The early diagnostic methods for non-small-cell lung cancer (NSCLC) are limited, lacking effective biomarkers, and the late stage surgery is difficult and has a high recurrence rate. We investigated whether the effects of FBXO45 in arcinogenesis and metastasis of NSCLC. The up-regulation of FBXO45 expression in NSCLC patients or cell lines were observed. FBXO45 gene promoted metastasis and Warburg effect, and reduced ferroptosis of NSCLC. FBXO45 induced ZEB1 expression to promote Warburg effect and reduced ferroptosis of NSCLC. Sh-FBXO45 reduced cancer growth of NSCLC in mice model. FBXO45 decreased the ubiquitination of ZEB1, leading to increased expression of ZEB1, which in turn promoted the Warburg effect and reduced ferroptosis in NSCLC. In vivo imaging, Sh-FBXO45 also reduced ZEB1 expression levels of lung tissue in mice model. FBXO45 in NSCLC through activating the Warburg effect, and the inhibition of ferroptosis of NSCLC by the suppression of ZEB1 ubiquitin, FBXO45 may be a potential therapeutic strategy for NSCLC.

目的 探讨原发性肝脏上皮样血管内皮细胞瘤(HEHE)的临床病理学特征、免疫组化、分子病理特征及鉴别诊断.方法 回顾性分析10例HEHE患者的临床资料、组织病理学与免疫组化特征以及基因检测结果.结果 10例HEHE患者中,男性5例,女性5例,其中大部分临床表现为腹部隐痛不适、腹胀、恶心伴疲倦乏力,少数病例为体检时发现肝脏占位.7例为肝内多发结节,3例为单发结节,其中2例伴肺部转移.镜下肿瘤细胞呈梭形或上皮样,排列呈条索状、巢片状,高倍镜下观察肿瘤细胞具有嗜酸性胞质,胞质内可见特征性空泡形成,肿瘤间质常伴黏液样变性,细胞核具有轻至中度异型性,偶见核分裂象和坏死.免疫组化结果:肿瘤细胞表达CD31、CD34、ERG、FⅧ等血管源性标志物,Ki-67增殖活性较低.其中1例行荧光原位杂交(FISH)结果检测到TFE 3基因断裂阳性.结论 HEHE为少见的血管源性恶性肿瘤,临床表现及辅助检查通常无特异性,需结合组织学、免疫组化及基因检测等诊断.

Non-small-cell lung cancer (NSCLC) is the major subtype of lung cancer, with a series of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and proteins involved in its pathogenesis. This study sought to investigate the functionality of lncRNA EPB41L4A antisense RNA 1 (lncRNA EPB41L4A-AS1) in the proliferation of NSCLC cells and provide a novel theoretical reference for NSCLC treatment. Levels of lncRNA EPB41L4A-AS1, miR-105-5p, and GTPase, IMAP family member 6 (GIMAP6) in tissues and cells were measured by RT-qPCR and the correlation between lncRNA EPB41L4A-AS1 and clinicopathological characteristics was analyzed. Cell proliferation was evaluated by cell counting kit-8 and colony formation assays. The subcellular localization of lncRNA EPB41L4A-AS1 was analyzed by the subcellular fractionation assay and the binding of miR-105-5p to lncRNA EPB41L4A-AS1 or GIMAP6 was analyzed by dual-luciferase and RNA pull-down assays. Functional rescue experiments were performed to analyze the role of miR-105-5p/GIMAP6 in NSCLC cell proliferation. lncRNA EPB41L4A-AS1 and GIMAP6 were downregulated while miR-105-5p was upregulated in NSCLC tissues and cells. lncRNA EPB41L4A-AS1 was correlated with tumor size and clinical staging and its overexpression reduced NSCLC cell proliferation. lncRNA EPB41L4A-AS1 was negatively correlated with miR-105-5p and positively correlated with GIMAP6 in NSCLC tissues, and lncRNA EPB41L4A-AS1 sponged miR-105-5p to promote GIMAP6 transcription in NSCLC cells. Overexpression of miR-105-5p or knockdown of GIMAP6 reversed the inhibition of lncRNA EPB41L4A-AS1 overexpression on NSCLC cell proliferation. lncRNA EPB41L4A-AS1 was downregulated in NSCLC and mitigated NSCLC cell proliferation through the miR-105-5p/GI-MAP6 axis.

The utilisation of neoadjuvant immunotherapy has demonstrated promising preliminary clinical outcomes for early-stage resectable non-small-cell lung cancer (NSCLC). Nevertheless, it is imperative to develop novel neoadjuvant combination therapy regimens incorporating immunotherapy to further enhance the proportion of patients who derive benefit. Recent studies have revealed that stereotactic body radiotherapy (SBRT) not only induces direct tumour cell death but also stimulates local and systemic antitumour immune responses. Numerous clinical trials have incorporated SBRT into immunotherapy for advanced NSCLC, revealing that this combination therapy effectively inhibits local tumour growth while simultaneously activating systemic antitumour immune responses. Consequently, the integration of SBRT with neoadjuvant immunotherapy has emerged as a promising strategy for treating resectable NSCLC, as it can enhance the systemic immune response to eradicate micrometastases and recurrent foci post-resection. This review aims to elucidate the potential mechanism of combination of SBRT and immunotherapy followed by surgery and identify optimal clinical treatment strategies. Initially, we delineate the interplay between SBRT and the local tumour immune microenvironment, as well as the systemic antitumour immune response. We subsequently introduce the preclinical foundation and preliminary clinical trials of neoadjuvant SBRT combined with immunotherapy for treating resectable NSCLC. Finally, we discussed the optimal dosage, schedule, and biomarkers for neoadjuvant combination therapy in its clinical application. In conclusion, the elucidation of potential mechanism of neoadjuvant SBRT combined immunotherapy not only offers a theoretical basis for ongoing clinical trials but also contributes to determining the most efficacious therapy scheme for future clinical application.

目的 分析平滑肌22 alpha蛋白(SM22α)、转化生长因子-β1(TGF-β1)在结直肠癌组织中的表达水平,并探讨其与肿瘤侵袭转移的关系.方法 回顾性选取咸阳市中心医院2018年4月至2019年5月期间收治的104例结直肠癌患者为研究组,按照肿瘤侵袭转移情况分为侵袭转移组(n=31)和非侵袭转移组(n=73),并选取同期于我院接受治疗的87例良性结直肠肿瘤患者作为对照组.采用免疫组化S-P法检测并比较各组患者结直肠病变组织中SM22α、TGF-β1表达水平,采用Spearman秩相关分析SM22α、TGF-β1表达水平与肿瘤侵袭转移的关系,并采用受试者特征曲线(ROC)评估SM22α和TGF-β1表达水平对结直肠癌患者肿瘤侵袭转移的评估效能.结果 研究组患者的SM22α阳性表达率为48.08％,明显低于对照组的64.37％,TGF-β1阳性表达率为69.23％,明显高于对照组的36.78％,差异均有统计学意义(P<0.05);C期/D期患者SM22α阳性表达率为32.61％,明显低于A期/B期的60.34％,TGF-β1阳性表达率为80.43％,明显高于A期/B期的60.34％,差异均有统计学意义(P<0.05);侵袭转移组患者的SM22α阳性表达率为32.26％,明显低于非侵袭转移组的54.79％,TGF-β1阳性表达率为87.10％,明显高于非侵袭转移组的64.38％,差异均有统计学意义(P<0.05);经Spearman秩相关分析结果显示,SM22α与肿瘤侵袭转移呈负相关(r=-0.471,P<0.05),TGF-β1与肿瘤侵袭转移呈正相关(r=0.543,P<0.05);ROC分析结果显示,SM22α、TGF-β1及联合检测肿瘤侵袭转移的ROC曲线下面积分别为0.663、0.690、0.731,检测灵敏度分别为80.3％、78.6％、84.5％,特异性分别为60.8％、60.0％、61.8％,并且联合检测的ROC曲线下面积高于单项检测,检测灵敏度和特异性高于单项检测.结论 结直肠癌组织中SM22α表达减少,TGF-β1表达增加,且与肿瘤侵袭转移密切相关,可用于初步诊断肿瘤侵袭转移,且两者联合检测诊断效能更好.

Hypoxia is a critical feature of solid tumors and is considered to be a key factor in promoting tumorigenesis and progression. Beyond inducing metabolic reprogramming of tumor cells to adapt to the hypoxia tumor microenvironment (TME), hypoxia can also promote tumor growth by affecting the secretion of exosomes. Exosomes are nano-sized (30-150 nm in diameter) extracellular vesicles that can carry numerous substances including lipids, proteins, nucleic acids, and metabolites. Notably, hypoxia-induced exosomes alterations not only exist in tumor cells, but also in various TME cells including stromal cells and immune cells. Besides promoting tumor invasion, angiogenesis, and drug resistance, the secretion of these altered exosomes has recently been found to negatively regulate anti-tumor immune responses. In this review, we focus on the hypoxia-induced changes in exosome secretion and found it can contributes to immune evasion and cancer progression by recruiting protumor immune cells into TME, as well as inhibiting antitumor immune cells. Next, we also describe the recent advances of exosomes in immunotherapy and future direction. In conclusion, ongoing discoveries in this field have brought new insights into hypoxia exosome-led immunosuppression, enabling the development of exosome-based therapeutics and elucidating their potential in immunotherapy.

患者,女性,47岁,以"反复晕厥4年,再发1d"为主诉于2020年6月8日人院.现病史:4年前站立位时出现短暂意识丧失,面色苍白,伴出汗,晕倒在地后约5 min内自行清醒.不伴抽搐、口吐白沫、恶心、呕吐.醒后无肢体活动障碍、语言及视听障碍.以后反复类似发作,家人目击多次并送住院诊疗,外院诊断为"直立性低血压",治疗无效.发作逐渐频繁,起初数月发作1次,3年来每日均有发作,平卧发作少,被迫长期卧床.2周来无诱因加重,坐起或下床即发作.就诊于咸阳市中心医院(我院),步入门诊大厅时再次出现意识丧失.急诊科查心电图:窦性心律,心率103次/min.血糖5.5 mmol/L.以"血管迷走性晕厥?"收住院.发病以来睡眠及食欲欠佳.无头痛、胸痛、心慌、呼吸困难、咳嗽等.二便正常.个人史:无特殊,无不良嗜好.婚姻史及家族史无特殊.既往健康.

腺泡状软组织肉瘤(alveolar soft part sarcoma , ASPS )发病率占所有软组织肉瘤的0 .5％ ～1％[1] ,多发于四肢尤其是右侧下肢[2 ].对于婴幼儿和儿童来说,头颈部区域最易受累,以往报道中41％ 发生在眼眶部,25％ 在口腔[3 ].陕西省咸阳市中心医院泌尿外科收治了1例发生在后腹腔的ASPS ,发生部位罕见,现报告如下.

目的 利用网络药理学技术预测藏药八味沉香散治疗心肌缺血的作用机制.方法 通过检索TCMSP、TCM-PTD、PubChem和SEA数据库获得八味沉香散成分及靶点,检索OMIM、Dis GeNET和DrugBank数据库获得心肌缺血相关靶点,疾病、化合物共有靶点,通过在线软件绘制韦恩图获取.将共有靶点输入Cytoscape 3.2.1构建成分-靶点网络,应用STRING平台构建蛋白-蛋白相互作用(PPI)网络模型.通过ClueGO插件结合CluePedia对关键靶点基因生物过程进行富集分析,采用DAVID6.8数据库对关键靶点进行通路富集分析.结果 对八味沉香散中化合物进行筛选,共获得38个成分,对应358个靶点,疾病靶点共检索出579个,映射后获得33个治疗心肌缺血相关靶点,PPI网络拓扑分析发现VEGFA、IL-1β、MMP9、TNF等27个靶点.ClueGo插件分析出60个生物过程相关条目,通路分析获得29条直接或间接与心肌缺血疾病相关通路.结论 本研究结果初步预测藏药八味沉香散治疗心肌缺血的作用机制,并为深入研究其作用机制奠定了良好基础.

目的:分析17例小汗腺汗孔瘤(EP)患者的临床表现、病理学特点及诊断、鉴别诊断.方法:对我院近8年明确诊断EP的患者进行临床资料分析,观察HE及免疫组化、PAS染色.结果:小汗腺汗孔瘤多见于四肢末端,表现多样,16例患者临床均误诊,镜下见肿瘤由增生一致的基底细胞样立方形细胞构成,界限清,从表皮下层向下延伸至真皮内,可见有单层细胞覆盖的有嗜酸性护膜的导管分化或正在形成导管的空泡化细胞及少数囊腔和角质小皮,瘤团周围无栅栏状排列,与基底细胞癌、脂溢性角化病及透明细胞汗腺瘤难以鉴别.结论:小汗腺汗孔瘤是一种少见的良性附属器肿瘤,易误诊,确诊必须依靠病理检查,手术单纯切除即可治愈.

目的 探讨整合素连接激酶(integrin linked kinase,ILK)对膀胱癌细胞增殖、凋亡、侵袭和活性氧(reactive oxygen spe-cies,ROS)的影响.方法 构建过表达ILK基因的人膀胱癌5637细胞系模型,并将实验分为转染了过表达ILK的5637/ILK组和未做任何处理的5637组.运用Am-Blue细胞活性检测试剂盒和克隆形成实验检测膀胱癌细胞的增殖.在膀胱癌治疗药物多西紫杉醇作用下,运用AnnexinⅤ-FITC/PI细胞凋亡检测试剂盒和流式细胞术检测ILK对膀胱癌细胞凋亡的影响,并采用Transwell实验检测ILK对膀胱癌细胞侵袭的影响.利用活性氧检测试剂盒检测细胞中ROS水平.结果 细胞增殖实验结果显示,5637/ILK组细胞的增殖率显著高于5637组.克隆形成实验显示,5637/ILK组细胞的克隆集落形成率显著高于5637组,差异具有统计学意义(t=15.69,P<0.05).细胞凋亡实验结果显示,在10μmol/L多西紫杉醇刺激下,5637/ILK组细胞的凋亡率与5637组相比显著降低(55.96％±0.23％vs 75.36％±1.06％);Transwell侵袭实验显示,5637/ILK组细胞平均视野侵袭细胞数为127.4±54.95个,而5637组细胞为48.3±42.95个,5637/ILK组细胞侵袭能力显著增加(t=23.518,P<0.05).活性氧检测试剂盒检测细胞中ROS水平显示,5637/ILK组ROS荧光强度显著高于5637组,差异具有统计学意义(t=18.69,P<0.05).结论 ILK过表达可以促进膀胱癌细胞增殖和克隆形成,显著提升细胞内氧化应激状态,并且在多西紫杉醇药物的作用下,膀胱癌细胞的凋亡减少,侵袭增加.进一步揭示ILK的促癌效应很可能与膀胱癌多西紫杉醇耐药和细胞内氧化应激状态有关.

目的 探讨整合素连接激酶(integrin linked kinase,ILK)调控polo样激酶1(polo-like kinase 1,PLK1)的表达对膀胱癌细胞恶性生物学行为的影响.方法 将构建好的针对ILK基因的过表达质粒在脂质体介导下稳定转染人膀胱癌5637细胞,并命名为5637/ILK组,同时设转染空质粒的5637细胞作为阴性对照,并命名为5637/NC组;运用Western blot分别检测5637/ILK和5637/NC组中ILK的表达.再将低表达PLK1的PLK1 siRNA质粒稳定转染过表达ILK的膀胱癌5637/ILK细胞,同时设未转染质粒的5637/ILK细胞为阴性对照,并将实验分为5637/ILK+PLK1 siRNA组和5637/ILK组.运用Western blot分别检测两组细胞中PLK1的表达;TUNEL细胞凋亡检测试剂盒检测两组细胞的凋亡;划痕实验检测两组细胞迁移能力;运用流式细胞仪检测两组细胞中活性氧(ROS)的含量.结果 Western blot结果显示,5637/ILK组ILK蛋白表达较5637/NC组明显增高(P<0.05);PLK1蛋白的表达在5637/ILK+PLK1 siRNA组明显低于5637/ILK组(P<0.05).TUNEL检测细胞凋亡结果显示,与5637/ILK组相比,5637/ILK+PLK1 siRNA组细胞的凋亡发生率显著增加(18.65％±1.26％vs 66.38％±0.73％,P<0.05).划痕实验结果显示,5637/ILK+PLK1 siRNA组细胞在24 h内迁移距离小于5637/ILK组[(953.73±95.24)μm vs(1771.47±92.86)μm],差异具有统计学意义(P<0.05).ROS实验显示,5637/ILK+PLK1 siRNA组细胞ROS荧光强度显著低于5637/ILK组,差异具有统计学意义(t=11.62,P<0.05).结论 下调PLK1的表达水平可使过表达ILK的膀胱癌5637/ILK细胞的凋亡明显增加,迁移能力显著降低,细胞内氧化应激状态减低,揭示ILK过表达所诱导的促癌效应很可能是通过对PLK1的激活作用来实现的.

目的:研究转录因子Snail及上皮钙黏素E-cadherin在乳腺浸润性导管癌中的表达,探讨二者与乳腺浸润性导管癌各临床病理因素之间的关系,并分析二者的相关性.方法:应用免疫组织化学SP法检测55例患者乳腺浸润性导管癌组织与癌旁组织中Snail及E-cadherin的表达情况.结果:E-cadherin在实验组中的阳性表达率为58.18％,在对照组中阳性表达率为98.18％,两者差异有统计学意义(P<0.01),E-cadherin的表达与患者年龄、乳腺浸润性导管癌组织学分级、HER-2相关.Snail在实验组中的阳性表达率为87.27％,在对照组中阳性表达率为12.73％,两者比较差异有统计学意义(P<0.01).Snail的表达与乳腺浸润性导管癌组织学分级、ER、HER-2相关.由癌旁组织到乳腺浸润性导管癌组织中,E-cadherin的阳性表达呈递减,而Snail的阳性表达呈递增,且E-cadherin和Snail的表达呈负相关(r=-0.341,P<0.01).结论:E-cadherin及Snail是患者乳腺浸润性导管癌发生、进展以及转移的重要生物学标志,与肿瘤的发生及肿瘤的浸润转移密切相关.

目的 通过研究膀胱癌中ILK、E-cadherin及Twist的表达,探讨其在膀胱癌发生、发展中的作用. 方法 运用免疫组织化学SP法检测ILK、E-cadherin及Twist在62例膀胱癌和25例癌旁正常组织中的表达,并分析其相关性. 结果 在膀胱癌和癌旁组织中,ILK的表达率分别为54.8％(34/62)和16.0％(4/25),两组相比差异具有统计学意义(x2=10.9,P＜0.05);E-cadherin的阳性表达分别为32.3％(20/62)和72.0％(18/25),两组相比差异具有统计学意义(x2=11.4,P＜0.05);Twist的阳性表达分别为64.5％(40/62)和4.0％(1/25),两组相比差异具有统计学意义(x2=26.2,P＜0.05).同时,ILK和Twist在高分化膀胱癌中的表达明显低于低分化癌,两组相比差异具有统计学意义(均P＜0.05),而E-cadherin在高分化膀胱癌中的表达明显高于低分化癌(P＜0.05).膀胱癌中E-cadherin与ILK和Twist的表达均呈负相关;而Twist与ILK表达呈正相关. 结论 ILK、E-cadherin及Twist蛋白在膀胱癌中均有异常表达,并与膀胱癌的分化程度密切相关,ILK、E-cadherin及Twist可能参与膀胱癌的发生、发展.

Background: Tripartite motif containing 14 (TRIM14) has been reported to play a critical role in tumor development. However, little is known about TRIM14 expression and its clinical significance in hepatocellular carcinoma (HCC). The aim of the present study was to investigate the expression and prognostic value of TRIM14 in patients with HCC. Materials and Methods: The mRNA and protein levels of TRIM14 in HCC were evaluated by quantitative real-time polymerase chain reaction, Western blot analysis, and immunohistochemistry. The association of TRIM14 expression with clinicopathological factors, overall survival (OS), and recurrence-free survival (RFS) was analyzed. Results: TRIM14 expression was significantly upregulated in HCC-related tissues. High TRIM14 expression correlated with C-reactive protein (p = 0.01), alanine aminotransferase (p = 0.02), tumor size (p = 0.005), lesion number (p = 0.023), vascular invasion (p = 0.041), tumor/node/metastasis (TNM) stage (p = 0.001), and Barcelona Clinic Liver Cancer (BCLC) stage (p = 0.003). In addition, high TRIM14 expression was associated with poor OS and RFS (both p < 0.001). Cox regression analysis revealed that high TRIM14 expression was an independent prognostic factor for both OS (hazard ratio (HR) 1.657, 95% confidence interval (CI) 1.031-2.687; p = 0.018) and RFS (HR 2.297, 95% CI 1.184-2.312; p = 0.007). Conclusion: TRIM14 is a potential prognostic predictor for OS and RFS in patients with HCC.

Cisplatin (CDDP)-based systematic chemotherapy remains the mainstay of treatment for muscle-invasive bladder cancer (MIBC). However, acquired resistance to CDDP, a multifactorial process governed by an array of signals acting at different levels, is the major problem in BC treatment. Here, we report for the first time that, expression of Paired-box gene 5 (PAX5), a B-cell essential transcription factor, was significantly induced in CDDP-resistant BC tissues and in experimentally-induced CDDP-resistant BC cells. Inhibition of PAX5 expression by shRNA treatment effectively improved CDDP sensitivity in BC cells, whereas overexpression of PAX5 potentiated CDDP resistance through supporting BC cell survival. Mechanistically, using luciferase reporter and chromatin immunoprecipitation assays, we identified prostaglandin-endoperoxide synthase 2 (PTGS2, also called COX2), a potent enzyme responsible for prostanoids formation and inflammatory response, as the direct down-stream target of PAX5. PAX5 exerted its oncogenic function during the pathogenesis of CDDP resistance via stimulation of PTGS2 transcription. These observations collectively suggest that dysregulation of PAX5/PTGS2 cascade plays a causal role in the induction of CDDP resistance and gene silencing approaches targeting this pathway may therefore provide a novel therapeutic strategy for overcoming CDDP resistance in BC.

Objective To investigate the expression of ILK,Cyclin D1 and MMP-9 in bladder tumor and to explore its significance in carcinogenesis and progression of bladder tumor.Methods The immunohistochemical SP method was used to detect the expression of ILK,Cyclin D1 and MMP-9 in 112 cases of bladder tumors and 35 cases of normal bladder tissues adjacent to carcinoma.Results The positive expression rates of ILK,Cyclin D1 and MMP-9 were 62.1％ and i5.0％,70.7％ and 20.0％,65.5％ and 15.0％ in bladder tumor and normal bladder tissues,respectively (P ＜ 0.05).Meanwhile,their positive expression rates increased with the decrease of tumor differentiation degree(P ＜ 0.05).The expression of ILK was positively correlated with the expression of Cyclin D1 and MMP-9 (P ＜0.05).Conclusion The ILK,Cyclin D1 and MMP-9 overexpress in bladder tumor,and are closely correlated with the pathological differentiation,which suggests that they may involve in the occurrence and metastasis of bladder tumor.They may be effective reference markers in diagnosis of clinical pathology staging,and their combined detection can help predict the clinical diagnosis and prognosis of bladder tumor.

患者女性,16岁,2个月前无明显诱因出现咳嗽、咯痰,痰液量多,为白色黏稠痰液,伴气喘、气短明显,活动后加重、声音嘶哑,无发热、胸痛、恶心、呕吐等症状.查体:精神差,喘息貌,甲状腺缺如,双肺呼吸音粗,可闻及广泛喘鸣及少许湿鸣音,其余未见明显异常.1年前因甲状腺囊肿于外院行手术切除甲状腺,术后病理诊断:甲状腺乳头状癌,术后并发甲减,长期服用优甲乐治疗.复查CT示:双侧甲状腺区未见明显甲状腺,环状软骨后方类圆形软组织密度影,其与食管上端分界不清,同平面气管腔轻度狭窄,腔内凹凸不平.胸廓入口处气管左侧淋巴结肿大.双肺炎症,右肺支气管腔团块状高密度影.右侧局部胸膜增厚,气管狭窄明显.气管镜检查:声门下约1 cm处可见占位性病变,堵塞气道约95％,表面有渗血,肿瘤灰白色,质软(图1),大部分清除,术后病理送检.

目的 探讨多种制片方法联合免疫细胞化学(ICC)在肺癌胸水细胞学诊断中的意义和应用策略.方法 胸水细胞学标本2523例,其中可疑肿瘤细胞标本例199例,分别采用细胞蜡块(92例)、传统细胞涂片(35例)和薄层液基细胞(TCT)(72例)制片方法与ICC相结合进行辅助诊断.结果 ICC与传统细胞涂片和TCT联合应用的诊断率比细胞蜡块的诊断率高,从91.5％提高到99.1％ (P ＜0.05);ICC联合3种制片方法的诊断率分别为95.75、82.9％、97.2％ (P ＜0.05);132例肺腺癌中TTF-1、NapsinA阳性病例分别为132和92例,灵敏度分别为100％和69.7％,特异度分别为95.5％和97％,差异显著(P＜0.05);小细胞癌3例,CgA、Syn、CD56阳性病例分别为1、3、3例,灵敏度分别为33.3％、100％、100％,特异度分别为100％、97.4％、95.4％,差异不显著(P＞0.05);1例间皮瘤及51例反应性间皮增生病例,Calretinin阳性48例,MC阳性43例,二者灵敏度分别为92.3％、82.7％,特异度分别为98.6％、98％,差异不显著(P＞0.05).结论 细胞蜡块、传统细胞涂片、TCT制片方法与ICC联合应用是提高肺癌胸水细胞学诊断率的有效手段,改进标本预处理措施、优化抗体套餐、一片多用对于标本有限的晚期患者尤其具有重要意义.

Mechanistic insight into estrogen deficiency by polycystic ovary syndrome (PCOS) remains a longstanding challenge in reproductive medicine. Recent advance suggest that Wingless-type MMTV integration site family members (WNTs), in concert with its Frizzled (FZD) receptors, regulate normal folliculogenesis, luteogenesis and ovarian steroidogenesis. However, no studies have so far investigated any causality between WNT-FZDs interactions and disrupted estrogen synthesis under certain pathological conditions. Here, we show that (i) FZD3 expression was significantly up-regulated in the cumulus cells (CCs) from PCOS patients. This up-regulation, along with the activation of WNT2/β-Catenin pathway, was tightly associated with insulin resistance and estrogen deficiency, two hallmarks of PCOS. (ii) Overexpression of exogenous FZD3 in human granulosa cell COV434 impaired long-term FSH incubation-induced CYP19A1 transactivation and the recruitment of β-Catenin onto CYP19A1 promoter, and subsequently compromised FSH-stimulated estrogen production. (iii) Conversely, inhibition of FZD3 expression exhibited a therapeutic effect on estrogen synthesis in PCOS CCs. Thus, excessive FZD3 expression in CCs may act as a brake on steroidogenic activation that is normally overcome by FSH stimulation. Future endeavor in this field should help to elucidate the complicated crosstalk between energy metabolism and endocrine cells through WNT/FZD signaling molecules.