Cyclooxygenase-2 expression is dependent upon epidermal growth factor receptor expression or activation in androgen independent prostate cancer

Aim： To investigate the expression of cyclooxygenase-2 （COX-2） and epidermal growth factor receptor （EGFR） and the possible mechanism in the development in androgen independent prostate cancer （AIPC）. Methods： Immunohistochemistry was performed on paraffin-embedded sections with goat polyclonal against COX-2 and mouse monoclonal antibody against EGFR in 30 AIPC and 18 androgen dependent prostate cancer （ADPC） specimens. The effect of epidermal growth factor （EGF） treatments on the expression of COX-2 and signal pathway in PC-3 and DU-145 cells was studied using reverse transcription-polymerase chain reaction （RT-PCR） and Western blot analysis. ELISA was used to measure prostaglandin E2 （PGE2） levels in the media of PC-3 and DU-145 incubated with EGF for 24 h. Results： COX-2 was positively expressed in AIPC and ADPC, which were predominantly in endochylema of prostate cancer （PCa） cells. Intense staining was seen in AIPC （80%） and in ADPC （55.5%）, but there was no significant association between the two groups. EGFR expression was also positive in the two groups （61.8% in ADPC and 90% in AIPC, P 〈 0.01）. A significant association was found between EGFR expression and a higher Gleason score （P 〈 0.05） or tumor stage （P 〈 0.05）. The expression of PGE2 was increased in PC-3 and DU-145 cells after being incubated with EGF. Both p38MAPK and PI-3K pathway were involved in the PC-3 cell COX-2 upregulation course. In DU- 145, only p38MAPK pathway was associated with COX-2 upregulation. Conclusion： EGFR activation induces COX-2 expression through PI-3K and/or p38MAPK pathways. COX-2 and EGFR inhibitors might have a cooperative anti-tumor effect in PCa.

Role of androgen receptor in prostate cancer

The growth of prostate cancer is sensitive to androgen, and hormonal therapy has been used for treatment of ad-vanced cancer. About 80% of prostate cancers initially respond to hormonal therapy, howerver, more than half of the re-sponders gradually become resistant to this therapy. Changes in tumors from an androgen-responsive to an androgen-unre-sponsive state have been widely discussed. Since androgen action is mediated by androgen receptor (AR), abnormalitiesof AR is believed to play an important role of the loss of androgen responsiveness in prostate cancer. This article focusedon the role of AR in the progression of prostate cancer. (Asian J Androl 1999 Sep; 1: 81-85)

In situ hybridization assay of androgen receptor gene in hepatocarcinogenesis

AIM To determine the correlation between expression of androgen receptor (AR) gene and hepatocarcinogenesis. METHODS Male SD rats were used as experimental animals and the animal model of experimental hepatocarcinoma was established by means of 3′ me DAB administration. Androgen receptor mRNA was detected by a non radioactive in situ hybridization assay in neoplastic and non neoplastic liver tissues. RESULTS The expression of androgen receptor mRNA was observed only in neoplastic cells and some atypical hyperplastic cells. In the liver tissue of control animal and the remaining normal liver cells adjacent to the carcinoma tissue, no positive signal was seen. CONCLUSION Androgen has an important correlation with hepatocarcinogenesis and the expression of androgen receptor gene might be a mark event during hepatocarcinogenesis.

Clinical significance of the leptin and leptin receptor expressions in prostate tissues

Aim： To evaluate the expression of leptin and leptin receptor in benign prostatic hyperplasia （BPH） and prostate cancer （PCa）, and to investigate whether they are associated with the development and progression of PCa. Methods： hnmunohistochemical staining was performed to examine the expression of leptin and leptin receptor in BPH and PCa. PCa was divided into three groups： localized PCa, locally advanced PCa and metastatic PCa. The positive staining was identified and the percentage of the positive staining was graded. We also assessed the relationship between both the Gleason score and body mass index （BMI） and PCa. Results： The percentage of the leptin expression in PCa was significantly higher than that in BPH （P 〈 0.01）. For the PCa group, the expressed levels of leptin showed a considerable correlation with localized PCa and metastatic PCa （P 〈 0.05）. Leptin receptor, however, did not reveal a definite difference between BPH and PCa. The expression of leptin indicated a significant difference between well-differentiated PCa （Gleason score ≤6） and poorly differentiated PCa （Gleason score 8-10） （P 〈 0.05）. The relation between the leptin expression level in PCa and the BMI was not remarkable （P = 0.447）. Conclusion： Our results suggest that leptin might have a promoting effect on the carcinogenesis and progression of PCa.

Human epidermal growth factor receptor type 2 protein expression in Chinese metastatic prostate cancer patients correlates with cancer specific survival and increases after exposure to hormonal therapy

Aim： To investigate human epidermal growth factor receptor type 2 （HER2） protein expression and gene amplification in Chinese metastatic prostate cancer patients and their potential value as prognostic factors. Methods： Immunohistochemistry （IHC） was performed to investigate HER2 protein expression in prostate biopsy specimens from 104 Chinese metastatic prostate cancer patients. After 3-11 months of hormonal therapy, 12 patients underwent transurethral resection of the prostate （TURP）. HER2 protein expression of TURP specimens was compared with that of the original biopsy specimens. Of these, 10 biopsy and 4 TURP specimens with HER2 IHC staining scores ≥ 2＋ were investigated for HER2 gene amplification status by fluorescent in situ hybridization （FISH）. Results： Of the 104 prostate biopsy specimens, HER2 protein expression was 0, 1＋, 2＋ and 3＋ in 49 （47.1%）, 45 （43.3%）, 8 （7.7%） and 2 （1.9%） cases, respectively. There was a significant association between HER2 expression and Gleason score （P = 0.026）. HER2 protein expression of prostate cancer tissues increased in 33.3% of patients after hormonal therapy. None of the 14 specimens with HER2 IHC scores 〉 2＋ showed HER2 gene amplification. Patients with HER2 scores 〉 2＋ had a significantly higher chance of dying from prostate cancer than those with HER2 scores of 0 （P = 0.004） and 1＋ （P = 0.034）. Multivariate Cox regression analysis showed that HER2 protein expression intensity was an independent predictor of cancer-related death （P = 0.039）. Conclusion： An HER2 IHC score 〉 2＋ should be defined as HER2 protein overexpression in prostate cancer. Overexpression of HER2 protein in cancer tissue might suggest an increased risk of dying from prostate cancer. HER2 protein expression increases in some individual patients after hormonal therapy.

Atypical chemokine receptor CCRL2 is overexpressed in prostate cancer cells

Atypical chemokine receptors have recently emerged as important molecular players in health and diseases; they affect chemokine availability and function and impact a multitude of pathophysiological events, including the tumorigenesis process. This family of atypical receptors comprises five members: ACKR1/DARC, ACKR2/D6,ACKR3/CXCR7, ACKR4/CCRL1, and ACKR5/CCRL2. This work evaluated the differential expression of these receptors in prostate cancer using quantitative PCR. Further evaluation of CCRL2 at the protein level confirmed its overexpression in a metastatic cell line and in malignant prostatic tissues from patients. CCRL2, a presumed member of the atypical chemokine receptor family, plays a key role in lung dendritic cell trafficking to peripheral lymph nodes.Recent studies have reported the expression of CCRL2 in different human cancer cell lines and tissues. However, its function and expression in prostate cancer has not been previously addressed.

Kinetics of testosterone recovery in clinically localized prostate cancer patients treated.with radical prostatectomy and subsequent short-term adjuvant androgen deprivation therapy

deprivation therapy （ADT） is a standard treatment for metastatic, recurrent and locally advanced prostate cancer （PCa）. The aim of this study is to investigate the timing and extent of testosterone recovery in clinically localized PCa patients treated with radical prostatectomy （RP） and subsequent short-term adjuvant ADT. A total of 95 localized PCa patients underwent RP and 9-month adjuvant ADT were included in this prospective study. Serum testosterone level was measured before adjuvant ADT, at ADT cessation, and at 1, 3, 6, 9 and 12 months after cessation of ADT. A Cox proportional hazards model was used to assess variables associated with the ti me of testosterone normalization. The results showed that median patient age was 67 years and median testosterone level before adjuvant ADT was 361 （230-905） ng d1-1. All patients finished 9-month adjuvant ADT and achieved castrate testosterone level. At 3 months after ADT cessation, testosterone recovered to supracastrate level in 97.9% patients and to normal level in 36.9% patients. The percentage of patients who recovered to normal testosterone level increased to 66.3%, 86.3% and 92.6% at 6, 9 and 12 months, respectively. Cox regression model found that higher baseline testosterone level （ 300 ng dl- 1） was the only variable associated with a shorter time to testosterone normalization （hazard ratio： 1.98; P -- 0.012）. In conclusion, in most patients, testosterone recovered to supracastrate level at 3 months and to normal level at 12 months after 9-month adjuvant ADT cessation. Patients with higher baseline testosterone level need shorter time of testosterone normalization.

Increased expressions of vascular endothelial growth factor(VEGF),VEGF-C and VEGF receptor-3 in prostate cancer tissue are associated with tumor progression

Aim： To investigate the differences in microvessel densities （MVD） and the expressions of vascular endothelial growth factor （VEGF）, VEGF-C and VEGF receptor-3 （VEGFR-3） between prostate cancer （PCa） tissues and adjacent benign tissues, and to explore the correlations among MVD, Jewett-Whitmore staging, Gleason scores and expressions of VEGF, VEGF-C and VEGFR-3 in the progression of PCa. Methods： An immunohistochemical approach was adopted to detect the expressions of CD34, VEGF, VEGF-C and VEGFR-3 in both cancer areas and peripheral benign areas of 71 primary prostatic adenocarcinoma specimens. A statistic analysis was then performed according to the experimental and clinic data. Results： Significantly upregulated expressions of VEGF, VEGF-C and VEGFR-3 were all found in malignant epithelium/cancer cells compared with adjacent benign epithelium （P 〈 0.01）. Patients in stage D had a significantly higher score than patients in stage A, B or C when comparing the expression of VEGF-C or VEGFR-3 in the tumor area （P 〈 0.01）. In addition, significant correlations were observed between Jewett-Whitmore staging and VEGF-C （rs = 0.738, P 〈 0.01）, clinical staging and VEGFR-3 （rs = 0.410, P 〈 0.01）, VEGF-C and Gleason scores （rs = 0.401, P 〈 0.01）, VEGFR-3 and Gleason scores （rs = 0.581, P 〈 0.001） and MVD and VEGF （rs = 0.492, P 〈 0.001）. Conclusion： Increased expressions of VEGF and VEGF-C were closely associ- ated with progression of PCa. The main contribution of increased VEGF expression for PCa progression was to upregulate MVD, which maintained the growth advantage of tumor tissue. However, the chief role of increased expressions of VEGF-C and VEGFR-3 was to enhance lymphangiogenesis and provide a main pathway for cancer cells to disseminate. （Asian J Androl 2006 Mar; 8： 169-175）

Effect of androgen withdrawal on activation of ERKs and expression of cell cycle regulation molecules in human prostate carcinoma cells

Objective: To explore the possible mechanisms of growth regression of human androgen dependent prostate carcinoma cells caused by androgen withdrawal. Methods: After 24 h of treatment with 1 × 10-9 mol/L dihydrotestosterone (DHT), the expression of phosphorylated ERK proteins and cell cycle regulation molecules including CDK2, CDK4, CDK6 and P27kip1 in human androgen dependent prostate carcinoma cell line LNCaP was measured by Western blot analysis 0 h, 8 h and 24 h of after androgen withdrawal. Human androgen independent prostate carcinoma cell line PC-3 was also examined as control. Results: Down-regulation of phosphorylated ERK, CDK2, CDK4 and CDK6 and up-regulation of P27kip1 were found initially in LNCaP cell line 8 h after androgen withdrawal. The levels of phosphorylated ERK and CDKs decreased continuously and reached the lowest after 24 h, while continuous elevation of P27kip1 was detected thereafter to 24 h. No expression change of phosphorylated ERK, CDKs and P27kip1 were detected in PC-3 cell line. Conclusion: The androgen withdrawal can cause ERKs activation decrease and cell cycle regulation molecules changes, which may be one of the mechanisms for inhibited growth of androgen dependent prostate carcinoma after androgen ablation by either operative or medicine methods.

长链非编码RNA参与前列腺癌相关信号通路调控介导肿瘤发生进展的研究进展

前列腺癌(prostate cancer,PCa)属于一类恶性程度极高的泌尿系肿瘤,在全球新发癌症病例中前列腺癌位居第四位。由于前列腺癌具有高度异质性及耐药性,目前尚无治愈药物问世,阐明前列腺癌恶性进展的分子机制将对改善前列腺癌药物抗性,提升病人预后大有裨益。在前列腺癌发生发展的过程中各类信号通路起到了重要调控作用,包括胞内磷脂酰肌醇激酶-丝氨酸/苏氨酸特异性蛋白激酶(PI3K-Akt)信号通路、雄激素受体(androgen receptor,AR)、无翼信号通路(WNT)、缺口信号通路(Notch)在内的多种信号通路失衡显著影响了前列腺癌的恶性进展,然而其深层的分子机制仍有待进一步阐述。长链非编码RNA(long noncoding RNA,lncRNA)是一类长度大于200 bp的RNA分子,在过去十多年随着测序技术的发展,lncRNA的重要作用逐渐被研究者所认知,在前列腺癌中多种lncRNA通过影响前列腺癌中关键信号通路发挥相应作用参与调控前列腺癌的进展。该文就lncRNA在前列腺癌相关信号通路发挥的作用及相应分子机制作一综述,以期给前列腺癌治疗提供新的思路与方案。

Proliferative response of human prostate cancer cell to hormone inhibited by androgen receptor antisense RNA

Background The failure of endocrine treatment for advanced prostate cancer might be related to aberrant activation of androgen receptor (AR) Prostate cancer cell line LNCaP contains AR that can be activated by androgen, estrogen and progesterone This study was set to investigate the effects of antisense AR RNA on growth of LNCaP cultured in medium containing varied concentrations of R1881, 17β-estradiol, and progesterone, respectively Methods LNCaP cells transfected with antisense AR RNA retroviral vector pL-AR-SN were designated as LNCaP as-AR . LNCaP cells containing empty vector pLXSN served as LNCaP Neo . LNCaP and LNCaP Neo were taken as controls In vitro cell growth assay, proliferative cells of LNCaP and tranfected LNCaPs were counted by typan staining when they cultured with synthetic androgen R1881, 17β-estradiol, and progesterone, respectively Results Growth of LNCaP as-AR was inhibited significantly ( P <0 05) compared with that of LNCaP and LNCaP Neo at 1 nmol/L R1881, 10 nmol/L 17β-estradiol, and 1 nmol/L progesterone, respectively No difference was seen between LNCaP and LNCaP Neo ( P >0 05) Microscopic observation showed that LNCaP and LNCaP Neo cells grew well, but only few LNCaP as-AR cells were alive Conclusions Our observations indicate that antisense AR RNA retroviral vector pL-AR-SN could change androgen-independent characteristics of LNCaP cells, which might shed some novel insights into the treatment of androgen-independent prostate cancer

两种方法联合间歇性雄激素抑制治疗中晚期前列腺癌的疗效观察

目的观察经尿道等离子前列腺电切术(TUPKP)和睾丸切除术联合间歇性雄激素抑制(IAD)治疗中晚期前列腺癌(Pca)的疗效。方法 40例中晚期Pca患者行TUPKP治疗并且行睾丸切除术和IAD治疗。结果 6个月后,国际前列腺症状评分(IPSS)、生活质量评分(QOL)、最大尿流率(MFR)、残余尿量(RV)、前列腺特异抗原(PSA)、前列腺体积等与术前比较差异有统计学意义(P<0.01)。结论 TUPKP和睾丸切除联合IAD治疗中晚期Pca的疗效确切,明显提高患者生活质量,值得临床推广应用。

雌激素和雄激素受体在肺癌中的表达

背景与目的男性与女性肺癌流行病学表现明显不同,可能与性激素水平有关,有数据显示性别因素是肺癌明显独立的预后因子。本研究通过检测雌激素受体(ER)、雄激素受体(AR)在肺癌中的表达,探讨其与临床和病理学特征之间的关系。方法应用免疫组化S-P法检测105例(男84,女21)肺癌组织标本中ER、AR的表达。结果ER和AR总阳性率分别为14.3%(15/105)和20%(21/105)。肺癌组织中ER阳性表达率与患者年龄、性别、肿瘤组织学类型、组织分化程度及TNM分期、肿块大小、淋巴结转移情况等无关。AR的阳性表达与患者年龄、性别、肿瘤组织学类型、组织分化程度及肿块大小等情况无关,而在Ⅲ期肺癌患者中显著高于Ⅰ期肺癌,淋巴结转移N2组与N0组之间也存在统计学差异(x^2=4.7828,P=0.0287)。结论ER阳性表达与肺癌的生物学行为可能无关。AR的阳性表达与肺癌进展和淋巴结转移程度可能相关。

不同ER、PR状态乳腺癌中AR的表达及其意义

目的探讨AR在不同ER、PR状态乳腺癌中的表达及意义。方法采用免疫组化方法检测AR、ER、PR在173例乳腺癌中的表达,依据结果分组:(1)AR状态分组:AR阳性组和AR阴性组;(2)ER、PR状态分组:En组(ER、PR均阴性)、Ep组[ER和(或)PR阳性];(3)AR、ER、PR联合分组:En-AR+(En组且AR阳性)、En-AR-(En组且AR阴性)、Ep-AR+(Ep组且AR阳性)、Ep-AR-(Ep组且AR阴性),其中En-AR-又称为均阴性组,其他三组统称为部分或完全阳性组。不同分组方法比较与临床病理特征的关系。结果Ep组AR阳性率62.8%(54/86),En组AR阳性率37.9%(33/87),两组差异有显著性(P=0.001),AR阳性组体积小、核分裂少、组织学分级低(P<0.05);En-AR-组表现为核分裂多、组织学分级高(P<0.01),此外En组内AR阳性者核分裂少、组织学分级低(P<0.05),Ep组内AR阳性者临床分期高(P=0.000),En-AR+、Ep-AR+、Ep-AR-比较均无差异。结论AR在不同激素状态乳腺癌中表达的意义不同,ER、PR均阴性乳腺癌表达AR者预后较好,ER、PR阳性乳腺癌表达AR者临床分期高。在选择针对性药物时应考虑到不同激素受体状态的组合。

45例人前列腺癌雄激素受体基因B～H外显子的突变研究

目的和方法 :为探讨雄激素受体 (AR)与前列腺癌 (PC)发生发展及内分泌治疗不敏感的关系 ,我们首先建立了用PC的穿刺和石蜡切片组织检测AR基因突变的PCR -SSCP(双链构象多态性 ) -双链DNA循环测序法。并用上述方法检测了 45例国人前列腺癌组织 (6例穿刺组织 ,39例石蜡切片 )AR基因B～H外显子的基因突变。结果 :在 6例患者的癌组织中证实有 7个SSCP泳动变位片段 (其中一患者有两个外显子异常 ) ,这 6例患者中 4例为低分化腺癌 ,其中 2例已有远处转移 ,而序列分析证实这 2例转移患者SSCP异常的外显子H片段各存在一错义突变 (Glu 872Gln、Met 886Ile)。这两种AR的基因突变国内外均未见报道 ,为在PC中新发现的突变。结论 :实验发现AR突变均发生在前列腺癌的中晚期 。

雄激素受体在前列腺癌细胞激素非依赖转化中的表达及调控

目的:研究雄激素受体(androgen receptor,AR)在激素依赖性前列腺癌(androgen dependent prostate can-cer,ADPC)细胞系LNCaP转化成激素非依赖性前列腺癌(androgen independent prostate cancer,AIPC)过程中的表达变化,以及其受Wnt信号通路和蛋白酶体降解通路调控的机制。方法:应用活性炭滤过的低激素胎牛血清培养LNCaP细胞,得到雄激素非依赖的LNCaP亚系LNCaP-AI(androgen independent)细胞。应用细胞增殖试验检测LNCaP-AI的细胞生长曲线。应用Western blot、RT-PCR分析激素依赖性转化过程中的AR、前列腺特异抗原(pros-tate specific antigen,PSA)的表达变化。在AIPC细胞中,应用Wnt信号通路阻滞剂IWR-1及蛋白酶体通路抑制剂乳胞素(lactacystin)处理细胞,观察Wnt信号通路和蛋白酶体信号通路对AR mRNA及蛋白表达的影响。结果:在体外低激素环境中生长6个月后,LNCaP细胞变成雄激素非依赖性的LNCaP亚系LNCaP-AI。表现为对雄激素依赖性减弱,细胞增殖加快,PSA的表达增高。在转化为LNCaP-AI的过程中,AR mRNA水平短期上调,后恢复到原始水平,但蛋白水平一直处于下调趋势。IWR-1处理的LNCaP-AI,AR mRNA及蛋白的表达下调。乳胞素处理的LNCaP-AI,AR mRNA无变化而蛋白表达上调。结论:在体外前列腺癌细胞由激素依赖性向非依赖性转化的过程中,AR mRNA表达仅有一过性增高,而蛋白表达呈现明显的下降趋势。进一步研究发现,Wnt信号通路和蛋白酶体通路可能对AR的蛋白表达有调控作用。Wnt信号通路的抑制或蛋白酶体信号通路的增强可能是AR蛋白表达下调的原因。

雄激素受体在三阴性乳腺癌的表达及其预后意义

目的探讨雄激素受体(AR)在三阴性乳腺癌(TNBC)的表达及其预后意义。方法免疫组化检测AR在153例TNBC的表达情况,分析其与TNBC的临床病理特征的相关性及其预后意义。结果 TNBC中AR阳性率为28.1%,与AR阴性者相比,受体阳性者具有更高的淋巴结阳性率。单因素分析显示,AR阳性与TNBC的5年无疾病进展时间(DFS)和总生存时间(OS)相关;多因素分析显示,淋巴结阳性率是影响TNBC 5年DFS和OS的独立预后因素,AR与TNBC的5年DFS具有相关性。结论 TNBC中AR阳性者预后差,AR可能成为TNBC的治疗新靶点。

LSD1和AR在前列腺癌中的表达及其意义

目的检测赖氨酸特异性组蛋白脱甲基酶(LSD1)和雄激素受体(AR)在前列腺癌中的表达,探讨其与前列腺癌的Gleason分级、临床分期、复发和转移之间的关系。方法收集150例前列腺癌患者随机标本制作组织芯片,另30例非肿瘤性前列腺组织作为对照。用免疫组织化学EnVision法检测两组标本中LSD1和AR的表达情况。结果前列腺癌组织中LSD1和AR阳性率分别为90.7%和80.3%,非肿瘤性前列腺组织中阳性率分别为20.0%和10.0%。相关分析表明,LSD1和AR在前列腺癌中的表达与Gleason分级以及复发相关,与临床分期和转移无相关性。结论 LSD1和AR可能是预测前列腺癌复发及预后的重要生物学指标。

雄激素受体在乳腺癌中的表达及其预后意义

目的·探讨雄激素受体(AR)在乳腺癌中的表达情况及其预后意义。方法·选取2013年10月-2016年12月就诊于上海交通大学医学院附属瑞金医院、仁济医院及苏州九龙医院的183例女性乳腺癌患者,采用免疫组织化学检测肿瘤组织中AR蛋白的表达,分析AR表达与临床病理特征的相关性;采用在线生存分析数据库(Kmplot)观察AR基因的表达与乳腺癌患者预后的相关性。结果·AR蛋白的阳性率为47.5%。AR阳性者具有相对较低的组织学分级[57.6%(G1/G2)vs 25.0%(G3),P<0.05]。在雌激素受体、孕激素受体及P53阳性者中,AR蛋白的阳性率高于阴性组(P<0.05)。分子分型为管腔型者AR蛋白的阳性率高于表皮生长因子受体-2过表达及三阴性乳腺癌组(51.7%vs 31.6%,P<0.05)。单因素分析结果显示,AR基因阳性的乳腺癌患者的无复发生存、总生存、无远处转移生存明显高于AR阴性者(P<0.05)。结论·乳腺癌中AR阳性患者的预后较好,AR通路抑制剂可能成为治疗AR阳性乳腺癌的选择。

女性外阴尖锐湿疣的克隆性

目的 根据女性体细胞中两条X染色体上雄激素受体 (AR)基因的长度多态性进行非放标克隆性检测 ,以探讨尖锐湿疣的克隆组成。方法 石蜡切片HE染色后进行显微解剖 ,提取基因组DNA ,Hha Ⅰ消化 ,巢式PCR扩增 ,变性聚丙烯酰胺凝胶电泳后银染显示单股DNA片段长度。结果 在 68例湿疣标本中 ,65例扩增成功 ,其中 53例 (81 5 % )具有AR位点的多态性 ;在适于分析的 45例中 ,9例 (2 0 % )显示AR位点长度多态性丢失 ,属于单克隆性增生 ;其余 36例 (80 % )无多态性丢失 ,提示为多克隆增生。单克隆性病变的核分裂指数明显高于多克隆病变 ,但二者的凋亡小体计数差异不显著。结论 大部分尖锐湿疣属于多克隆性病变 ,属反应性增生 ;少部分是克隆性增生 。