1 267例乳腺癌临床与免疫组化指标的相关性分析

分析乳腺浸润性导管癌的临床特征及6种免疫组化指标表达的关系,探讨其临床意义。方法:采用免疫组化SP法对1 267例乳腺癌患者的术后肿瘤石蜡标本进行ER、PR、C-erbB-2、P53、Ki-67、VEGF检测,并与患者的临床特征进行相关分析。结果:乳腺癌组织中ER、PR、C-erbB-2的阳性表达率分别为61.4%、53.0%、36.6%;P53、Ki-67、VEGF的阳性表达率分别为42.0%、91.6%、74.7%。肿瘤直径≤2 cm组中,ER和PR表达率最高（66.8%和58.8%）,而C-erbB-2的表达率最低（32.9%）。在低年龄组（≤50岁）和临床I期的患者中,PR表达率均最高,为57.9%和58.5%。C-erbB-2在临床晚期（Ⅲ,Ⅳ期）表达率最高（45.9%）。P53、Ki-67的阳性表达均与ER阳性表达呈负相关。而P53、Ki-67、VEGF的阳性表达与C-erbB-2的表达均呈正相关。淋巴结阳性组中P53、Ki-67与ER及P53与C-erbB-2的相关程度均较淋巴结阴性组大。结论:乳腺浸润性导管癌组织中ER、PR、C-erbB-2与P53、Ki-67和VEGF之间有一定的相关性,联合检测有助于指导该类肿瘤的治疗。      

Expression of ER,PR, C-erbB-2 and Ki-67 in Endometrial Carcinoma and their Relationships with the Clinicopathological Features

Background: To analyze the expression of estrogen receptors (ER), progesterone receptors (PR), C-erbB-2and Ki-67 in endometrial carcinoma (EC) and their relationships with the clinicopathological features. Materialsand Methods: Sixty-seven EC samples, 53 normal endometrial samples and 53 atypical hyperplasia endometrialsamples were all selected in Shaanxi Provincial People’s Hospital from Jun., 2012 to Jun., 2014. The expression ofER, PR, C-erbB-2 and Ki-67 in EC tissue, normal endometrial tissue and atypical hyperplasia endometrial tissuewas respectively detected using immunohistochemical SP method. The relationships between the expression of ER,PR, C-erbB-2 and Ki-67 and the patients’ clinicopathological features as well as their correlations in EC tissuewere also analyzed. Results: The positive expression rates of ER and PR in EC tissue were 44.8% and 41.8%,respectively, dramatically lower than in atypical hyperplasia endometrial tissue and normal endometrial tissue(P<0.01). The positive expression rates of C-erbB-2 and Ki-67 in EC tissue were 80.6% and 64.2%, respectively,significantly higher than in atypical hyperplasia endometrial tissue and normal endometrial tissue (P<0.01).In EC tissue, the expression of ER and PR was closely associated with the differentiated degrees and depth ofmyometrial invasion (P<0.05), while that of C-erbB-2 and Ki-67 with the clinical staging, differentiated degrees,depth of myometrial invasion and presence or absence of lymph node metastasis (P<0.05). Spearman correlationanalysis further displayed that the expression of ER was positively correlated with PR (r=0.393, P=0.001), butnegatively with C-erbB-2 and Ki-67 (r=-0.469, P=0.000; r=-0.329, P=0.007); The expression of PR was negativelycorrelated with C-erbB-2 and Ki-67 (r=-0.273, P=0.025; r=-0.251, P=0.041), but that of C-erbB-2 positivelywith Ki-67 (r=0.342, P=0.005). Conclusions: Abnormal expression of ER, PR, C-erbB2 and Ki-67 might playan important role in endometrial malignant transformation and cell differentiation, so their joint detection islikely to be a comprehensive combination of immune factors, which is of great importance for EC prognosis.     

The Evolution of Estrogen Receptor Signaling in the Progression of Endometriosis to Endometriosis-Associated Ovarian Cancer

To investigate changes in estrogen receptor alpha (ERα) signaling during progression of endometriosis to endometriosis-associated ovarian cancer (EAOC) as a driver of malignant transformation. We procured tissue samples of normal endometrium, endometriosis (benign, atypical, concurrent with EAOC), and EAOC. We evaluated expression of a 236-gene signature of estrogen signaling. ANOVA and unsupervised clustering were used to identify gene expression profiles across disease states. These profiles were compared to profiles of estrogen regulation in cancer models from the Gene Expression Omnibus (GEO). Gene Set Enrichment Analysis (GSEA) was performed to determine whether gene expression in EAOC was consistent with ERα activity. ANOVA revealed 158 differentially expressed genes (q?<?0.05) and unsupervised clustering identified five distinct gene clusters. The estrogen signaling profile of EAOC was not consistent with activated ERα in pre-clinical models. Gene set enrichment analysis did not identify signatures of activated ERα in EAOC but instead identified expression patterns consistent with loss of ERα function and development of endocrine resistance. Gene expression data suggest that ERα signaling becomes inactivated throughout the progression of endometriosis to EAOC. The gene expression pattern in EAOC is more consistent with profiles of endocrine resistance.     

Expression of estrogen receptor,progesterone receptor,and insulin-like growth factor receptor-1 and of MIB-1 in patients with recurrent pleomorphic adenoma of the parotid gland

BACKGROUND: Patients with recurrent pleomorphic adenomas of the parotid gland are difficult to manage without considerable risk of facial nerve injury. The prognostic significance of progesterone receptor (PR) and estrogen receptor (ER) reported in these adenomas was evaluated in patients with recurrent pleomorphic adenomas, comparing the results in a group of patients with primary adenomas without recurrences during 10 years of follow-up. METHODS: Paraffin embedded tumor samples from 52 patients with recurrent pleomorphic adenoma of the parotid gland were collected and stained immunohistochemically. Expression of PR, ER, Ki-67 antigen, and insulin-like growth factor receptor-1 (IGFR-1) was analyzed in resected samples of recurrent tumors and was compared with samples from a control group of patients with primary pleomorphic adenoma. RESULTS: A difference (P < 0.05) in the type of tumor was observed between the recurrent group (more cell-poor variants) and the control group. ER expression was low in both groups (19% and 17%, respectively), but immunoreactivity for ER was higher (48%) in normal parotid gland tissue. PR expression in the recurrent group (96%) was higher compared with PR expression in the control group (61%; P < 0.001). PR expression and IGFR-1 expression were correlated weakly (correlation coefficient = 0.660; P = 0.053) in the recurrent group. The expression of growth fraction (Ki-67 score) and IGFR-1 was similar in both groups but was more extensive compared with normal parotid gland tissue. CONCLUSIONS: PR seems to be a prognostic factor in recurrent pleomorphic adenoma of the parotid gland. The PR pathway can be considered a potential target for hormone treatment in patients with these recurrent adenomas.     

Utility of cytology microarray constructed from effusion cell blocks for immunomarker validation

BACKGROUND: Tissue microarray allows rapid and efficient evaluation of gene expression at the protein level and of immunochemical markers. To our knowledge, there has been no report of constructing cytology microarray using effusion cell blocks and testing its utility in immunochemical marker validation. METHODS: A total of 23 malignant effusions (primary tumor of breast [5], GI tract [5], lung [5] and ovary [8]) were used to construct a cytology microarray so that 3 cores of 0.6 mm in diameter were taken from the original cell blocks. Antibodies including AE1/AE3, EMA, and Ki-67 were applied to all cases, and CK7, CK20, TTF-1, WT-1, ER, and PR antibodies were used for selected cases. The cellularity, composition of cells, the staining pattern, and the intensity of each antibody were compared between corresponding cell block sections and CMA cores. RESULTS: The composition of tumor cells in the original block and the cores (including Sections 1 and 45) on cytology microarray were similar, ranging from 5% to 90%. Immunostains of AE1/AE3 and EMA were all positive and 100% concordant between the originals and cytology microarray. Similarly, CK7, CK20, ER, PR, TTF-1, and WT-1 stained both original blocks and cytology microarray with a high level of agreement with respect to percentage of positive cells, staining pattern (cytoplasm or nuclear), and intensity. Ki-67 stain showed slightly lower concordance (84%) with a few cases not in agreement because of low tumor burden in the original block coupled with low percentage of staining by antibody. CONCLUSIONS: Three 0.6 mm cores of cytology microarray are representative of the original cell block with cellularity and antibody staining pattern, intensity, and percentage. Therefore, CMA has a great potential in clinical research and practice as it allows rapid validation of immunocytochemical markers.     

ER、PR与C-erbB-2、Ki-67在乳腺癌中的表达及其临床意义

目的 探讨乳腺癌组织中ER、PR与C-erbB-2、Ki-67的表达及它们的相关性.方法 采用免疫组化检测,对356例乳腺癌患者ER、PR、C-erbB-2及Ki-67的表达、临床病理特征以及它们的相关性进行回顾性分析.结果 ER、PR、C-erbB-2及Ki-67的表达与淋巴结转移相关(P<0.05);乳腺癌组织分级...     

PTEN与预后相关因子在乳腺癌组织芯片中的相关性

目的:构建乳腺癌组织芯片,研究PTEN与乳腺癌预后相关因子ER、PR、c-erbB-2、Ki67在原发性乳腺癌中的蛋白表达及其相关性。方法:制作乳腺癌组织芯片,用免疫组织化学法检测芯片上165例乳腺癌组织中PTEN、ER、PR、c-erb B-2和Ki67蛋白的表达。结果:乳腺癌组织中PTEN的高表达例数为66/163(40.5%),ER、PR、c-erb B-2和Ki67阳性率分别为51.5%、35.6%、34.4%、44.8%。PTEN阳性表达随腋淋巴结转移数、组织学分级和TNM分期的增高而降低,呈负相关性P<0.05),与肿瘤的大小和发生年龄无明显相关。乳腺癌中PTEN与ER、PR蛋白表达呈显著正相关,与c-erb B-2、Ki67蛋白表达呈负相关。结论:PTEN蛋白低表达及表达缺失与性激素失调及乳腺肿瘤细胞的生长、预后之间存在一定的联系,PTEN可作为判断乳腺癌恶性程度的潜在标志物。同时检测PTEN、ER、PR、c-erb B-2和Ki67对乳腺癌的辅助治疗具有重要意义及实用价值。     

KLF4与S100A14在子宫内膜异位症相关性卵巢癌中的表达及临床意义

目的:探求子宫内膜异位症相关性卵巢癌中Krüppel样因子4（KLF4）与钙离子结合蛋白14（S100A14）的表达情况及临床意义。方法:免疫组化判定KLF4及S100A14分别在36例正常/良性卵巢组织（对照组）、30例卵巢子宫内膜异位症组织（ovarian endometriosis，OE）和49例子宫内膜异位症相关性卵巢癌组织(endometriosis associated ovarian carcinoma，EAOC)中的表达情况，并分析二者与EAOC患者相关临床参数的关系。结果:KLF4在对照组、OE组以及EAOC组中的阳性表达率分别为72.2%（26/36）、63.3%（19/30）、32.7%（16/49），差异有统计学意义（P＜0.01）。S100A14在三组中表达的阳性率分别为61.1%（22/36）、63.3%（19/30）、87.8%（43/49），差异有统计学意义(P＜0.05)。在EAOC中，KLF4表达与淋巴结转移有显著相关性（P＜0.05）。KLF4与S100A14呈负相关(r=-0.138)。结论:KLF4低表达和S100A14高表达可能参与了卵巢子宫内膜异位症恶变，同时KLF4可能促进了EAOC的转移。     

49例卵巢子宫内膜异位症恶变的临床病理分析

背景与目的:卵巢子宫内膜异位症是常见妇科良性疾病,异位的子宫内膜与原位的子宫内膜一样,都具有恶性潜能.本研究探讨49例卵巢子宫内膜异位症恶变的临床病理学特征.以及雌激素受体(estrogen receptor,ER)和孕激素受体(progesterone receptor,PR)在卵巢子宫内膜异位症恶变和无恶变卵巢子宫内膜异位症之间的表达差异.方法:对49例卵巢子宫内膜异位症恶变(恶变组)的临床病理学特征进行回顾性研究,应用ER、PR抗体对恶变组及49例无恶变卵巢子宫内膜异位症(对照组)进行免疫组织化学染色和统计学分析.结果:49例卵巢子宫内膜异位症恶变患者为29～70岁,中位年龄49岁.首发症状多为发现盆腔包块,B超检查提示盆腔混合性囊实性包块.术后肉眼检查见包块呈囊实性,直径4.0 cm～20.0 cm,囊内壁粗糙呈棕或黄色,内有咖啡色粘稠液体,实性区呈菜花样或乳头状的增生物,质脆或嫩,直径0.5 cm～15.0 cm.镜下见恶变组中的异位宫内膜腺上皮发生不典型增生及恶变.恶变组和对照组ER阳性率分别为20.4%(10/49)和95.9%(47/49),PR阳性率分别为14.3%(7/49)和95.9%(47/49),两者之间都有统计学意义(P＜0.05).结论:卵巢子宫内膜异位症恶变多发于围绝经期妇女,结合患者临床表现、B超结果以及病理检查都有助于疾病诊断.异位子宫内膜ER、PR抗体的表达阴性可作为诊断的依据之一.     

乳腺癌组织中ER、PR、cerbB-2、Ki-67表达及其意义

目的探讨乳腺癌组织中雌激素受体（ER）、孕激素受体（PR）、cerbB-2和Ki-67基因的表达及其临床意义。方法采用S-P免疫组化方法,检测107例乳腺癌组织中ER、PR、cerbB-2、Ki-67的表达水平,并结合其患者的相关临床资料进行分析。结果乳腺癌组织中ER、PR、cerbB-2、Ki-67阳性表达率分别为56.1%、82.2%、71.0%、67.3%。ER、PR、cerbB-2、Ki-67阳性表达与乳腺癌腋窝淋巴结转移和临床分期显著相关（P〈0.05）。而与患者年龄、肿瘤大小无相关性（P〉0.05）。相关分析结果显示ER与PR表达呈正相关（P=0.000）,与Ki-67表达呈负相关（P=0.000）;PR与cerbB-2、Ki-67表达呈负相关（P=0.012、0.006）。结论 ER、PR和cerbB-2、Ki-67与乳腺癌的发生、发展有关,联合检测ER、PR、cerbB-2和Ki-67,有助于客观评估乳腺癌的生物学行为,从而指导临床治疗和预后判断。     

乳腺浸润性导管癌组织Ki-67表达及其分子分型的意义

目的:探讨Ki-67增殖抗原在乳腺浸润性导管癌组织中的表达及与临床病理特征、雌激素受体(ER)、孕激素受体(PR)、人表皮生长因子受体-2(C-erbB-2)和抑癌基因p53的关系.方法:采用Elivison二步法进行免疫组化染色,检测102例单侧乳腺浸润性导管癌组织中Ki-67、ER、PR、C-erbB-2和p53的表达水平,并结合患者相关临床资料进行分析.结果:Ki-67高表达(≥14％)比例占82.4％ (84/102).不同分子亚型中,luminalA型Ki-67表达率最低,三阴性(导管)最高.Ki-67表达水平与单侧浸润性导管癌患者的淋巴结转移(x2=5.007,P=0.025)、TNM分期(u=705.000,P=0.032)和组织分级(单侧Fisher:P=0.042)有明显的相关性,与患者的年龄(t=1.996,P=0.052)、肿块大小(u=859.000,P=0.502)和侵犯脉管情况(xc2=0.762,P=0.383)无明显的相关性.Ki-67表达水平与ER(r=-0.273,P=0.005)、PR(r=-0.332,P=0.001)表达程度呈负相关;与C-erbB-2(r=0.327,P=0.001)、p53(r=0.343,P=0.000)表达程度呈正相关.结论:Ki-67表达与目前乳腺癌分子分型相关,其高表达是预后不良因素.     

LRP16基因在乳腺癌组织中的表达及其临床意义

背景与目的:既往研究表明雌激素通过其受体!直接上调LRP16的表达,LRP16基因的高表达促进乳腺癌细胞的增殖。本研究旨在探讨LRP16基因在乳腺癌组织中的表达状况及其与临床病理特征的关系。方法:收集52例乳腺癌组织及其配对癌旁组织,Northernblot与半定量RT-PCR法分别检测22例和30例标本中LRP16mRNA水平。免疫组化法检测肿瘤组织中雌激素受体(ER)、孕激素受体(PR)及Ki-67的表达情况。结果:Northernblot检测结果表明,22例癌组织LRP16mRNA的表达较癌旁组织高2倍的有9例,高表达率为40.9%(9/22)。高表达LRP16的9例中有7例ER阳性,8例PR阳性;而非高表达13例中ER阳性6例,PR阳性5例,两组ER与PR阳性率均有显著性差异(P<0.05)。LRP16高表达的9例中只有1例PR和ER同时阴性,而非高表达的13例中有7例。22例患者中,13例肿瘤直径3.0～4.5cm,其中LRP16基因高表达组占8例;有腋窝淋巴结转移的12例中8例LRP16高表达。8例高表达Ki-67患者中6例LRP16高表达。半定量RT-PCR检测结果表明,30例肿瘤标本中9例(30.0%)LRP16mRNA的表达水平明显高于癌旁组织,9例LRP16高表达者ER、PR均阳性,Ki-67高表达,且瘤体直径均大于3.5cm,均有腋窝淋巴结转移,与非高表达组比较差异有显著性(P<0.05)。结论:LRP16基因表达水平与ER/PR阳性率、细胞增殖活性、肿瘤直径、远处淋巴结转移密切相关,提示LRP16基因可能参与促进乳腺癌的增殖与转移。     

新辅助化疗对乳腺癌的组织学分级和生物学指标表达的影响

目的 探讨新辅助化疗对乳腺癌的组织学分级和生物学指标表达的影响.方法 67例接受新辅助化疗的原发性乳腺癌女性患者在化疗前均有核芯针活检结果作为组织学诊断依据,化疗后效果的组织学评估参照日本乳腺癌学会制定的判定标准,分为无效(G1)、轻度有效(G2)、中度有效(G3)、显著有效(G4)和完全有效(G5)5级.采用免疫组化EnVision法对化疗前后的肿瘤组织进行染色,比较化疗前后雌激素受体(ER)、孕激素受体(PR)、人表皮生长因子受体2(Her-2)和Ki-67的表达变化.结果 全组67例患者化疗效果的组织学评估结果显示,G1、G2、G3、G4和G5的患者分别为5例(7.5%)、19例(28.4%)、20例(29.9%)、17例(25.4%)和6例(9.0%).全组有49例患者在化疗前后具有ER、PR、Her-2和Ki-67表达情况的评估结果.化疗后PR阳性率为71.4%,与化疗前(91.8%)相比,差异有统计学意义(P=0.021);而化疗前后ER和Her-2的表达保持稳定.14例浸润性导管癌患者在新辅助化疗后组织学分级发生变化,其中降1级者12例,占85.7%.新辅助化疗后,组织学分级有变化者在G1、G2、G3和G4组中所占的比例分别为0、5.9%、41.2%和54.5%(P=0.013).Ki-67的平均表达率从化疗前的28.3%下降到化疗后的11.0%(P=0.011).化疗后Ki-67的表达率下降＞10%、＞20%、＞30%、＞40%和＞50%者在G1和G2组、G3组、G4和G5组中所占的比例均呈增加趋势,且差异均有统计学意义(均P＜0.05).结论 新辅助化疗后,乳腺癌组织的PR表达显著降低,而ER和Her-2的表达保持稳定;乳腺癌组织的组织学分级和Ki-67的表达也降低,并且好的化疗效果与组织学分级和Ki-67的表达降低相关.     

Ki-67与乳腺癌临床病理特征及新辅助化疗疗效的相关性

目的：分析Ki-67与乳腺癌临床病理特征对新辅助化疗（neoadjuvant chemotherapy,NCT）疗效和预后的影响,探讨NCT疗效的预测因素。方法用免疫组化法检测320例局部晚期乳腺癌患者癌组织中ER、PR、HER-2及Ki-67表达状况。进行NCT 4～6个周期后手术。分析临床病理特征与病理完全缓解率（patho-logic complete response,pCR）之间的关系。临床病理参数与疗效分析用χ2检验,影响预后因素用Cox多因素回归分析。结果 Ki-67表达与ER（r=－0.174,P=0.002）和PR（r=－0.132,P=0.019）呈负相关,与HER2（r=0.140, P=0.012）和乳腺肿瘤大小（r=0.132,P=0.019）呈正相关;ER阴性组pCR率显著高于ER阳性组（26.9%vs 7.4%,χ2=22.761,P=0.000）;PR阴性组pCR率显著高于阳性组（22.7%vs 10.9%,χ2=7.950,P=0.005）;Ki-67高表达组pCR率18.0%（41/228）优于Ki-67低表达组8.6%（8/92）（χ2=4.552,P=0.033）;化疗后Ki-67表达下降组pCR率19.8%（48/243）优于未下降组1.3%（1/77）（χ2=15.356,P=0.000）;各分子亚型间化疗疗效差异显著,Luminal A型pCR率为1.4%（1/71）,Luminal B型pCR率为15.3%（25/163）,HER2过表达型pCR率为31.3%（14/45）,三阴性型pCR率为22.0%（9/41）（χ2=20.639,P=0.000）;用Kaplan-Meier法进行生存分析,Ki-67低表达组无病生存时间（DFS）和总生存时间（OS）均优于Ki-67高表达组,两者均为P=0.034。结论 Ki-67高表达患者对化疗更敏感,但预后较差。化疗前Ki-67的表达和化疗后Ki-67变化是影响DFS独立的预后因素。ER、PR、Ki-67指数及分子分型可以作为NCT疗效的预测指标,Ki-67指数与ER、PR、HER2之间存在相关性。     

ER，PR，Her-2及Ki-67在乳腺癌原发灶和前哨淋巴结转移灶中的表达对比研究

目的:探讨ER、PR、Her-2及Ki-67在乳腺癌原发灶和前哨淋巴结转移灶中的表达变化及其临床病理意义。方法:收集50例具有乳腺癌原发灶和前哨淋巴结转移灶的病例,采用免疫组化及原位杂交分析原发灶和前哨淋巴结转移灶中ER、PR、Her-2及Ki-67的表达有无差异。结果:ER在乳腺癌原发灶和SLN转移灶中表达一致率为100%。PR原发灶和转移灶一致率为92%,变化率为8%,Her-2原发灶和转移灶一致率为96%,变化率为4%,表达变化均无统计学意义（P＞0.05）。Ki-67在乳腺癌原发灶表达率为（30.3±20.2）%,SLN转移灶表达率（25.1±17.6）%,差异具有统计学意义（P＜0.05）;Ki-67原发灶和转移灶表达一致率为70%,变化率为30%,但表达变化无统计学意义（P＞0.05）。补充腋窝淋巴结阳性率在原发灶高表达、SLN转移灶中变为低表达组22.2%（2/9）明显低于无变化组62.5%（15/24）,差异具有统计学意义（P=0.04）。结论:原发灶基本能反应SLN转移灶ER、PR、Her-2表达状态,但针对个体而言,SLN转移灶分子状态重新评价仍有益。Ki-67在SLN转移灶表达率降低,原发灶高表达而SLN转移灶变为低表达可能预测补充腋窝淋巴结的低转移率。     

Immunohistochemical analysis of 1,25-dihydroxyvitamin-D3-receptors,estrogen and progesterone receptors and Ki-67 in ovarian carcinoma

BACKGROUND: The aim of this study was to analyze immunohistochemically the expression of VDR in normal and carcinomatous ovarian tissue to evaluate whether ovarian tissue may be a new potential target for biologically active vitamin D analogues. MATERIALS AND METHODS: The expression of 1,25-dihydroxyvitamin-D3-receptors (VDR) was immunohistochemically investigated in ovarian carcinomas (n=40). VDR immunoreactivity (mAb 9A7gamma) was compared with the staining pattern of the proliferation marker Ki-67, of the estrogen receptors (ER) and of the progesterone receptors (PR). The percentage of positive tumour cells (PP), the intensity of staining (SI) and a resulting immunoreactivity score (IRS) were determined for the semiquantitative evaluation of VDR-, ER- and PR-expression. RESULTS: A total of 16.7% of the normal surface ovarian epithelium was VDR-negative, while the remaining 83.3% revealed weak to moderate VDR immunoreactivity. Moderate to strong nuclear immunoreactivity for VDR was detected in almost all ovarian carcinomas analyzed. Both the intensity of VDR immunostaining and the number of VDR-positive cells were significantly increased in ovarian carcinomas as compared to normal ovarian tissue. Analyzing coexpression of VDR with the proliferation marker Ki-67 or with the estrogen and progesterone receptors, no significant correlation was found. CONCLUSION: Our findings indicate that: (I) VDR expression is increased in ovarian carcinomas as compared to normal ovarian tissue. (II) Up-regulation of VDR in ovarian carcinomas is not exclusively induced by an increase of proliferation, but by different unknown mechanisms. (III) Expression of VDR in ovarian carcinomas is independently regulated from the expression of ER and PR. (IV) Ovarian tissue may be a new target organ for therapeutically applied vitamin D analogues exerting fewer calcemic side-effects. New vitamin D analogues may be promising drugs for the treatment of advanced ovarian carcinomas.     

C-erbB-2、p53、Ki-67及VEGF在乳腺癌中的表达及相关性

目的探讨C-erbB-2、p53、Ki-67及VEGF在乳腺癌组织中的表达及其与乳腺癌临床病理特征之间的相关性。方法采用免疫组化SP法检测72例乳腺癌组织中C-erbB-2、p53、Ki-67及VEGF表达情况,并结合临床病理特征进行相关性分析。结果乳腺癌患者C-erbB-2、p53、Ki-67及VEGF阳性表达率分别为47.2%、48.6%、56.9%、65.3%。C-erbB-2、p53表达与淋巴结转移、雌激素受体、孕激素受体相关(P<0.05);Ki-67、VEGF与肿瘤直径、淋巴结转移相关(P<0.05);ER和PR呈正相关(P<0.05);C-erbB2与ER、PR呈负相关(P<0.05);p53与ER和PR呈负相关(P<0.05);p53、Ki-67、VEGF之间均呈正相关(P<0.05)。结论 C-erbB-2、p53、Ki-67及VEGF检测对判断乳腺癌预后有重要意义。     

Histopathology and ARID1A Expression in Endometriosis- Associated Ovarian Carcinoma (EAOC) Carcinogenesis Model with Endometrial Autoimplantation and DMBA Induction

Background: Ovarian carcinoma is one of the most deadly malignancies in the gynecologic field. The cause is not yet known, and the clinical symptoms are not specific. Endometrioid carcinoma and ovarian clear cell carcinoma can originate from endometriosis and are known as endometriosis-related ovarian carcinoma (EAOC). Development of EAOC experimental animal models is needed for basic research and clinical preparation of human tissue tests. This study aimed to determine the role of the ARID1A gene mutation in the carcinogenetic process of EAOC in experimental animal models induced with DMBA. Methods: In this study, the EAOC experimental model was developed using the autoimplantation technique and DMBA induction. This study involved placebo surgery mice (sham), endometrial autoimplantation, and a combination of endometrial autoimplantation and DMBA induction, which were sacrificed at weeks 5, 10, and 20, respectively. Histopathological assessment and immunohistochemical ARID1A staining with an assessment of positive percentages were carried out on 200 cells. Results: This study produced 1 (20%) atypical endometriosis and 1 (20%) clear cell carcinoma at implantation and after 10 weeks of DMBA induction, and 100% endometrioid carcinoma in the DMBA-induced group. ARID1A staining did not show any significant difference (p = 0.313) in all groups. Conclusion: The combination of endometrial autoimplantation techniques and DMBA induction in the ovary produced atypical endometriosis, clear cell carcinoma, and endometrioid carcinoma, where time is an important factor. There was no significant difference in ARID1A expression between the treatment and control groups.