FAT10 level in human gastric cancer and its relation with mutant p53 level,lymph node metastasis and TNM staging

AIM:To investigate the role of FAT10 and mutant p53 in the pathogenesis,severity and prognosis of gastric cancer.METHODS:FAT10,mutant p53 mRNA and protein levels were measured by reverse transcription(RT)-PCR and immunohistochemistry in gastric cancer tissue(n = 62),tumoradjacent tissue(n = 62) and normal gastric tissue(n = 62).Relation of FAT10 and mutant p53 expression with clinicopathological features and clinical outcomes of gastric cancer patients were analyzed.RESULTS:The FAT10,mutant p53 mRNA and protein levels were signif icantly higher in gastric cancer than in its adjacent and normal tissue.The FAT10 and mutant p53 levels in gastric cancer tissue were significantly correlated with lymph node metastasis and tumor,nodes,metastasis(TNM) staging.Moreover,the high FAT10 level was associated with the overall survival rate of patients.Multivariate Cox-proportional hazards model analysis showed that mRNA and protein levels of FAT10 and mutant p53,lymph node metastasis,distant metastasis and TNM stage were the independent prognostic factors for gastric cancer.CONCLUSION:FAT10 may be involved in gastric carcinogenesis,and is a potential marker for the prognosis of gastric cancer patients.FAT10 and mutant p53 may play a common role in the carcinogenesis of gastric cancer.

靶向突变p53蛋白的抗肿瘤药物

p53蛋白是人体内十分重要的肿瘤抑制因子,通过调节细胞周期阻滞、诱导细胞凋亡等作用发挥肿瘤抑制功能。突变后的p53蛋白不仅具有显性负性效应(dominant negative effect,DN)抑制野生型p53蛋白功能,而且还通过功能获得性效应(gain of function,GOF)调节细胞代谢、侵袭、迁移等方式促进肿瘤的发生。p53蛋白在超过50%的肿瘤组织中发生突变,是肿瘤细胞区别于正常细胞的一个特异性药物靶点。因此,针对突变p53蛋白开发新型抗癌药物一直是研究的热点。长期以来,由于突变p53蛋白表面较为光滑,缺乏药物结合口袋,使其被认为是一个不可成药的靶点。随着高通量筛选技术的发展以及对突变p53蛋白结构的深入了解,许多靶向突变p53蛋白的小分子化合物被报道并在体外展现出较好的抗肿瘤活性,多款基于突变p53蛋白研发的化合物已经进入临床试验阶段。本文就靶向p53蛋白治疗肿瘤的直接和间接策略进行综述,重点针对突变p53蛋白重激活剂与降解突变p53蛋白的小分子化合物作用机制进行梳理,以期为后续开发靶向突变p53蛋白药物的创新提供帮助。

Expression of hMSH2 gene and mutant p53 in sporadic digestive tract tumors

Objective To investigate the role of mutated mismatch repair gene hMSH2 and mutant p53 gene in the carcinogenesis and development of sporadic digestive tract tumors. Methods hMSH2 gene in normal and tumor tissue of 30 digestive tract tumor specimens was examined using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) silver staining. The PCR product with an abnormal strand was sequenced directly. Mutant p53 protein in the tumor tissue was analyzed immunohistochemically. Results Six patients were identified as having mutated strands, three on hMSH2 exon 1 and three on hMSH2 exon 5. DNA sequencing revealed that all 6 patients had mutated basic groups that led to decrease in function of the hMSH2 protein. Forty percent (12/30) of patients were p53 positive. The frequency of mutated hMSH2 in p53 positive patients (41.7%) was significantly higher than in p53 negative patients (5.6%, P<0.05). Conclusion The mutation of hMSH2 plays an important role in the carcinogenesis and development of digestive tract tumors through stimulating p53 mutation.

BCL7C suppresses ovarian cancer growth by inactivating mutant p53

B-cell CLL/lymphoma 7 protein family member C (BCL7C) located at chromosome 16p11.2 shares partial sequence homology with the other two family members, BCL7A and BCL7B. Its role in cancer remains completely unknown. Here, we report our finding of its tumor-suppressive role in ovarian cancer. Supporting this is that BCL7C is downregulated in human ovarian carcinomas, and its underexpression is associated with unfavorable prognosis of ovarian cancer as well as some other types of human cancers. Also, ectopic BCL7C restrains cell proliferation and invasion of ovarian cancer cells. Consistently, depletion of BCL7C reduces apoptosis and promotes cell proliferation and invasion of these cancer cells. Mechanistically, BCL7C suppresses mutant p53-mediated gene transcription by binding to mutant p53, while knockdown of BCL7C enhances the expression of mutant p53 target genes in ovarian cancer cells. Primary ovarian carcinomas that sustain low levels of BCL7C often show the elevated expression of mutant p53 target genes. In line with these results, BCL7C abrogates mutant p53-induced cell proliferation and invasion, but had no impact on proliferation and invasion of cancer cells with depleted p53 or harboring wild-type p53. Altogether, our results demonstrate that BCL7C can act as a tumor suppressor to prevent ovarian tumorigenesis and progression by counteracting mutant p53 activity.

Ubiquitin ligase DTX3 empowers mutant p53 to promote ovarian cancer development

The deltex family protein DTX3 is believed to possess E3 ubiquitin ligase activity,as it contains a classic RING finger domain.However,its biological role and the underlying mechanism in cancer remain largely elusive.Here,we identified DTX3 as a novel mutant p53-interacting protein in ovarian carcinoma.Mechanistically,DTX3 mediated mutant p53 ubiqui-tination and stabilization by perturbing the MDM2-mutant p53 interaction,consequently leading to activation of diverse.mutant p53 target genes.Importantly,a positive correlation between the expression of DTX3 and mutant p53 target genes was further validated in ovarian carcinomas.Ectopic DTX3 promoted,while depletion of DTX3 suppressed,ovarian cancer cell proliferation and invasion.Remarkably,the pro-tumorigenic effect of DTX3 is dependent on mutant p53,because ablation of mutant p53 significantly impaired DTX3-induced gene expression and ovarian cancer cell growth and propagation.Furthermore,DTX3 elevated the expressi on of muta nt p53 target genes and boosted ovarian tumor growth in vivo.Fin ally,DTX3 was amplified and overexpressed in ovarian carci no mas,which is sign ificantly associated with unfavorable prognosis.Altogether,our findings unveil the oncogenic role of DTX3 in ovarian cancer development by bolstering mutant p53 activity.

Ki-67、突变型p53表达和CT与直肠腺癌亚型、病理分化程度的相关性及临床价值分析

目的探究核基因Ki-67、突变型p53表达和CT与直肠腺癌亚型、病理分化程度的相关性及临床价值。方法选取2021年1月~2022年12月启东市人民医院收治的直肠腺癌患者90例,采用免疫组织化学法对患者的Ki-67及突变型p53表达情况进行测定,并对患者进行CT影像检查。探究患者Ki-67及突变型p53表达情况及CT检查结果与直肠腺癌亚型、病理分化程度的相关性,并采用受试者工作特征曲线(ROC)探究各指标对患者直肠腺癌高度分化的诊断价值。结果根据患者直肠腺癌亚型将90例患者分为A组(n=73,管状腺癌)和B组(n=17,黏液腺癌);根据患者的分化程度将患者分为C组(n=74,低分化)及D组(n=16,中分化及高分化)。Ki-67在A、B组中的阳性率分别为76.71%、47.06%,C、D组中的阳性率分别为47.30%、87.50%,差异有统计学意义(χ^(2)=4.547、8.573,P<0.05);突变型p53在A、B组中的阳性率分别为53.42%、23.53%,在C、D组中的阳性率分别为36.49%、81.25%,差异有统计学意义(χ^(2)=4.939、10.676,P<0.05)。C、D组间肿瘤位置、肿瘤肠壁长度、厚度、强化程度、增强后低密度区比较差异无统计学意义(P>0.05);但与C组相比较,D组肠壁偏向性、环形增厚占比、重度肠周浸润占比较大,差异有统计学意义(P<0.05)。Ki-67、突变型p53的阳性表达情况及肠壁偏向性环形增厚和重度肠周浸润对直肠腺癌管状腺癌高分化的ROC曲线下面积分别为0.701、0.724、0.636、0.639,但肠壁偏向性环形增厚和重度肠周浸润诊断差异无统计学意义(P>0.05)。结论Ki-67及突变型p53的阳性表达情况对直肠腺癌亚型和病理分化程度具有一定诊断意义,CT影像特征可以在一定程度上反映直肠腺癌患者病理分化程度,但诊断价值较低。

子宫内膜癌组织中HAX1和突变型p53表达的相关性及其临床意义

目的:探讨造血干细胞特异性相关结合蛋白1(HAX1)和突变型p53在子宫内膜癌组织中的表达模式、相关性及与预后的关系。方法:采用UALCAN数据库及qRT-PCR分析新鲜子宫内膜癌组织中HAX1 mRNA的表达水平;利用Western blotting检测新鲜子宫内膜癌组织中HAX1的蛋白表达水平;应用免疫组化检测120例子宫内膜癌患者癌组织及相应的癌旁组织石蜡标本中HAX1和p53蛋白的表达水平,分析两者的相关性及与患者临床病理特征和预后的关系;利用GEPIA数据库对HAX1与子宫内膜癌相关基因的关系进行分析。结果:HAX1 mRNA和蛋白在子宫内膜癌组织中均高表达;HAX1阳性表达和突变型p53的表达中度正相关(χ^(2)=36.468,r=0.551,P<0.05),且均与淋巴结转移、FIGO分期、血CEA水平以及Ki-67的表达密切正相关(P<0.05),但与患者总生存率呈负相关;HAX1阳性表达(P=0.008)、突变型p53表达(P=0.022)、淋巴结有转移(P=0.003)、FIGO高分期(P<0.001)及术后辅助治疗方法(P<0.001)是患者预后的独立危险因子;基因相关性分析结果显示HAX1与TP53、MKI67、BAX、CCNE1、POLE1、MSH2、MSN6及PMS2的表达相关。结论:HAX1在子宫内膜癌组织中高表达,与突变型p53表达正相关,两者表达模式可综合评估该肿瘤的恶性程度、进展情况及患者的预后情况,为子宫内膜癌的术后治疗提供新思路。

Mutant p53 promotes cell spreading and migration via ARHGAP44

The tumor suppressor p53 protein is either lost or mutated in about half of all human cancers.Loss of p53 function is well known to influence cell spreading,migration and invasion.While expression of mutant p53 is not equivalent to p53 loss,mutant p53 can acquire new functions to drive cell spreading and migration via different mechanisms.In our study,we found that mutant p53 significantly increased cell spreading and migration when comparing with p53-null cells.RNA-Seq analysis suggested that Rho GTPase activating protein 44(ARHGAP44) is a new target of mutant p53,which suppressed AKHGAP44 transcription.ARHGAP44 has GAP activity and catalyze GTP hydrolysis on Cdc42.Higher level of GTP-Cdc42 was correlated with increase expression of mutant p53 and reduced ARHGAP44.Importantly,wt-ARHGAP44 but not mutant ARHGAP44(R291A) suppressed mutant p53 mediated cell spreading and migration.Bioinformatics analysis indicated lower expression of ARHGAP44 in lung carcinoma compared with normal tissues,which was verified by RT-qPCR using specimens from patients.More interestingly,ARHGAP44 mRNA level was lower in tumors with mutant p53 than those with normal p53.Collectively,our results disclose a new mechanism by which mutant p53 stimulates cell spreading and migration.

Expression of mutant type-p53 products in H pylori-associated chronic gastritis

AIM:To investigate the mutation of p 53 immuno-histochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.METHODS:53 subjects(36 male,17 female,mean age ± SEM,57.1 ± 12.1)undergoing endoscopic examination were included in this study.42 of 53 patients were H pylori-positive,and 11 were H pylori-negative.All H pylori-positive patients had successful eradication therapy.Biopsy specimens were taken from five points of the stomach,as recommended by the updated Sydney system.Immunohistochemical studies were performed by using primary antibodies against p53(DO-7 and PAb240).RESULTS:p53(DO-7 and PAb240)immunoreactivity was shown in the neck region of the gastric pits,however,quite a few cells were found to be immunopositive for p 53(PAb240)in the H pylori-infected gastric mucosa.The proportion of patients immunopositive for p 53(PAb240)was significantly reduced 6 mo after eradication [28/42(66.7%)to 6/42(14.3%)](P < 0.05),while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53(PAb240).p53(PAb240)-positive patients were divided into two groups by the number of positive cells detected:one with more than six positive cells per 10 gastric pits(group A,n = 12),and the other with less than five positive cells per 10 gastric pits(group B,n = 30).Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum(group A:2.00 ± 0.14 vs group B:1.40 ± 0.15,P = 0.012),the lesser curvature of the corpus(group A:2.00 ± 0.21 vs group B:1.07 ± 0.23,P = 0.017),and the greater curvature of the corpus(group A:1.20 ± 0.30vs group B:0.47 ± 0.21,P = 0.031).Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum(group A:2.10 ± 0.41 vs group B:1.12 ± 0.29,P = 0.035).CONCLUSION:H pylori-associated chronic gastritis expressed the mutant-type p53,which was significantly associated with more severe atrophic and metaplastic changes.H pylori eradication led to a significant reduction in the expression of the mutant-type p53.It is considered that H pylori-infected chronic gastritis is associated with a genetic instability that leads to gastric carcinogenesis,and H pylori eradication may prevent gastric cancer.

乳腺癌组织COX-2蛋白c-erbB-2 P53 VEGF-C蛋白表达及其与临床病理参数和预后的关系

目的:分析乳腺癌组织环氧化酶-2(COX-2)蛋白、人表皮生长因子受体2(c-erbB-2)、突变型P53蛋白、血管内皮生长因子C(VEGF-C)蛋白表达及其与临床病理参数和预后的关系。方法:选取2017年3月至2019年5月到我院就诊103例乳腺癌患者的手术切除标本。免疫组化法测定患者入组时的COX-2、c-erbB-2、P53、VEGF-C蛋白阳性率;比较上述各指标水平与患者TNM分期、分化程度等病理参数的关系;随访患者术后3年生存资料,Kaplan-Meier分析COX-2、c-erbB-2、P53、VEGF-C蛋白水平对预后生存的影响。结果:患者TNM分期、分化程度与COX-2阳性相关(P<0.05);肿瘤直径≥3cm、淋巴结转移与c-erbB-2阳性相关(P<0.05);TNM分期、分化程度、淋巴结转移与P53阳性相关(P<0.05);淋巴结转移与VEGF-C阳性相关(P<0.05)。103例患者随访3年,随访率为100%,截止至2022年5月死亡20例(19.42%),存活83例(80.58%);根据死亡情况将阳性患者分为存活亚组及死亡亚组,死亡亚组患者入组时的组化评分均明显高于存活亚组(P<0.05)。Log-rank χ^(2)检验显示随访3年P53、VEGF-C阳性及阴性的累积存活率比较差异有统计学意义(χ^(2)=14.000、5.206,P均<0.05);COX-2、c-erbB-2阳性及阴性患者的累积存活率比较差异无统计学意义(χ^(2)=1.761、2.830,P=0.184、0.093)。结论:乳腺癌组织中COX-2、c-erbB-2、P53、VEGF-C蛋白阳性率与TNM分期、淋巴结转移、分化程度等病理参数相关,在患者预后评估中具有一定指导意义。

VEGF和突变型p53在胃癌组织表达及意义

目的:通过检测胃癌及癌前病变患者活检组织中血管内皮生长因子(VEGF)和突变型p53基因(mtp53)的表达,探讨VEGF和突变型p53基因在胃癌发生发展中的临床意义。方法:通过胃镜组织活检收集19例正常胃组织、22例肠上皮化生、47例胃肠黏膜不典型增生、54例胃癌样本,通过免疫组织化学染色检测组织中VEGF和mtp53的表达水平。结果:VEGF、mtp53的表达水平在正常胃组织,肠上皮化生,不典型增生以及胃癌中呈逐渐增高的规律。胃癌组织中VEGF和mtp53表达较正常胃组织、肠上皮化生组织显著增高(P<0.05),而与不典型增生组织差异无统计学意义(P>0.05)。结论:VEGF与突变型p53的异常表达可能与胃组织病变的恶化程度有关。

肺癌中血管内皮生长因子及突变型p53基因表达及其临床意义研究

目的 探讨血管内皮生长因子 (VEGF)、突变型p5 3(mtp5 3)基因表达水平与肺癌病理生理学特征之间的关系。方法 采用免疫组化方法 (LSAB法 ) ,检测 12 0例肺癌组织及相应癌旁组织 ,40例肺良性病变组织中的VEGF、mtp5 3表达水平。结果 肺癌组织中VEGF、mtp5 3基因的表达水平显著高于癌旁肺组织和肺良性病变组织 (P <0 .0 1)。VEGF、mtp5 3基因表达水平与肺癌患者性别、年龄、吸烟史、组织学类型均无明显关系 (P >0 .0 5 ) ,与原发肿瘤大小、细胞分化程度、淋巴结转移状态、P_TNM分期均有密切关系 (P <0 .0 1)。mtp5 3基因表达水平与VEGF表达水平呈显著正相关 (P <0 .0 1)。结论 VEGF、mtp5 3基因可能参与了肺癌的发生、发展进程 ,可以作为肺癌生物学行为恶化的一项指标。

芹菜素诱导乳腺癌MDA-MB-231细胞系非P53依赖性凋亡的研究

目的:探讨芹菜素(Apigenin)对乳腺癌MDA-MB-231细胞系凋亡的影响。方法:常规培养MDA-MB-231细胞,应用四甲基偶氮唑盐(MTT)法评价芹菜素对乳腺癌MDA-MB-231细胞增殖的影响。荧光染色法观察细胞形态学变化。流式细胞术(FCM)Annexin V/PI双染法检测细胞凋亡率。Western blot检测不同浓度芹菜素对Caspase-3,PARP,突变型P53,P73,PIG3,Bax,Bcl-2等凋亡相关蛋白表达的影响。RNA干扰技术检测P73对凋亡及下游靶基因PIG3表达的影响。结果:MTT结果显示,芹菜素10、20及40μM分别处理细胞24 h,发现芹菜素可有效抑制MDA-MB-231细胞增殖,且具有浓度依赖性和时间依赖性,实验组与对照组比较差异具有统计学意义(P<0.05),两组组间比较差异具有统计学意义(P<0.05);荧光染色结果显示,对照组未观察到凋亡细胞,芹菜素10μM、20μM及40μM组细胞中均可见凋亡小体,其数目随芹菜素浓度的增加而逐渐增加,具有浓度依赖性;流式细胞术结果显示,与对照组比较,芹菜素10μM,20μM及40μM组早期凋亡率逐渐增加,呈明显的量效关系,实验组与对照组比较差异具有统计学意义(P<0.05);Western blot结果显示,与对照组相比,芹菜素10μM、20μM及40μM组Caspase-3、PARP剪切带含量明显增加,P73、PIG3及Bax表达增加,而突变型P53与Bcl-2表达减少,且具有浓度依赖性。RNA干扰结果显示,与阴性对照组相比,p73-siRNA可有效抑制芹菜素诱导的PIG3表达,Caspase-3和PARP剪切含量也相应降低,实验组与对照组比较差异具有统计学意义(P<0.05)。结论:芹菜素可通过非P53依赖性凋亡有效抑制乳腺癌MDA-MB-231细胞增殖,其机制可能与下调突变型p53表达,上调P73介导的PIG3表达,以及Bax/Bcl-2比值增加有关。

突变P53功能研究新进展与个性化的肿瘤治疗新策略

p53是迄今为止研究最多的一种抑癌蛋白,最新研究仍在不断地揭示p53在调控机体代谢、生殖方面的新功能。同时,也揭示了不同p53突变蛋白的获得性新功能在肿瘤发生中的促进作用。这些研究对于了解p53突变的个性化新功能,寻找再激活野生型p53,校正突变p53的新途径奠定了基础,不同突变p53蛋白的个性化治疗将是未来肿瘤治疗的热点。文章综述了已发现的一些突变p53的获得性新功能,及针对不同的p53功能缺陷进行的p53蛋白功能再激活的策略:通过小分子或多肽再激活肿瘤细胞中的p53突变蛋白的野生型功能;通过重组的腺病毒在肿瘤细胞中表达野生型p53蛋白;通过抑制MDM2与p53的相互作用稳定野生型p53蛋白。对p53不同位点突变的深入研究可以帮助我们制定更合理的个性化治疗方案,寻求更有效的肿瘤治疗新途径。

原发性膀胱移行细胞癌Pgp与突变p53蛋白、EGFR的相互关系

目的 :探讨mdr1基因表达产物Pgp与突变 p5 3蛋白、EGFR是否存在相关性及其临床意义。方法 :采用免疫组化SP法 ,检测 10 7例原发性膀胱移行细胞癌中Pgp、突变 p5 3蛋白、EGFR表达情况。结果 :Pgp、突变p5 3蛋白、EGFR的阳性表达率分别为 6 3 .6 % ,72 .9%和 6 6 .4% ,三者的过表达均与膀胱癌的病理分级、分期和术后的复发有关 ;相关性研究显示Pgp表达与突变 p5 3蛋白和EGFR的表达密切相关 (P <0 .0 1)。结论 :Pgp、突变 p5 3蛋白和EGFR过表达不仅是判定原发性膀胱移行细胞癌恶性程度和预后的重要指标 ,而且提示原发性膀胱移行细胞癌中Pgp的表达可能与其他肿瘤一样 ,受到 p5 3和EGFR等的调控。

突变体p53研究进展

抑癌基因突变是癌症发生过程中一个极为关键的事件。p53作为体内最重要的抑癌基因之一,在人类癌症中发生突变的频率高达50%。同时,p53突变也是人类遗传病Li-Fraumeni综合征的主要病因。p53最常见的突变形式是错义突变,所形成的突变体p53不但失去了野生型p53的抑癌功能,而且还获得了一系列类似于癌基因的功能,促进了肿瘤的进程。文章拟对突变体p53的结构功能改变,获得癌基因活性的分子机制,以及近年来对封闭突变体p53活性所进行的探索等研究方向所取得的进展做一综述。

胶质瘤LDHA和突变型p53蛋白联合表达的临床病理学意义

目的探讨LDHA/p53联合表达在胶质瘤临床病理学中的意义。方法按照2016年WHO中枢神经系统肿瘤新分类,分析68例胶质瘤LDHA和突变型p53蛋白的表达特点及其与临床病理特征的关系。结果 68例胶质瘤中,LDHA单独高表达多为高级别胶质瘤,占48.5%;突变型p53高表达则多为胶质母细胞瘤,占26.5%。LDHA/p53联合表达在胶质母细胞瘤中显著增高,占22.1%(P=0.005)。高级别胶质瘤中LDHA/p53联合表达增多,占27.9%(P=0.002)。结论 LDHA/p53联合表达有助于高级别胶质瘤的诊断,对胶质母细胞瘤的诊断也具有提示作用。

凋亡诱导因子和突变型p53在胃癌前病变组织及胃癌组织中的表达及其相关性研究

目的探讨凋亡诱导因子(AIF)与突变型p53(mp53)在胃癌前病变组织及胃癌组织中的表达及其相关性。方法胃癌根治术切除标本及胃镜活检标本125例,其中20例正常胃黏膜标本,42例低级别上皮内瘤变胃黏膜标本,23例高级别上皮内瘤变胃黏膜标本,40例胃癌组织标本,采用免疫组织化学染色技术检测各组的AIF及mp53的表达情况。结果 AIF在正常胃黏膜、低级别上皮内瘤变胃黏膜、高级别上皮内瘤变胃黏膜及绝大多数胃癌细胞胞质中表达,在少数胃癌细胞胞核中表达;mp53均在细胞核内表达。AIF与mp53的表达无相关性(P>0.05)。AIF和mp53在低级别上皮内瘤变胃黏膜、高级别上皮内瘤变胃黏膜及胃癌组织中的表达显著高于正常胃黏膜(P<0.01)。结论 AIF和mp53异常表达可能在胃癌发生发展过程中发挥作用。AIF蛋白表达量升高和p53基因发生突变在胃癌发生过程中均是早期事件。AIF在胃癌发生过程中可能执行氧化还原酶和细胞凋亡的双重功能,对其分子作用机制的深入探讨可能为胃癌的早期诊治提供新的思路。

膀胱移行细胞癌mp53、VEGF表达的相关性及临床意义

目的探讨膀胱移行细胞癌(BTCC)mp53、VEGF表达的相关性及临床意义。方法应用免疫组化二步法,检测50例BTCC组织(BTCC组)和10例正常膀胱黏膜(正常对照组)中mp53、VEGF的表达,结合临床病理资料进行统计分析。结果(1)50例BTCC中的mp53阳性表达率为66%,VEGF阳性表达率为72%;10例正常膀胱黏膜mp53和VEGF的表达均为阴性,BTCC组与正常组比较,差异具有高度统计学意义(P<0.01)。(2)浸润型肿瘤组较表浅型肿瘤组mp53和VEGF阳性表达率高(P<0.05),G2和G3级肿瘤组较G1级肿瘤组mp53和VEGF阳性表达率高(P<0.01)。(3)mp53和VEGF表达呈正相关,具有高度统计学意义(P<0.01)。结论mp53和VEGF表达呈正相关,两者均与BTCC浸润性、低分化、高复发率相关,可作为判断膀胱癌预后的标志物。

长链非编码RNA H19,EZH2,Ki-67及突变型P53联合检测在子宫颈癌诊断中的意义

目的:研究长链非编码RNA(long non-coding RNA,lncRNA) H19,EZH2,Ki-67,突变型P53联合检测在子宫颈癌诊断中的意义。方法:取子宫颈活检或手术组织标本进行病检,其中50例子宫颈癌为研究组,50例非瘤子宫颈为对照组。采用qRT-PCR检测lncRNA H19在各组组织中的表达量。利用免疫组织化学SP法检测以上2组宫颈组织石蜡标本中EZH2,Ki-67,突变型P53的表达。应用SPSS 13.0软件包统计分析各组H19,EZH2,Ki-67及突变型P53的表达与子宫颈癌临床和病理诊断结果的相关性。结果:研究组H19的表达量低于对照组(P<0.05);研究组EZH2,Ki-67,突变型P53阳性表达量高于对照组,差异具有统计学意义(P<0.05)。结论:临床工作中联合检测H19,EZH2,Ki-67,突变型P53更有利于子宫颈癌的诊断。