前列腺癌术后 Gleason 分级与 PSA、P504s、Ki -67蛋白表达相关性分析

目的：探讨前列腺癌 Gleason 分级评分与 PSA、P504s、Ki -67蛋白免疫组化表达的关系。方法：采用免疫组化 SP 法检测45例前列腺癌患者术后石蜡包埋组织中 PSA、P504s、Ki -67的表达，并根据 HE 切片进行 Gleason 分级评分。结果：前列腺癌 Gleason 分值越高，PSA 阳性表达越弱（P ﹤0.05），Ki -67阳性表达越强（P ﹤0.05）；P504s 强表达，与 Gleason 评分无相关性（P ﹥0.05）。结论：PSA 表达越弱、Ki -67表达越强，前列腺癌组织分化程度越差，预后越差。P504s 在前列腺癌中强表达，可应用于诊断，与预后无明显相关性。     

前列腺癌组织FHIT和PSA表达的初步研究

目的:探讨脆性组氨酸三联体(fragile histidine triad, FHIT)与前列腺特异性抗原(prostate specific antigen, PSA)在前列腺癌组织中的表达及意义.方法:选取不同分级的前列腺癌组织(64例)和前列腺增生组织(32例),采用免疫组织化学SP法染色,检测FHIT及PSA的表达情况.结果:64例前列腺癌组织中病理分级(按Gleason分级系统)分化良好癌、中等分化癌和分化不良癌组织中FHIT的蛋白表达率分别为84.2%(16/19)、45.4%(10/22)和17.4%(4/23).随着Gleason评分增加,FHIT蛋白表达率显著下降,P<0.05.病理分级中分化良好癌、中等分化癌和分化不良癌PSA的蛋白表达率分别为100%(19/19)、68.2%(15/22)和34.8%(8/23),随着Gleason评分增加,PSA蛋白表达率显著下降,P<0.05.结论:FHIT的表达与前列腺癌的Gleason评分负相关;PSA的表达与Gleason评分负相关;FHIT和PSA的表达呈正相关.     

联合PTEN、Gleason评分与PSA在预测前列腺癌进展中的价值

目的研究第10号染色体缺失的磷酸酶和张力蛋白同源物基因(PTEN)、Gleason评分、前列腺特异性抗原(PSA)在预测前列腺癌进展中的价值。方法应用S-P法测定29例前列腺癌(Pca)与20例前列腺增生(BPH)组织切片中PTEN蛋白的表达,回顾性研究上述Pca、BPH患者Gleason评分及PSA资料。结果BPH与Pca两组中PTEN总体表达有差异性(P<0.05),两组PSA值总体差异性显著(P<0.05)。PTEN与临床资料关系中,术前PSA<4ng/ml与>10ng/ml两组间PTEN表达有差异(P<0.05),余无差异性。Gleason评分2～4分与5～7分两组PTEN表达无差异(P>0.05),两组与8～10分组PTEN表达比较差异均有显著性(P<0.01);高分化与低分化组PTEN表达有显著差异(P<0.01);临床A、B期与C、D期PTEN表达差异性显著(P<0.01)。结论联合PTEN、Gleason评分及PSA对诊断并预测Pca进展有一定的临床意义。     

PTEN蛋白缺失与中国前列腺癌患者根治术后生化复发风险关系的研究

背景与目的：张力蛋白同源第10号染色体缺失的磷酸酶基因(phosphatase and tensin homolog deleted on chromosome 10,PTEN)缺失是西方国家前列腺癌中最常见的基因异常之一,与肿瘤的进展、预后均有一定相关性。鉴于前列腺癌的异质性,不同地区、人群间其基因表达谱存在广泛差异,本研究主要探讨PTEN蛋白缺失在中国前列腺癌患者中的发生率以及与生化复发的相关性。方法：选取2006—2011年225例局限性前列腺癌并采取根治切除术的患者为研究对象,回顾性收集所有患者的临床病理资料,包括确诊时年龄、血清前列腺特异性抗原(prostate-specific antigen,PSA)值、Gleason分级评分、TNM分期、手术切缘和术后生化复发与否及时间。将225例局限性前列腺癌根治切除标本的肿瘤组织及癌旁组织制成组织芯片(tissue microarray,TMA),采用免疫组织化学技术检测PTEN蛋白在肿瘤及癌旁组织中的表达。采用χ²检验分析前列腺癌组织中PTEN蛋白缺失与患者临床病理特征的相关性。运用Kaplan-Meier生存分析模型、Cox比例风险模型分析PTEN蛋白缺失及患者临床病理特征与生化复发的关系。结果：前列腺癌患者中PTEN蛋白缺失率为15%(33/217),且存在PTEN蛋白缺失的前列腺癌患者其确诊时血清PSA值(P=0.030)及年龄(P=0.009)要显著高于PTEN表达的前列腺癌患者。单因素生存分析显示,PTEN表达情况(P=0.013 1)、确诊时血清PSA值(P=0.000 4)和Gleason分级评分(P=0.019 8)与前列腺癌患者的生化复发相关。Cox多因素分析结果表明,PTEN蛋白表达情况(HR=0.536,P=0.044)、确诊时血清PSA值(HR=1.879,P=0.001)和Gleason分级评分(HR=1.361,P=0.030)为前列腺癌患者生化复发的独立预后因素。结论：PTEN蛋白表达情况是局限性前列腺癌患者根治术后生化复发的独立预后因素,检测PTEN蛋白有望改善根治术后前列腺癌患者的管理及指导进一步治疗。     

前列腺特异性膜抗原和前列腺特异性抗原表达强度与前列腺癌Gleason评分之间的相关性研究

目的研究前列腺特异性膜抗原(PSMA)和前列腺特异性抗原(PSA)的表达强度与前列腺癌Gleason评分之间的相关性。方法制备抗PSMA膜外段表位的单克隆抗体,应用免疫组织化学方法检测前列腺癌中PSMA的表达,统计分析其与Gleason评分之间的相关性,并和PSA与Gleason评分之间的相关性进行对比。结果制备出8株分泌抗PSMA膜外段表位的单抗的杂交瘤细胞株。免疫组化结果表明,PSMA的表达强度与前列腺癌的Gleason评分之间存在相关性。在分化差的前列腺癌中,PSMA水平高于分化中等和分化良好的前列腺癌(P<0.01),而PSA在前列腺癌中的表达无明显差异(P>0.05)。结论PSMA表达水平在分化差的前列腺癌中明显升高,与Gleason评分存在相关性,可以作为前列腺癌的Gleason分级的标记物,提示PSMA可以作为对激素疗法效果不敏感的低分化前列腺癌抗体介导的免疫治疗靶点。     

联合检测血清HMGB1 PSA在局限性前列腺癌冷冻术后复发中的应用价值

  目的   探讨局限性前列腺癌经前列腺癌氩氦冷冻治疗后血清HMGB1和PSA表达在预测治疗后复发中的临床价值。  方法   应用酶联免疫吸附试验(ELISA) 测定80例局限性前列腺癌患者(Pca组) 冷冻治疗前、后和30例前列腺良性增生患者(BPH组)、20例健康对照者血清HMGB1和PSA表达。Pca组术后PSA、MRI随访, 经病理穿刺活检证实: 局部复发9例, 远处转移3例。比较Pca组术后血清HMGB1表达, 及预测前列腺癌复发的价值。  结果   Pca组术前血清HMGB1 (94.0±77.4 ng/mL) 相比BPH组(33.2±7.4 ng/mL) 和健康对照组(24.7±7.3 ng/mL) 显著升高(P < 0.001)。Pca组术后血清HMGB1 (55.0±11.0 ng/mL) 较术前显著降低(P=0.005);Pca组冷冻治疗后, 复发者术后HMGB1平均值为(70.8±2.7) ng/mL, 无复发者术后HMGB1平均值为(55.0±10.8) ng/mL, 差异有统计学意义(P=0.001);3例远处转移患者血清HMGB1水平较9例局部复发者显著升高(94.2±17.9 vs.73.1±7.9ng/mL)。术后血清HMGB1相比PSA预测复发性Pca的敏感性高(83.3%Vs.66.7%), 而两者联合诊断的特异性较单一PSA高(95.6%vs.82.4%)。Pca组术后HMGB1表达与临床分期、复发和转移(P < 0.001) 相关, 与Gleason评分无显著相关性(P > 0.05)。  结论   血清HMGB1在Pca中高表达, 提示血清HMGB1可作为一项预测和预后指标。此外, Pca患者冷冻治疗后联合检测HMGB1和PSA对于复发患者可提高早期诊断率, 有效的指导病理穿刺活检及后续治疗。      

前列腺癌患者血清和病理组织中miRNA-375的表达及意义

目的探讨前列腺癌患者血清和病理组织中miRNA-375的表达及临床意义。方法选取2015年3月至2016年3月间我院收治的前列腺癌患者30例为观察组,另选择同期前列腺增生患者30例为对照组,检测并比较两组患者血清及病理组织中miRNA-375变化,观察血清miRNA-375表达与临床病理关系,分析病理组织与血清中mi-RNA-375相关性及前列腺癌患者血清miRNA-375与血清PSA的相关性。结果与前列腺增生患者比较,前列腺癌患者PCR定量检测miRNA-375血清中2-△Ct显著增高,病理组织中miRNA-375表达显著升高,差异有统计学意义(P<0.05)。病理分期T3~T4期、Gleason评分>7分、存在转移及PSA>10μg/L者显著高于病理分期T1~T2期、Gleason评分≤7分、无转移及PSA≤10μg/L者,差异有统计学意义(P<0.05)。前列腺癌患者mi-RNA-375与血清PSA呈线性相关(r=0.714,P<0.05)。前列腺癌病理组织与血清中mi-RNA-375呈线性相关(r=0.911,P<0.05)。结论前列腺癌患者血清miRNA-375水平存在明显升高,且与患者临床病理特征存在相关性。     

前列腺癌组织Clusterin与Survivin表达与PSA的相关性分析

目的:分析蛋白Clusterin和Survivin在前列腺癌(PCa)组织中的表达与前列腺特异性抗原(PSA)的相关性及在前列腺癌诊断中的应用价值。方法:应用免疫组织化学方法检测80例前列腺癌和50例前列腺增生组织凋亡蛋白Clusterin、Survivin的表达和相应患者血浆中PSA值。结果:前列腺癌组织中Clusterin、Survivin蛋白的阳性表达率分别为57.5%(46/80)、48.8%(39/80),Clusterin和Survivin蛋白在前列腺增生组织中的阳性表达率分别为0(0/50)、0(0/50),差异具有统计学意义(P<0.05)。Clusterin和Survivin蛋白表达与前列腺癌病理分级、临床分期、转移情况和PSA具有相关性(P<0.05),前列腺癌组织中Survivin与Clusterin的表达无相关性(P>0.001)。结论:联合检测Clusterin及Survivin表达与前列腺特异抗原(PSA)可为前列腺癌的防治和治疗提供新的思路。     

EPO-R 和CD31 在前列腺癌中的表达及其意义

 目的 探讨EPO-R和CD31在前列腺癌中表达及其临床意义。方法 采用免疫组化的方法对51例前列腺癌手术标本及10例前列腺增生手术标本进行标记及分析。结果 显示EPO-R和CD31表达与前列腺癌的病理分级、Gleason评分及转移密切相关，并具有显著性差异，但与血清前列腺特异性抗原(PSA)水平无关。结论 EPO-R和CD31的表达可能在前列腺癌的发展及转移过程中起重要作用。     

尿PCA3在前列腺癌中的临床价值

目的探讨尿前列腺癌抗原3(PCA3)基因表达水平及与血清前列腺特异性抗原(PSA)的表达水平,及其与肿瘤分化程度的关系。方法选择81例因血清PSA表达升高和(或)直肠指诊异常行前列腺穿刺活检的患者。采用苏木精-伊红(HE)染色及免疫组化鸡尾酒染色明确病理活检结果,定量-实时逆转录聚合酶链反应(qRT-PCR)检测尿PCA3 m RNA表达水平,并分析其与肿瘤分化程度的关系。前列腺癌患者尿PCA3 mRNA和血清PSA表达水平间的相关性采用线性回归分析。结果 81例患者的前列腺活检组织中,诊断前列腺癌阳性53例,阴性28例。前列腺癌患者尿PCA3 mRNA和血清PSA表达水平,均明显高于非前列腺癌患者(P﹤0.01);前列腺癌患者尿PCA3 m RNA表达水平与血清PSA表达水平无线性相关关系(P﹥0.05)。PCA3 mRNA高表达组患者Gleason评分明显高于低表达组患者(P﹤0.01),尿PCA3高表达倾向低、中度分化(P﹤0.01)。尿PCA3 mRNA高表达组患者NME1、NME3和SPARCL1 mRNA表达水平均明显低于低水平组患者(P﹤0.01);SPOCK1和survivin m RNA表达水平均明显高于低表达组患者(P﹤0.01)。结论前列腺癌患者尿PCA3 mRNA及血清PSA表达水平明显升高,但二者间无线性关系。前列腺癌患者尿PCA3 mRNA高表达时,NME1、NME3和SPARCL1mRNA表达水平及分化程度均降低,SPOCK1和survivin mRNA表达水平升高。     

BRAF and KRAS mutations in prostatic adenocarcinoma

Constitutive activation of the kinase cascade involving RAS, RAF, MEK and ERK is common to human cancers, and mutations of KRAS and BRAF are mutually exclusive and serve as alternatives to activate the RAS/RAF/ERK signaling pathway. RAS mutations are known to occur in prostate adenocarcinomas, but little is known about BRAF mutations in these tumors. In the present study, BRAF and KRAS mutations were characterized in 206 prostate adenocarcinomas by enhanced PCR-RFLP and direct sequencing. The identified KRAS and BRAF mutations were then analyzed with respect to preoperative serum PSA levels, Gleason scores and tumor stages. Mutations in codon 600 of BRAF were identified in 21 (10.2%) of 206 prostate adenocarcinomas. KRAS mutations in codons 12 or 13 were found in 15 (7.3%) of 206 prostate adenocarcinomas. However, no tumor specimen contained both BRAF and KRAS mutations. Prostate adenocarcinomas with a BRAF mutation tended to show higher preoperative serum PSA levels, Gleason scores and tumor stages than prostate adenocarcinomas with a KRAS mutation. The results obtained show that BRAF mutations are as uncommon as KRAS mutations in prostate adenocarcinoma. Although BRAF and KRAS are members of the same RAS/ERK signaling pathway, prostate adenocarcinomas with a BRAF mutation showed clinicopathologic features that differed from those of prostate adenocarcinoma with a KRAS mutation.     

前列腺癌组织中Kindlin-2和Clusterin蛋白表达及与PSA含量的相关性

目的:探讨前列腺特异性抗原（PSA）含量和前列腺癌（PCA）组织中Clusterin、Kindlin-2蛋白阳性表达的相关性,研究前列腺癌的治疗策略。方法:45例前列腺增生和55例前列腺癌组织应用免疫组织化学方法检测凋亡蛋白Kindlin-2、Clusterin的表达并检测对应病例的血浆PSA含量。结果:Clusterin、Kindlin-2蛋白在前列腺癌组织中的阳性表达率分别为50.9%(28/55)、63.6%(35/55),Clusterin和Kindlin-2蛋白在前列腺增生组织中的阳性表达率分别为0(0/45)、51.1%(23/45)。在前列腺癌和前列腺增生组织中Clusterin和Kindlin-2阳性表达率具有统计学差异(P<0.05);Clusterin和Kindlin-2蛋白表达与前列腺癌病理分级、临床分期、转移情况和PSA含量相关,差异有统计学意义（P<0.05）。结论:联合检测Kindlin-2、Clusterin蛋白和PSA可为前列腺癌提供一种新的联合检查方法。     

前列腺癌组织中p27和Survivin的表达与前列腺特异性抗原的相关性

目的:通过分析蛋白p27和Survivin在前列腺癌(PCa)组织中的阳性表达与前列腺特异性抗原(PSA)的相关性,探讨前列腺癌的治疗方法.方法:应用免疫组织化学方法检测75例前列腺癌和60例前列腺增生组织中p27、Survivin蛋白的表达和相应患者血浆中的PSA值.结果:前列腺癌组织中p27、Survivin蛋白的阳性表达率分别为37.3%(28/75)、68.0%(51/75),p27和Survivin蛋白在前列腺增生组织中的阳性表达率分别为63.3%(38/60)、0(0/60),在前列腺增生和前列腺癌组织中Survivin和p27蛋白的阳性表达率差异均具有统计学意义(P<0.05).p27和Survivin蛋白表达与前列腺癌病理分级、临床分期、转移情况和PSA值具有统计学意义(P<0.05).结论:临床中联合检测p27及Survivin表达与前列腺特异性抗原的关系和相互作用机制,为前列腺癌的防治和治疗提供新的思路.     

A case-control study of the androgen receptor gene CAG repeat polymorphism in Australian prostate carcinoma subjects

BACKGROUND: The development of prostate carcinoma is androgen-dependent. The coding sequence of the androgen receptor (AR) gene contains a CAG repeat polymorphism that has been shown to influence AR activity in vitro. Studies of this polymorphism as a prostate carcinoma risk factor have been conflicting. METHODS: A matched case-control design was used in a clinic-based multicenter study of Australian prostate carcinoma subjects. Cancer subjects were matched by age and locality with controls, all of whom had a serum prostate specific antigen (PSA) level of less than 4 mg/L. Conditional logistic regression was used to determine the relative risk of prostate carcinoma dependent on AR gene CAG number. The association of disease characteristics at diagnosis with the polymorphism also was assessed. RESULTS: Five hundred forty-five cases of prostate carcinoma and 456 matched case-control pairs were recruited. Association studies of disease characteristics at diagnosis showed age at diagnosis to be associated with AR CAG number by univariate (P = 0.004) and multivariate (adjusting for PSA, stage, and grade) linear regression (P = 0.018). No association was observed between the polymorphism and disease stage (TNM-based categories; P = 0.277), histologic grade (P = 0.41), or PSA level at diagnosis (P = 0.48). In the pairwise case-control analysis, the odds ratio of prostate carcinoma for a change of 5 CAG repeats gave an odds ratio of 0.9821 (95% confidence interval, 0.84-1.15). CONCLUSIONS: In this Australian study population, the AR CAG repeat polymorphism was not a risk factor for prostate carcinoma, but a shorter repeat sequence was associated with earlier age at diagnosis.     

前列腺癌患者全血锌浓度的改变及诊断价值

目的:研究全血锌浓度与前列腺癌的关系,并将其与血清前列腺特异性抗原(PSA)联合,探讨在前列腺癌诊断中的应用价值.方法:收集自2005年7月至2008年10月东南大学附属中大医院和南京大学医学院附属鼓楼医院收治的前列腺癌患者95例,前列腺增生症患者91例,采用火焰吸收原子分光光度法测定全血锌浓度,采用放射免疫法测定血清PSA值.结果:全血锌浓度前列腺癌组(4.73±1.51)μg/mL,前列腺增生症组(6.82±1.63)μg/mL,两组间有显著差异(P＜0.001).两组血清PSA值总体分布有显著差异(P＜0.01),但在4.0～10.0ng/mL区间,两组例数比例无显著差异(P=0.143).以前列腺增生症组为对照,全血锌浓度诊断前列腺癌的ROC曲线下面积为0.82;在血清PSA4.0～10.0ng/mL区间范围,此曲线下面积为0.79.在血清PSA4.0～10.0ng/mL区间范围,全血锌浓度取5.24μg/mL界值时有最佳的诊断准确性,Youden指数0.46;其与血清PSA取界值4.0ng/mL串联应用,诊断的特异度为75%,是血清PSA单独诊断时的2.34倍,Youden指数为0.51,是血清PSA单独诊断的2.22倍,并联无助于诊断,Youden指数仅0.14.结论:全血锌浓度检测有助于前列腺癌与前列腺增生症的鉴别诊断,其与血清PSA联合应用(串联),能够显著改善血清PSA 4.0～10.0ng/mL区间内的诊断阳性率,可为前列腺癌的诊断提供有价值的参考,有一定的临床应用前景.     

The accumulation of angiostatin-like fragments in human prostate carcinoma.

PURPOSE: Angiostatin, a potent inhibitor of angiogenesis and, hence, the growth of tumor cell metastasis, is generated by a proteolytic enzyme from plasminogen. However, its localization and specific enzymes have yet to be ascertained in human tissue. EXPERIMENTAL DESIGN: To elucidate the generation and the localization of angiostatin in prostate carcinoma, we examined angiostatin generation in a panel of human prostate cancer cell lines and performed immunohistochemistry with the antibodies to angiostatin and prostate-specific antigen (PSA), a potent proteolytic enzyme of angiostatin in 55 cases of prostate carcinoma. RESULTS: We demonstrated that the lysates of human prostate carcinoma cell lines could generate angiostatin-like fragments from purified human plasminogen but could not generate angiostatin in the absence of exogenous plasminogen. The fragmented proteins were reacted with the monoclonal antibody specific for plasminogen lysine-binding site 1 (LBS-1). Immunohistochemically, the intracytoplasmic immunostaining of LBS-1 was positive in 87.3% (48 of 55) of prostate carcinoma cases, and the immunostaining of miniplasminogen was negative in all cases. There was a significant relationship between the positive immunostaining of LBS-1 and Gleason score (P = 0.0007). The intracytoplasmic immunostaining of PSA was positive in 37.0% (20 of 54) of prostate carcinoma cases, but there was no significant relationship between the expression of PSA and Gleason score, or between the positive immunostaining of LBS-1 and PSA. CONCLUSIONS: These findings suggest that angiostatin is generated by prostate carcinoma cells and is accumulated within the cytoplasm. In addition, the generation of angiostatin-like fragments was correlated with tumor grade; however, PSA may not be the only enzyme for angiostatin generation in human prostate carcinoma.     

Prospective study of correlations between biopsy-detected high grade prostatic intraepithelial neoplasia, serum prostate specific antigen concentration, and race

BACKGROUND: High grade prostatic intraepithelial neoplasia (HGPIN), a premalignant lesion of the prostate gland, is more common in black men than in white men. The influence of HGPIN on the serum prostate specific antigen (PSA) concentration is controversial, and correlations between HGPIN and PSA in black men and white men have not been investigated. METHODS: Between January 1992 and December 1998, 411 black men and 639 white men with suspected prostate carcinoma underwent an initial benign prostate biopsy at a single medical center. The presence or absence of HGPIN in the biopsy specimens was determined by one uropathologist. RESULTS: HGPIN was identified in 8.9% of the specimens. When stratified by PSA concentration (< 4.0 ng/mL, 4.0-9.9 ng/mL, and > or = 10.0 ng/mL), HGPIN was associated with an increased PSA concentration only among men with PSA concentrations < 4.0 ng/mL (P = 0.01). The prevalence of HGPIN in the black and white patients was 13.4% and 5.9%, respectively (P < 0.0001), and was significantly greater in black men than in white men with PSA concentrations < 4.0 ng/mL (P = 0.002). Among the patients with PSA concentrations < 4.0 ng/mL, black race was an independent predictor of an increased PSA concentration when adjusted for patient age, prostate volume, and the presence or absence of HGPIN (P = 0.03). CONCLUSIONS: HGPIN is more common in black men than in white men and may produce an increase in the PSA concentration. However, racial differences in the prevalence of HGPIN may not contribute to racial differences in PSA concentrations among men with no clinical or histologic evidence of carcinoma.     

Prognostic significance of p16 and CDK4 proteins in localized prostate carcinoma

BACKGROUND: In prostate carcinoma, a very low frequency of point mutations of the tumor suppressor gene CDKN2/MTS1 (p16(INK4) ) has been reported, but deletions of 9p21 and inactivation by promoter methylation are observed more frequently. In the current study the authors evaluated the expression of p16 and CDK4 proteins and their prognostic significance in patients with clinically localized prostate carcinoma. METHODS: The levels of p16 and CDK4 proteins were quantitated by immunofluorescence flow cytometry, using paraffin embedded material, in 104 adenocarcinomas of the prostate after radical prostatectomy. These levels then were compared with 25 cases of benign prostate hyperplasia (BPH). RESULTS: In prostatic carcinoma specimens, p16 protein was elevated significantly compared with BPH, with a median fluorescence index (FI) of 15.4 versus 10.7, respectively (P = 0.010). This was not the case for CDK4 protein, although p16 protein expression correlated significantly with CDK4 protein expression in BPH (Spearman rank correlation [R(S)] = 0.63) and carcinoma (R(S) = 0.78). In univariate survival analysis of the first 5 years, high levels of p16 protein expression (FI > 11.7) (P = 0.005), tumor greatest dimension, World Health Organization (WHO) histologic grade, capsular penetration, seminal vesicle invasion, positive surgical margins, lymph node involvement, and preoperative serum prostate specific antigen > 20 ng/mL all were significant predictors of biochemical failure. In multivariate survival analysis, high p16 protein expression (P = 0.015), age, WHO histologic grade, capsular penetration, and seminal vesicle involvement remained as independent predictors of biochemical failure. CONCLUSIONS: These data suggest that increased expression of p16 protein, but not CDK4 protein, may be involved in the development of prostate carcinoma and may represent an independent predictor of biochemical failure after radical prostatectomy.     

Histopathologic effects of hypofractionated robotic radiation therapy on malignant and benign prostate tissue

We describe the first histopathologic analysis of prostatic tissue following hypofractionated robotic radiation therapy. A 66 year-old man presented with stage II, low risk adenocarcinoma of the prostate and underwent elective conformal hypofractionated radiation therapy. His pretreatment evaluation revealed T1c adenocarcinoma, Gleason's grade 3 + 3 = 6 and a prostate specific antigen (PSA) level of 4.87 ng/ml. Hypofractionated radiation therapy (37.5 Gy in five daily fractions of 7.5 Gy) was completed on an Internal Review Board approved protocol. One year later, he developed progressive urinary retention. Transurethral prostatic resection was performed to alleviate obstructive symptoms. Bilobar hypertrophy was observed without evidence of stricture. Histolopathologic analyses of resected prostate tissues revealed changes consistent with radiation treatment, including cellular changes, inflammation, glandular atrophy and hyperplasia. There was no evidence of residual cancer, fibrosis or necrosis. The patient's postoperative course was uneventful with post-treatment PSA of 0.5 ng/ml and residual grade 1 stress incontinence.