from ductal carcinoma in situ (DCIS) to invasive breast carcinoma (IBC) remains to be determined. A retrospective review of clinicopathologic features and analysis of the expression of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER-2), and Ki-67 in patients with MIC (90 cases), DCIS (268 cases) and IBC (1504 cases) was performed. Most MICs (93.3%) exhibited an intermediate to high nuclear grade, and this proportion was larger than that of DCIS (62.7%, P < 0.001) or IBC (85.4%, P = 0.036). The incidence of sentinel lymph node metastasis in MIC (12.5%) was higher than that of DCIS (1.6%, P < 0.001), but much lower than that of IBC (39.7%, P < 0.001). MICs had higher expression of HER-2 and lower expression of ER and PR compared to DCIS and IBC; and MIC was more likely to present with a HER-2+ subtype. Furthermore, DCIS exhibited greater HER-2 overexpression or gene amplification (P < 0.001) levels and lower proliferation index of Ki-67 (P < 0.001) compared to IBC. Our results suggest that the clinicopathologic and molecular phenotype of MIC are different from DCIS and IBC. Thus, MIC may be a distinct entity rather than an interim stage in the progression from DCIS to IBC. The prognosis of MIC and the biologic behavior of this uncommon subset need to be further explored.     

SLP-2基因在喉鳞状细胞癌和乳腺浸润性癌组织中的表达及其与预后的关系

目的 探讨两种恶性上皮性肿瘤组织--喉鳞状细胞癌(简称喉癌)和乳腺浸润性癌(简称乳腺癌)中stomatin like protein-2(SLP-2)基因在mRNA和蛋白水平的表达,及其与肿瘤的临床病理参数和预后的相关性.方法 应用逆转录聚合酶链反应(RT-PCR)检测了46对喉癌及喉正常上皮组织中SLP-2基因的表达,Western blot方法检测了其中10对标本的SLP-2蛋白表达,同时采用免疫组织化学方法分别检测了104例喉癌组织芯片和263例乳腺癌组织芯片中SLP-2蛋白的表达水平,分析SLP-2蛋白的表达与临床病理变量之间的关系.结果 RT-PCR结果显示SLP-2基因在46例喉癌中的38例肿瘤组织中的表达升高(83%,38/46),喉正常上皮组织中表达阴性.Western blot结果显示,有7例喉癌组织中SLP-2蛋白表达显著高于对应的喉正常上皮组织.喉癌组织芯片的免疫组织化学染色结果显示,与全部20例喉正常上皮组织的阴性表达(0/20)相比,SLP-2蛋白染色在104例喉癌组织中有36例出现了过表达(34.6%,36/104;P=0.000).与喉正常上皮表达相比,喉癌组织中SLP-2基因在mRNA和蛋白水平的表达均明显升高.SLP-2蛋白过表达与喉癌患者的临床分期较晚(P<0.01)和淋巴结发生转移(P=0.003)密切相关.乳腺癌组织芯片免疫组织化学染色结果显示,与在正常乳腺组织中的阴性表达(0/10)相比,SLP-2蛋白在乳腺癌组织中呈现过表达(52.5%,138/263),差异有统计学意义(P:0.000),且该蛋白的过表达与乳腺肿物的大小(P=0.020)、淋巴结转移(P<0.01)、临床分期Ⅲ期(P<0.01)以及发生远处转移(P=0.002)密切相关.此外,还与HER2/neu蛋白的表达存在显著相关性(P:0.037),生存分析表明,SLP-2蛋白过表达乳腺癌患者总生存率显著降低.多因素分析显示淋巴结状态、HER2/neu蛋白表达和SLP-2蛋白表达可能作为独立的预后因子.结论 SLP-2蛋白的过表达可能与喉癌和乳腺癌的侵袭、转移过程密切相关,并可能作为独立的预后指标提示乳腺癌患者预后不良.     

Morphometric grading in breast cancer: Tfor mitotic counts

Three hundred sixty-four cases of invasive ductal breast cancer diagnosed during the years 1988 to 1991 were analyzed to determine quantitative thresholds for mitotic activity. Mitotic counts were calculated in each sample and expressed as standardized mitotic index (SMI) and mitotic activity index (MAI). Based on Kaplan-Meier curves, univariate and multivariate analysis of Cox's regression, and maximum efficiencies of ROC analysis, optimal thresholds were determined on the basis of survival and recurrence of disease. In our material, with a follow-up time of 5 years 9 months, we found two thresholds-a lower and a higher-for both SMI (17 mitoses/mm²and 32 mitoses/mm²) and MAI (13 mitoses/10 HPF and 35 mitoses/10 HPF). The thresholds were the same in the whole material and in subgroups divided according to the patients' age and axillary lymph node status at the time of diagnosis, and tumor size. The thresholds clearly separated patients with favorable, intermediate, and unfavourable outcome of disease. In our material, the risk of breast cancer death associated with the determined thresholds (ranging from 4.7 to 3.8) clearly exceeded those of menopausal status, axillary lymph node status and tumor size. The risk of breast cancer death associated with the determined thresholds was still emphasized in the groups of premenopausal and axillary lymph node-negative patients, and with tumor size less than 2 cm in diameter (risk ratios, 11.8, 6.0, and 6.7, respectively). The results suggest that the presented quantitative thresholds could be applied in grading of invasive ductal breast cancer.     

High-level SLP-2 expression and HER-2/neu protein expression are associated with decreased breast cancer patient survival

There is sufficient evidence that human stomatin-like protein 2 (SLP-2) is a novel cancer-related gene. Its protein is overexpressed in many human cancers. SLP-2 can contribute to the promotion of cell growth, cell adhesion, and tumorigenesis in esophageal squamous cell carcinoma and lymph node metastasis in laryngeal squamous cell carcinoma. Immunohistochemical detection of SLP-2, estrogen and progesterone receptors, and HER-2/neu were performed on 263 cases of primary invasive breast cancer with a tissue microarray. Of 263 cases, 138 (52.5%) showed high expression of SLP-2 protein, and 125 (47.5%) showed low or absent expression. In addition, there were significant positive associations between tumor stage and size (P = .020), lymph node metastasis (P < .001), clinical stage (P < .001), distant metastasis (P = .002), and HER-2/neu protein expression (P = .037) and high-level SLP-2 expression. High-level SLP-2 expression was associated with decreased overall survival (P = .011) and was more often found in patients with tumors larger than 20 mm, lymph node metastasis, advanced clinical stage, distant metastasis, and HER-2/neu protein-positive expression. More important, lymph node metastasis, HER-2/neu-positive expression, and high-level SLP-2 expression were associated with significantly decreased survival.     

p27kip1、p16蛋白和增殖细胞核抗原在鼻咽癌中的表达及其意义

目的 研究p27^kip1、p16蛋白及增殖细胞核抗原(PCNA)在鼻咽癌(NPC)组织中的表达,探讨它们之间的关系及其与．NPC生物学行为及预后的相关性。方法应用免疫组织化学EnVision两步法检测66例鼻咽非角化性癌(NKC)组织和25例鼻咽黏膜慢性炎症(NP)组织中p27^kip1、p16蛋白及PCNA表达水平。结果(1)．NKC组织中p27^kip1、p16阳性表达率分别为65％、68％;与NP组比较,差异有统计学意义(P＜0．05)。(2)＜、p16蛋白在NKC中的表达与NKC颅神经侵犯及治疗后5年生存率有关(P＜0．05),与临床分期、淋巴结转移无关(P＞0．05);PCNA表达与．NKC临床分期及治疗后5年生存率有关(P＜0．05),与淋巴结转移、颅神经侵犯无关(P＞0．05)。(3)p27^kip1、p16及PCNA阳性表达之间有相关性(P＜0．05)。结论检测p27^kip1、p16蛋白及PCNA有助于综合评估NKC的预后。     

卵巢上皮-间质肿瘤中B7-H3、B7-H4的表达及临床病理意义

目的探讨B7-H3、B7-H4在卵巢上皮-间质肿瘤中的表达及其临床病理意义。方法用RT-PCR技术及免疫组化PV9000两步法研究86例卵巢恶性上皮-间质肿瘤(恶性组),40例卵巢交界性上皮-间质肿瘤(交界组)和40例卵巢良性上皮-间质肿瘤(良性组)B7-H3与B7-H4mRNA及蛋白表达情况,并结合临床病理参数进行分析。结果 B7-H3、B7-H4mRNA在3组卵巢肿瘤组织中均有表达,且各自的3组卵巢肿瘤组织的mRNA光密度值差异均有统计学意义(P<0.05);B7-H3与B7-H4蛋白在恶性组中均呈细胞质和(或)细胞膜表达,其中B7-H3阳性率为81.4%(70/86),明显高于交界组22.5%(9/40)和良性组5.0%(2/40)的表达,差异有统计学意义(P<0.05);B7-H4阳性率为77.9%(67/86),明显高于交界组35.0%(14/40)和良性组5.0%(2/40)的表达,差异有统计学意义(P<0.05)。恶性组的卵巢癌组织中B7-H3蛋白在非黏液性卵巢癌中较黏液性卵巢癌高表达,差异有显著性(P<0.01),与临床分期、病理分级、患者年龄、腹水细胞学和淋巴结转移差异均无统计学意义(P>0.05)。B7-H4蛋白表达与组织病理学类型、临床分期、病理分级、患者年龄、腹水细胞学和淋巴结转移差异均无统计学意义(P>0.05)。结论 B7-H3与B7-H4在卵巢恶性上皮-间质肿瘤表达提示其可能与肿瘤的发生、发展有关,可为卵巢恶性肿瘤的诊断及治疗提供新的依据。     

乳腺癌非前哨淋巴结转移的预测

目的 :预测非前哨淋巴结 (non SLN)转移 ,以筛选出转移局限于前哨淋巴结 (SLN)的乳腺癌患者。方法 :采用99mTc SC作为示踪剂 ,对 95例乳腺癌患者行前哨淋巴结活检 ,对乳腺癌非前哨淋巴结转移进行单因素和多因素分析。结果 :95例患者中成功发现 91例患者有SLN (95 8% ) ,其中 85例患者SLN能准确反映腋窝淋巴结的病理状况 (93 4% )。临床肿块大小(P =0 0 2 8)、肿瘤分级 (P =0 0 40 )和原发灶cyclinD1蛋白 (P =0 0 17)的表达与non SLN转移显著相关。而Logistic多因素分析证实 ,临床肿块大小、肿瘤分级为独立的预测非前哨淋巴结转移的因子。结论 :可根据临床病理学特征 ,筛选出乳腺癌转移只局限于前哨淋巴结的患者 ,也存在免除腋窝淋巴结清扫的可能性