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1.
目的 研究前列腺癌组织中PTEN蛋白的表达和微血管密度(MVD)的相关性及其意义。方法 应用免疫组化SP法检测3 2例前列腺癌及5例良性前列腺增生组织中PTEN蛋白表达及微血管计数,分析其意义和相关性。结果 3 2例前列腺癌中8例PTEN蛋白表达阳性(2 5 % ,8/3 2 ) ,并随病理分级升高阳性表达率下降,高分化组同中分化组间差异无显著性(P >0 .0 5 ) ,但高分化、中分化组同低分化组之间差异有显著性(P <0 .0 5 ) ,且在浸润型肿瘤(C D)期与局限性肿瘤(A B)期的差异有显著性(P <0 .0 1)。前列腺癌组织中MVD(5 2 .86±17.87) ,MVD随病理分级和临床分期的升高而升高,并同PTEN蛋白的表达成负相关(r =-0 .65 3 ,P <0 .0 1)。结论 PTEN蛋白低表达和微血管的形成在前列腺癌的发生、发展中起重要作用。检测PTEN蛋白的表达和MVD有助于判断病情及预后。PTEN蛋白的低表达与肿瘤微血管的形成相关。  相似文献   

2.
目的 通过进行系统回顾和Meta分析,评估牙周病与前列腺癌发病风险的相关性。方法 在PubMed、Web of Science、维普、中国知网、万方数据库中检索2021年3月23日之间公开发表关于牙周病患者前列腺癌患病风险的相关研究,对文献进行数据提取,并采用Review Manager 5.4软件进行Meta分析。结果 通过阅读题目、摘要和全文,排除重复文献,再根据纳入和排除标准,共9项研究纳入meta分析。分析结果显示,牙周病患者发生前列腺癌风险是非牙周病人群的1.17倍,差异有统计学意义(HR=1.17,95%CI 1.02~1.35)。结论牙周病与前列腺癌的发病呈正相关,牙周病是前列腺癌的危险因素。牙周病与前列腺癌的关系受地域影响,亚洲地区比欧美地区影响更明显。  相似文献   

3.
目的:通过开展基于既往相关队列研究和病例对照研究的荟萃分析,研究男性脱发与前列腺癌发病风险的相关性。方法:文献检索自PubMed、Web of Science和中国知网数据库,检索截止时间为2017年5月30日。DerSimonian-Laird随机效应模型被用于计算合并后的RR和95%CI。结果:本项荟萃分析共纳入15项研究。在总体分析中,男性脱发(任何类型)与前列腺癌发病风险之间无相关性(RR=1.03,95%CI:0.96~1.11)。纳入研究之间存在显著的异质性(P=0.078,I^2=36.4%)。对脱发类型进行亚组分析,发现头顶脱发和前列腺癌发病风险显著相关(RR=1.24,95%CI:1.05~1.46),而其他类型的脱发则无相关性。结论:头顶脱发的男性可能具有较高的前列腺癌发病风险,但由于总体分析以及大多数的亚组分析结果阴性,并且研究之间存在一定的异质性,本研究结果还需进一步设计良好的前瞻性队列研究来验证。  相似文献   

4.
5.
目的:探讨中国人群输精管结扎术与前列腺癌发病间的相关性。方法:系统检索3个中文文献数据库(CNKI、万方、维普)及3个英文文献数据库(Pud Med、Embase、Cochrane Library)截至2014年12月之前发表的有关中国人群输精管结扎术与前列腺癌关系的文献。由两位研究者独立按纳入和排除标准筛选文献,进行质量评价和数据提取,并采用STATA 12.0软件进行Meta分析。结果:共纳入合格的研究文献9篇,包括前列腺癌病例1 202例,对照4 496例。采用随机效应模型合并分析后的结果未发现中国人群输精管结扎术与前列腺癌相关(OR=1.05;95%CI,0.62~1.79),且异质性明显(P0.001,I2=85.7%)。尚不能认为目前纳入的研究存在发表偏倚(Egger,P=0.824;Begg,P=0.348)。结论:Meta分析结果提示中国人群输精管结扎术不会增加前列腺癌的发病风险。  相似文献   

6.
目的探讨前列腺癌(PCa)组织中PTEN蛋白的表达与血清PSA水平的相关性。方法采用免疫组织化学SABC法对32例PCa和10例前列腺增生(BPH)组织中PTEN蛋白的表达进行检测,并比较各组间PTEN蛋白表达水平的差异及其与血清PSA水平、PCa病理分级、临床分期及预后的关系。结果PTEN在PCa、BPH组织中的阳性表达率分别为31.3%和100.0%,二者比较有显著性差异(P<0.05),且PCa组织中PTEN蛋白的表达与血清PSA水平、病理分级、临床分期和肿瘤转移呈负相关(P<0.05)。结论随着肿瘤细胞病理分级、临床分期的增高,PTEN蛋白阳性表达率降低,它的异常表达在PCa的发生、发展中起重要作用,检测PTEN蛋白的表达有助于判断病情及预后。  相似文献   

7.
目的:探讨输精管结扎与前列腺癌发病间的相关性。方法:以"输精管结扎术"、"前列腺癌"及其同义词和近义词为关键词,在CBMDisc、CMCC、CMAC、CNKI(1978年~2014年1月1日)和PubMed(1965年~2014年1月1日)等国内外数据库上进行全面检索,按文献纳入及剔除标准筛选出符合要求的文献,采用Meta分析方法进行综合分析。结果:共有17篇病例对照研究文献纳入本次研究,符合研究标准的研究对象33 841例,其中病例12 243例,对照21 598例。合并OR值(95%CI)为1.03(0.87,1.23)。结论:输精管结扎不增加前列腺癌的发病风险。  相似文献   

8.
PTEN蛋白在前列腺癌中的表达及临床意义   总被引:1,自引:0,他引:1  
目的 探讨PTEN蛋白表达与前列腺癌临床病理特征及临床分期的关系。方法 应用免疫组织化学法检测 3 2例前列腺癌及 5例良性前列腺增生组织中PTEN蛋白的表达。结果  3 2例前列腺癌中有 8例 (2 5 .0 % )呈不同程度的阳性表达。随肿瘤细胞病理分级 ,临床分期增高 ,PTEN蛋白表达率降低 ,高分化组与中分化间表达率的差异无显著性 ,但高、中分化组与低分化组间的差异有显著性 (P <0 .0 5 )。在A、B期的表达率明显高于C、D期 (P <0 .0 5 )。结论 抑癌基因PTEN的表达缺乏在前列腺癌的发生、发展中起重要作用 ,检测PTEN蛋白的表达有助于判断病情及预后。  相似文献   

9.
胰腺癌PTEN蛋白表达及其与p53表达相关性的研究   总被引:1,自引:0,他引:1  
目的 分析胰腺癌PTEN蛋白表达以揭示其与胰腺癌生物学行为的关系,通过PTEN与p53蛋白表达相关性的研究,探讨p53突变对PTEN蛋白表达的影响。方法 应用免疫组织化学方法分析41例胰腺癌PTEN和p53蛋白表达。结果 41例胰腺癌中p53阳性表达16例。阴性表达25例;所有标本都有PTEN蛋白表达,其阳性物质定位与癌周正常组织相同,其中22例呈高表达(++),19例呈低表达(+),其表达高低与胰腺癌TNM分期有相关性(P<0.01);并与p53蛋白表达呈现相关(P<0.05);而与肿瘤分化程度无相关性。结论 胰腺癌罕见PTEN的完全失活;胰腺癌PTEN蛋白的亚细胞定位与正常组织相同;但其表达有高低之别,并与胰腺癌TNM分期有相关性,表明PTEN表达下降与胰腺癌侵袭行为及病程进展有关;而p53突变则是导致PTEN表达下降原因之一。  相似文献   

10.
前列腺癌组织中Skp2、PTEN的表达及临床意义   总被引:2,自引:0,他引:2  
目的:探讨Skp2和第10号染色体缺失的磷酸酶和张力蛋白同源物基因(Phosphatase and tensin homologue deleted on chromosome 10.PTEN)在前列腺癌中的表达及临床意义。方法:用免疫组织化学EnVision^TM办法检测Skp2和PTEN蛋白在41例前列腺癌和20例BPH组织中的表达情况。结果:在前列腺癌中的Skp2蛋白染色阳性率显著高于BPH(P〈0.01),Skp2蛋白表达与前列腺癌术前血清前列腺特异抗原(PSA)水平、局部浸润、肿瘤分期、病理分级呈密切正相关(P〈0.05)。在前列腺癌中的PTEN蛋白染色阳性率显著低于BPH(P〈0.01),PTEN蛋白表达与上述临床病理特征呈负相关(P〈0.05)。前列腺癌中Skp2蛋白与PTEN蛋白表达呈负相关(P〈0.01)。结论:Skp2蛋白在前列腺癌的发生发展中起重要作用,抑癌基因PTEN可能参与Skp2表达的调节。  相似文献   

11.
膀胱癌组织中PTEN的表达及其与微血管密度的相关性   总被引:1,自引:0,他引:1  
张建华  杨为民  周四维 《临床外科杂志》2005,13(8):491-493,i0001
目的研究膀胱癌组织中抑癌基因PTEN的表达及其与微血管密度(MVD)之间的关系,评价PTEN在膀胱癌发生发展中的作用。方法应用免疫组织化学SP法检测62例膀胱癌组织和18例良性膀胱病变组织中PTEN的表达和MVD,同时结合肿瘤分期分级进行分析。结果62例膀胱癌组织中PTEN阳性率为53.23%(33/62),18例良性膀胱病变组织PTEN全部阳性表达;PTEN的表达与肿瘤分级密切相关(P〈0.05);肿瘤组织MVD明显高于良性病变组织;PTEN表达与MVD呈负相关(P〈0.05)。结论PTEN基因突变或缺失所导致的表达障碍可能在膀胱癌的恶性进展和血管生成过程中发挥重要的作用。  相似文献   

12.

Purpose

Increasing evidence has demonstrated that men taking the anticoagulant warfarin have a lower risk of developing prostate cancer. This phenomenon is not observed in other cancers. We sought to determine if the target of warfarin, vitamin K epoxide reductase (VKOR), is expressed in benign and cancerous prostate tissues and if a functional single nucleotide polymorphism (SNP) in the VKOR gene is associated with prostate cancer risk.

Materials and methods

The expression of VKOR was quantified by immunohistochemistry in an institutional series of 54 radical prostatectomy samples and metastatic biopsies, as well as in 40 other cancers and matched benign tissues on a tissue microarray. Genotyping of SNP rs2359612 was performed in a prospective series of 57 patients.

Results

VKOR is highly expressed in benign human prostate epithelial cells but is not expressed or expressed at very low levels in cancerous cells. This expression pattern is unique to prostate cancer. Additionally, the proportion of the carrier C allele of rs2359612 in the patients with prostate cancer was significantly higher than in the population, suggesting an association between this allele and the risk of having a diagnosis of prostate cancer.

Conclusions

The expression of VKOR in benign prostate epithelial cells, along with the association between a functional VKOR SNP and prostate cancer risk, suggests a possible role for VKOR in mediating the effect of warfarin on prostate cancer risk. Larger multi-institutional cohort studies are warranted, as are molecular studies on the role of VKOR in prostate cancer development.  相似文献   

13.
14.
FHIT和PTEN在前列腺腺癌中的表达及其意义   总被引:2,自引:0,他引:2  
目的:探讨脆性组氨酸三联体(FHIT)、磷酸酶和张力蛋白同源基因(PTEN)在前列腺腺癌中的表达及其意义。方法:应用免疫组化PV-6000法对85例前列腺腺癌及30例良性前列腺增生(BPH)标本进行FHIT、PTEN检测。结果:FHIT、PTEN在前列腺腺癌组织中阳性表达率分别为34.1%、42.4%;在前列腺结节性增生组织中阳性表达率分别为96.7%、90.0%。前列腺腺癌组织中FHIT、PTEN阳性表达明显低于BPH,差异具有统计学意义(P<0.01)。FHIT、PTEN在前列腺腺癌Gleason分级为高分化组内阳性表达率分别为44.4%、55.6%;中分化组内阳性表达率分别为38.9%、44.4%;低分化组内阳性表达率分别为25.0%、37.5%。FHIT、PTEN阳性表达率在前列腺腺癌高分化、中分化、低分化组别之间有差异,差异亦有统计学意义(P<0.05)。前列腺腺癌组织中FHIT的表达与PTEN的表达无明显相关性(P>0.05)。结论:FHIT和PTEN在前列腺腺癌发生、发展、浸润的过程可能发挥了一定作用。  相似文献   

15.
目的:研究卵巢癌组织中PTEN蛋白表达与临床病理因素的关系。方法运用免疫组织化学的方法检测67例卵巢癌组织,25例良性卵巢肿瘤和10例正常卵巢组织中PTEN蛋白的表达。结果在67例卵巢癌组织中有35例为阳性表达,卵巢良性肿瘤有22例阳性表达,正常卵巢组织中均为阳性表达,其间存在显著相关性(P<0.05),PTEN蛋白表达与卵巢癌的的病理分级、临床分期和淋巴结转移存在显著相关性(P<0.05),而与卵巢癌的组织类型无显著相关性(P>0.05)。结论 PTEN蛋白的阳性表达及表达缺失对于评价卵巢癌的恶性程度、转移及预后有显著的临床价值。  相似文献   

16.

Background

Ki-67 for quantifying tumor proliferation is widely used. In localized prostate cancer (PCa), despite a suggested predictive role of Ki-67 for outcomes after therapies, it has not been incorporated into clinical practice. Herein, we conduct a systematic review and meta-analysis of the literature reporting the association of Ki-67 and disease outcomes in PCa treated radically.

Methods

Medline and EMBASE databases were searched without date or language restrictions, using “KI67” and “prostate cancer” MeSH terms. Studies reporting Ki-67 association with clinical outcomes (disease-free survival [DFS], biochemical failure-free survival, rate of distant metastases [DM], disease-specific survival [DSS], or overall survival [OS], or all of these) in patients with PCa managed actively were included, and relevant data extracted by 2 independent reviewers. Odds ratios (OR) were weighted and pooled in a meta-analysis using Mantel-Haenszel random-effect modeling.

Results

Twenty-one studies comprising 5,419 patients met eligibility for analysis, and 67.6% of patients had low Ki-67. Mean Ki-67 was 6.14%. High Ki-67 was strongly associated with worse clinical outcomes. DFS was better in those patients with low Ki-67 at 5 and 10 years (OR = 0.32, 95% CI: 0.23–0.44, P<0.00001; OR = 0.31, 95% CI: 0.20–0.48, P<0.00001). Similarly, low Ki-67 was related to improved DSS at 5 and 10 years (OR = 0.15, 95% CI: 0.10–0.21, P<0.00001; OR = 0.16, 95% CI: 0.06–0.40, P<0.00001). Association between low Ki-67 scores with improved OS (OR = 0.47; 95% CI: 0.37–0.61; P<0.00001) and high Ki-67 scores with DM at 5 years (OR = 4.07; 95% CI: 2.52–6.58; P<0.00001) was consistently observed.

Conclusions

High Ki-67 expression in localized PCa is a factor of poor prognosis for DSS, biochemical failure-free survival, DFS, DM, and OS after curative-intent treatments. Incorporation into clinical routine of this widely available and standardized biomarker should be strongly considered.  相似文献   

17.
OBJECTIVE: Bone metastasis is a major cause of morbidity in prostatic cancer. Therefore, detecting and monitoring bone lesions are crucial for treatment of prostatic carcinoma. We aimed to evaluate total body bone mineral density and regional bone mineral density in patients with prostate cancer with and without metastases, and to compare them with bone scintigraphy. METHODS: Fifty-four patients with prostatic carcinoma and 20 healthy subjects were investigated with bone scintigraphy and dual-energy X-ray absorptiometry. The bone scintigraphic findings were classified as normal (score 0: n = 22), abnormal but not typical for metastases (score 1: n = 18), and typical pattern of metastases (score 2: n = 14). RESULTS: The patients with bone metastases prostate cancer had significantly higher total bone mineral density and regional bone mineral density of trunk and pelvis than healthy controls and prostate cancer patients without bone metastases. There was a significant positive correlation between bone scan score and total bone mineral density and regional bone mineral density of trunk and pelvis (r = 0.328, P < 0.05, r = 0.60, P < 0.001, r = 0.480, P < 0.001, respectively). CONCLUSION: Our results show that patients of prostate cancer with bone metastases have increased bone mineral density (BMD) in the pelvis and trunk, possibly because of a predominance of osteoblastic over osteolytic metastases demonstrated by Tc-99m MDP bone scan.  相似文献   

18.

Purpose/objective(s)

Brachytherapy (BT) monotherapy is a well-established treatment modality for favorable intermediate risk (FIR) prostate cancer. However, patients with unfavorable intermediate risk (UIR) disease are often recommended trimodality therapy involving BT, androgen deprivation therapy (ADT), and external beam radiation therapy (EBRT). We sought to investigate the relative benefit of supplemental therapies (ADT and/or EBRT) for FIR and UIR prostate cancer in a large dataset.

Materials/methods

We identified 3,723 patients with intermediate risk prostate cancer treated with BT between 1997 and 2013, including 1,989 and 1,734 patients with FIR and UIR disease, respectively. For the FIR cohort, Fine and Gray’s competing risks regression model was used to evaluate whether there was a difference in prostate cancer specific mortality (PCSM) between BT vs. BT + supplemental therapy (ADT, EBRT, or both). For the UIR cohort, this regression model was used to evaluate whether supplemental ADT, EBRT, or both decreased PCSM beyond BT alone. Both regression models were adjusted for clinical and treatment-related factors.

Results

The median follow-up periods were 7.7 years (interquartile range: 5.4–10.5) for the FIR cohort and 7.8 years (interquartile range: 5.3–10.6) for the UIR cohort. For the FIR cohort, there was no difference in PCSM between BT monotherapy vs. BT + supplemental therapy (adjusted hazard ratio [AHR] = 1.70; 95% CI: 0.46–6.29; P = 0.43). For the UIR cohort, supplemental EBRT (AHR = 2.66; 95% CI: 1.12–6.34; P = 0.03), ADT (AHR = 0.96; 95% CI: 0.38–2.43; P = 0.93), or both (AHR = 1.46; 95% CI: 0.42–5.01; P = 0.55) were not associated with improved PCSM compared with BT alone.

Conclusion

In our analysis, supplemental therapies did not offer an improvement in PCSM compared with BT alone for FIR or UIR prostate cancers. Further prospective clinical trials are required to determine whether BT monotherapy may be sufficient for a subset of patients with UIR disease.  相似文献   

19.
The management of low risk prostate cancer, defined as Gleason’s sum ≤6, PSA <10 ng/ml, and clinical stage T1c to T2a, remains controversial. There is substantiating evidence to suggest that a subset of early stage, low risk cancers can cause significant patient morbidity and death in the long term. Studies have shown that the natural history of untreated prostate cancer is to progress, particularly after 15 years of followup. The majority of men seeking definitive surgical treatment in contemporary series fall within 55 to 65 years of age and are expected to enjoy an overall life expectancy ranging from about 15 to 30 years, placing these men at long-term risk for disease progression and prostate cancer-specific death if managed expectantly. During the past 2 decades, refinements in surgical technique and in the delivery of external beam radiation have resulted in excellent long-term cancer control and favorable quality of life outcomes following treatment. Active surveillance with selective delayed intervention assumes that an individual’s cancer will not progress outside the window of curability during the surveillance period, that markers for disease progression are reliable, and that patients are compliant. Until we understand better the long-term natural history of untreated prostate cancer, have more reliable and accurate markers to detect disease progression with certainty, and can risk stratify more precisely the subgroup of men with low risk cancers who will eventually succumb to their disease, early definitive therapy seems prudent.  相似文献   

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