癌蛋白bcl—2在前列腺增生组织中的表达及其意义

采用抗ｂｃｌ－２单克隆抗体对２０例前列腺增生和１２例正常前列腺组织的冰冻切片进行免疫组织化学染色。结果表明，正常前列腺的外周区ｂｃｌ－２蛋白主要位于腺体的基底细胞，腺上皮细胞偶见着色，移行区仅部分基底细胞阳性关色。前列腺增生组织中的上皮基底细胞和大部分腔上皮细胞呈强阳性，阳性的细胞数和染色强度均高于正常前列腺组织。     

癌蛋白bcl－2在前列腺增生组织中的表达及其意义

采用抗ｂｃｌ－２单克隆抗体对２０例前列腺增生（ＢＰＨ）和１２例正常前列腺组织的冰冻切片进行免疫组织化学染色。结果表明，正常前列腺的外周区ｂｃｌ－２蛋白主要位于腺体的基底细胞，腺上皮细胞偶见着色，移行区仅部分基底细胞阳性着色。前列腺增生组织中的上皮基底细胞和大部分腔上皮细胞均呈强阳性，阳性的细胞数和染色强度均高于正常前列腺组织。具有抑制细胞凋亡的ｂｃｌ－２蛋白在ＢＰＨ组织中的过表达提示ＢＰＨ的发生可能与上皮细胞可以不依赖于激素的生长和（或）细胞寿命延长，凋亡的细胞数目减少有关。     

高分子质量细胞角蛋白结合前列腺特异性抗原及P53标记物在前列腺癌鉴别诊断中的临床意义

目的:提高对前列腺良、恶性病变的临床认识和鉴别诊断水平。方法:用免疫组化染色法分别对前列腺腺癌13例、前列腺上皮内瘤和不典型腺瘤样增生22例、良性前列腺增生74例患者病变组织作抗高分子质量细胞角蛋白抗体(CK34BE12)、前列腺特异性抗原(PSA)及突变型P53的表达。结果:9例前列腺癌的腺体基底细胞区CK34BE12染色为阴性;4例染色大部分区域呈现阴性,染色区域部分腺体CK34BE12的染色呈现断续的阳性反应,PSA表达阴性,P53表达呈阳性,阳性细胞标记指数>15%。13例前列腺上皮内瘤和不典型腺瘤样增生腺体基底细胞区CK34BE12染色呈阳性,9例基底细胞区CK34BE12染色呈现断续阳性的区域占主体,染色小部分区域呈现阴性,染色区域PSA表达减弱,P53表达呈阳性,阳性细胞标记指数<15%。74例良性前列腺增生的腺体基底细胞对CK34BE12染色均呈强阳性,染色的反应带呈现不规则粗线形连续环状强阳性着色围绕在腺周,染色区域中PSA表达呈现阳性,P53表达呈阴性。结论:在组织形态学观察的基础上联合应用CK34BE12及PSA标记物可特异地显示前列腺腺体基底细胞的存在及间接了解其基底细胞层的完整性与否,结合P53的表达判断致癌基因的存在;对前列腺良、恶性病变的鉴别诊断及肿瘤恶性程度的准确判断具有很大帮助,且对前列腺癌的早期诊断也有很好的应用价值。     

Caspase-3在前列腺组织中的表达和意义

目的 研究Caspase-3在良性前列腺增生(BPH)和前列腺癌(Pca)组织中的表达,了解Caspase-3在BPH和Pca发病及细胞凋亡中的作用。方法 30例BPH组织、22例Pca组织及7例正常前列腺石蜡切片组织用多克隆抗体Caspase-3行LSAB免疫组化染色,按表达的阳性率分0(阴性)、1 (<25％)、2 (25％～75％)、4 (>75％)统计染色等级。结果Caspase-3在93％(28/30)BPH组织有不同程度的表达(0～3 ),主要在分泌性上皮和基底细胞表达,而在基质平滑肌罕见表达,且BPH上皮表达明显少于正常组织。Capase-3在22例Pca组织表达阳性率为100％,普遍表达强阳性(4 ),且明显多于非癌性组织,Caspase-3表达与Pca病理分级无相关。结论 Caspase-3表达异常与BPH上皮与基质增生有关;Caspase-3在国人Pca细胞凋亡中有重要作用。     

生长调控因子异常与前列腺增生的关系

目的 探讨多种生长调控因子在前列腺增生过程中的作用.方法 采用免疫组织化学Max vision二步法检测61例前列腺增生(BPH)和15例正常前列腺组织中TGF-β1、b-FGF、EGFR和TGF-α的表达.结果 TGF-β1主要定位于前列腺上皮细胞浆、间质细胞浆内,呈棕黄色颗粒,BPH及正常前列腺组织中上皮细胞阳性率分别为45.90%、13.33%;间质细胞阳性率分别为24.59%、6.67%,BPH中前腺上皮细胞和间质细胞总阳性率为52.46%,正常前列腺组织中上皮细胞和间质细胞总阳性率为20.00%,两组比较差异有统计学意义P<0.05.b-FGF定位于前列腺间质细胞浆内,部分上皮细胞浆阳性,呈棕黄色颗粒,上皮细胞阳性率为26.23%,间质细胞阳性率为75.41%,BPH中前腺上皮细胞和间质细胞总阳性率为75.41%,正常前列腺中上皮细胞阳性率为0%,间质细胞阳性率为13.33%,总阳性率为13.33%,P<0.05.EGFR主要定位于前列腺上皮细胞膜上,呈棕黄色颗粒,偶见于细胞浆内,阳性表达率为55.74%,TGF-α定位于前列腺间质细胞浆内,呈棕黄色颗粒,阳性表达率为88.52%,前列腺增生与正常前列腺两组间比较,差异有统计学意义(P<0.05).在腺体增生为主和间质增生为主两组间,TGF-β1、b-FGF、EGFR和TGF-α表达差异均无统计学意义(P>0.05).结论 TGF-β1、b-FGF、EGFR和TGF-α是促进BPH的重要因素,TGF-β1、b-FGF和TGF-α主要与前列腺间质增生有关,EGFR主要与前列腺上皮增生有关.     

bcl-2和bad蛋白表达与乳腺癌的相关性研究

目的探讨bcl 2、bad基因在乳腺癌前病变及其在癌组织中的表达 ,以及与ER、PR及淋巴结转移间的关系。方法采用免疫组织化学染色SABC法 ,观察 19例乳腺单纯性增生 ,2 0例乳腺非典型增生 ,4 8例乳腺癌组织中bcl 2、bad蛋白的表达 ,并同时检测 4 8例乳腺癌组织中ER、PR的表达。结果bcl 2在正常组和乳腺单纯性增生组 10 0 %表达 ,非典型增生组 ,乳腺癌组的表达率分别为 85 0 %和 5 8 33% ,二组之间比较差异有显著性 ( χ2 =3 37,P <0 0 5 )。bad蛋白在各组中的表达率较bcl 2表达有下降趋势 ,分别为 87 5 % ,84 2 % ,5 5 % ,4 7 91%。bcl 2、bad在各组中表达阳性率差异有显著性 ( χ2 =2 3 0 5 ,P <0 0 0 1,χ2 =11 2 9,P <0 0 1)。结论bcl 2、bad基因在乳腺癌的恶性转化中起重要作用 ;同时其表达与雌激素的调节有密切关系 ;bcl 2蛋白表达与乳腺癌淋巴结转移有关     

前列腺组织中EGF、bFGF的表达

目的：研究EGF、bFGF在前列腺组织中的表达。方法：应用mRNA斑点杂交、原位杂交、免疫组织化学及原位杂交与免疫组织化学双染法检测6例正常前列腺（NP）、27例良性前列腺增生症（BPH）前列腺组织中EGF及bFGF的表达。结果：BPH前列腺组织和NP组织中无均无EGF mRNA表达,EGF蛋白表达呈弱阳性,两组间差异无显著性意义（P＞0.05）;NP组织上皮细胞有较多bFGF mRNA表达,但无bFGF翻译,基底基质细胞有少量mRNA及蛋白表达,二者表达水平基本一致;BPH前列腺组织上皮细胞无bFGF mRNA表达,但局灶性增殖上皮细胞细胞膜上有bFGF,基底基质细胞有大量bFGF mRNA转录及蛋白质翻译,以局灶性增殖区最为明显。结论：NP及BPH的前列腺组织中无EGF分泌细胞;bFGF在前列腺基底基质细胞过度表达,以自分泌、旁分泌方式促进了基质和上皮的非均一性增殖。     

PSP94在前列腺癌和良性前列腺增生组织中的表达

目的检测前列腺分泌蛋白94（PSP94）在良性前列腺增生组织、前列腺癌组织及正常前列腺组织中的表达。方法分别从良性前列腺增生患者、前列腺癌患者及正常男性体内获取前列腺组织标本，采用免疫组化方法分析各类组织中PSP94的表达水平。结果PSP94染色阳性主要见于前列腺增生组织和正常前列腺组织的上皮细胞胞浆中及前列腺液中。与前列腺增生组织相比，前列腺癌组织标本中PSP94染色强度较低，该类标本组织前列腺液中PSP94染色阴性及弱阳性较为普遍：而在基质细胞中，前列腺增生组织和前列腺癌组织的PSP94染色均为阴性。人多数分化较差的前列腺癌组织PSP94染色为阴性或弱阳性，而相比之下大多数分化较好的前列腺癌组织PSP94染色为弱阳性或中度阳性。结论与前列腺增生组织及正常前列腺组织相比，PSP94在前列腺癌组织中表达水平较低，尤其是低分化前列腺癌。     

MUC1在甲状腺癌及甲状腺良性病变组织中的表达及意义

目的检测多态性上皮粘蛋白 (polymorphicepithelialmucin ,PEM ,又名MUC1)在甲状腺癌及甲状腺良性病变组织 (结节性甲状腺肿 ,甲状腺腺瘤 )中的表达 ,探讨其在甲状腺癌诊断和免疫治疗中的意义。方法采用免疫组化方法检测 6 8例甲状腺癌及 18例甲状腺良性病变组织、10例甲状腺正常组织中MUC1的表达。结果甲状腺癌组织中MUC1阳性表达 5 1例 ,免疫组化染色表现为胞浆内深棕色或棕黄色颗粒 ;结节性甲状腺肿 ,甲状腺腺瘤MUC1阳性表达 4例 ,甲状腺滤泡上皮腺腔缘为黄色或棕黄色颗粒 ;正常甲状腺组织中阳性表达 1例。MUC1在甲状腺癌组织中的阳性表达率与甲状腺良性病变组织及甲状腺正常组织相比 ,差异有显著性 (χ2 =17 2 0 ,P <0 0 1)。MUC1在甲状腺癌组织中阳性表达与甲状腺癌的病理类型和颈淋巴结有无转移无关 (χ2 =0 72 ,P >0 0 5 )。结论MUC1在甲状腺癌组织中的表达及其分布特点可作为甲状腺癌的鉴别诊断指标。     

细胞增殖核抗原在前列腺上皮内瘤中的表达

目的:研究细胞增殖核抗原(PCNA)在前列腺上皮内瘤(PIN)组织中的表达,探讨细胞增殖在前列腺肿瘤形成过程中的作用.方法:采用免疫组织化学方法检测12例PIN和12例良性前列腺增生(BPH)组织中PCNA的表达.结果:PIN组织中PCNA阳性细胞主要分布于腺上皮的基底细胞层与分泌细胞层,在BPH组织中主要见于腺上皮基底细胞层.PIN和BPH组织中细胞增殖指数分别为(15.92±4.40)%和(8.33±2.93)%,两组间比较差异有统计学意义(P＜0.01).结论:PIN组织中细胞增殖活性显著高于BPH,增强的细胞增殖活性参与了前列腺上皮的恶性转化,在前列腺肿瘤的发生、发展中起重要作用.     

Immunohistochemical localization of a prostatic secretory protein of 94 amino acids in normal prostatic tissue, in primary prostatic tumors and in their metastases

Using the immunoperoxidase technique, we have studied in normal, hyperplastic and adenocarcinomatous prostates the tissue localization of an abundant 94 amino acid protein secreted by prostatic epithelial cells. In normal and hyperplastic prostates, strong immunoreactivity was found exclusively in glandular epithelial cells. No reaction was observed over the stroma. In well differentiated adenocarcinoma, the acinar cells were generally stained less intensely than in benign prostatic hyperplasia while in poorly differentiated tissue, strongly positive immunoperoxidase staining was found in some cancer cells scattered in the stroma. All prostatic cancer tissues examined (N = 21), with the exception of one, exhibited at least a few positive immunoreactive areas for the 94 amino acid secretory protein. In addition, immunoperoxidase staining was observed in lung and bone marrow metastases respectively in two patients with prostatic carcinoma. All other normal tissues and non-prostatic cancers studied to date were negative. These results suggest that this new marker could be a useful addition to prostatic acid phosphatase and prostate specific antigen.     

The proliferative function of basal cells in the normal and hyperplastic human prostate

To obtain more insight into the proliferative function of basal and secretory cell types in human prostate, we studied the immunoprofile of three well-characterized proliferation-associated antigens (Ki-67, PCNA, MIB 1) in normal and hyperplastic prostate tissue. Distinction between labeled basal and secretory cell types was made by simultaneous demonstration of the proliferation-associated antigens and basal cell-specific cytokeratins in identical sections. In normal and hyperplastic acini, approximately 70% of labeled cells were of the basal cell phenotype. These data clearly suggest that the proliferative compartment of the normal and hyperplastic epithelium is located in the basal cell layer. Compared to normal and hyperplastic conditions, severe proliferative abnormalities were detected in high-grade prostate intraepithelial neoplasias (PIN), as documented by the extension of the proliferative compartment up to the luminal border. Conversely, approximately 70% of proliferating cells detected in atypical hyperplasias that progressed in invasive carcinomas were localized in the remaining basal cell layer. These findings may indicate the proliferative role of basal cells in the epithelial renewal, and the development of hyperplastic and neoplastic disorders in the human prostate. © 1994 Wiley-Liss, Inc.     

Structural changes and alteration in expression of TGF-beta1 and its receptors in prostatic intraepithelial neoplasia (PIN) in the ventral prostate of noble rats

BACKGROUND: Prostatic intraepithelial neoplasia (PIN) is the most likely pre-cancereous lesion and represents the major target for chemoprevention of prostate cancer. The multi-functional role of TGF-beta1, together with its receptors, in normal prostate and development of prostatic neoplasia remains controversial and requires further investigation. METHODS: Ventral prostates were removed from Noble rats treated with a combination of testosterone (T) and estradiol (E(2)) for various periods of time, and processed for ultrastructural examination and histopathological grading. To evaluate the role of TGF-beta1 and TGFbeta receptor types I and II in normal prostate and high-grade PIN development, expression pattern of TGF-beta1 and TGFbeta-RI and TGFbeta-RII were studied on prostate samples with PIN lesions. RESULTS: Pathologically, low-grade PIN (LGPIN) and high-grade PIN (HGPIN) were observed in ducts or alveoli after three and five months of T + E(2) treatment, respectively. EM study revealed that HGPIN cells were characterized by a reduction in abundance of secretory apparatus and the nucleus with highly irregular and undulated membrane and often with inclusion bodies although the basal lamina remained largely normal. This was associated with a high level of expression of TGF-beta1 in stromal tissue subjacent to foci of HGPIN. No definite positive reactivity of TGF-beta1 was identified in glandular epithelial cells of HGPIN. These results implicated that the major site for the TGF-beta1 production remained to be restricted to stromal compartment at the stage of HGPIN, and a paracrine regulation of TGF-beta1 might be involved in the development of HGPIN. Positive staining for the TGFbeta-RI was found in the cytoplasm of luminal epithelial cells of normal ventral prostate. The intense positive reactivity for TGFbeta-RI was also identified in prostates with HGPIN lesions. Similar expression pattern of TGFbeta-RII was also observed. CONCLUSIONS: Based on the EM study, we concluded that HGPIN in ventral prostate was accompanied with alterations in nuclear morphology together with a change in secretory activity. The over expression of TGFbeta-RI and RII in HGPIN cells as well as TGF-beta1 in stromal tissue subjacent to HGPIN implicated a growth-stimulating role instead of inhibiting role of this peptide growth factor during the early stage of prostatic neoplasia.     

Announcement

Histologic specimens of ventral and dorsolateral prostate from ACI male rats of varying ages (3, 6, 12, 18, 24, and 29–32 months) were examined to identify changes associated with the development of adenocarcinoma. The same specimens were examined immunohistochemically for their distribution of prolactin binding sites. At 3 months of age ventral lobes of these ACI rats exhibited normal histology and prolactin binding patterns. At 6 and 12 months of age most ventral prostate alveoli showed epithelial cell atrophy, along with occasional acini containing normal-looking epithelial cells. Prolactin binding activity was present in most epithelial cells at 6 months of age but disappeared from atrophied cells at 12 months of age. At 18 months of age epithelial atrophy was more advanced and devoid of prolactin binding activity while zones of epithelial cell proliferation were expanded containing populations of normal-looking cells, and cells that were either hyperplastic or dysplastic (abnormal looking), all of which were capable of binding prolactin. Older rats, 24–32 months of age, also showed prostatic adenocarcinoma in ventral prostate and these cancerous cells bound prolactin. A continuum was frequently seen between areas of normal epithelial cells, hyperplasia, dysplasia, and adenocarcinoma of ventral prostate. Morphology and prolactin binding patterns in dorsal and lateral prostates of old ACI rats were similar to young adult rats and did not contain adenocarcinoma. In conclusion, age-dependent atrophy of the ventral prostate gland of ACI rats occurs early in life and precedes adenocarcinoma. Precancerous dysplastic changes appear to arise from normal and hyperplastic epithelial cells that are capable of binding prolactin rather than those that undergo precocious atrophy and lose their prolactin binding activity. Although atrophic epithelial cells do not appear to be progenitors of prostatic cancer, the possible relationship between precocious senescence (atrophy) and adenocarcinoma in ventral prostates of ACI rats is discussed.     

Branching activity in the human prostate: a closer look at the structure of small glandular buds

OBJECTIVE: Knowledge regarding cell biologic characteristics of small solid glandular buds in the prostate and their relationship with branching activity in the human prostate is still fragmentary. Our object was to demonstrate, on the basis of immunophenotype, loci that harbor the potential for branching activity within the adult human prostate. MATERIALS AND METHODS: Semiserial sectioning was performed on 13 adult prostates in an effort to identify structures in the prostate that could be considered foci of growth. Selected slides were stained with biomarkers for basal/luminal cells (keratins), proliferation (MIB-1), apoptosis inhibitor (bcl-2), intercellular adhesion (E-cadherin), and stromal-epithelial interactions (tenascin-C). Results were compared with fetal and prepubertal human prostates and microdissected rat prostates. RESULTS: Five histologic epithelial structures were identified in 19 paraffin blocks, which on serial sectioning showed morphologic transitions with a common pattern, consisting of reduction in number and caliber of acini until small solid buds of epithelial cells were reached. Immunophenotypically, the small solid glandular buds had a basal-cell keratin phenotype, expression of bcl-2 in virtually all cells, high proliferative activity, prominent intracellular localization of E-cadherin, and enhanced periglandular tenascin-C immunoreactivity. The budding tips in fetal and prepubertal prostates revealed an immunostaining pattern identical to the small solid glandular buds in the adult, but different to the rat prostate. CONCLUSIONS: Our data suggest that dispersed small solid glandular buds have a capacity for growth, and as such may be considered foci of resumed reawakening branching activity with in the adult human prostate.     

波形蛋白、细胞角蛋白5,18,19在人胚胎前列腺发育不同阶段的表达及意义

目的 探讨波形蛋白（Vimentin），细胞角蛋白（Cytokeratin）5、18、19（CK5、18、19）在人胚胎前列腺发育不同阶段组织及细胞中的定位表达变化及其在前列腺胚胎发育中的意义。方法 应用免疫组织化学方法研究Vimentin、CK5、CK18、CK19在不同胎龄前列腺组织中的表达变化。结果 胚胎前列腺上皮细胞中波形蛋白随胎龄增大其表达呈由弱到强，又由强减弱的变化趋势；CK5和CK18的表达起初分布无规律，但是随胎龄增大，CK5和CK18逐渐分别定位表达于基底细胞层和管腔上皮细胞层；CK19则在基底细胞层和管腔上皮细胞层中均有表达，且强度较一致，基本不随胎龄增大而变化。结论 胚胎前列腺上皮细胞Vimentin的表达，可能有助于上皮细胞的游走迁移，以形成早期原始腺体。CK5、CK18以及CK19阳性细胞在原始腺体中的动态分布与胚胎前列腺上皮细胞的分化状态有关。     

人创面愈合过程中同源异形框基因的表达及意义

目的 探讨人胎儿及成人皮肤创面愈合过程中，几种同源异形框基因的表达及在胎儿无瘢痕愈合中的作用。方法 采用原位杂交方法，对正常成人和胎儿皮肤及创面愈合过程中PRX—2、H0XBl3、H0X2．2和H0X2．3的表达进行观察。结果 (1)在正常胎儿和成人皮肤中可见PRX—2阳性表达，以前阳性程度为强。分布部位有所不同，在正常胎儿皮肤中，阳性表达主要见于真皮乳头层毛干部周围细胞，表皮中也可见阳性表达；而在正常成人皮肤中，表皮基底层细胞呈弱阳性表达，真皮组织中未见阳性表达。胎儿皮肤创伤后，接近切口的组织中阳性表达明显增强，而成人皮肤创伤后，阳性表达未见明显变化，仍局限于表皮基底层细胞；(2)在正常胎儿及成人皮肤均可见H0XBl3阳性表达，真皮部分主要集中在毛囊细胞，表皮部分主要集中在基底层细胞，创伤后其表达明显减弱，尤其是胎儿皮肤；(3)在正常胎儿皮肤中H0X2．2和H0X2．3阳性表达主要见于表皮全层，表皮基底层阳性表达比较强，真皮中可见弱阳性表达，创伤后近切口的组织中，表达增强。在正常成人皮肤及其创面，未见到阳性表达。结论 同源异形框基因作为与发育生物学密切相关的基因，在人胎儿及成人皮肤创面愈合过程中的表达有所不同，这可能是二创面愈合差异的根本原因。     

胰岛素样生长因子－I mRNA在前列腺组织中的表达

对１５例良性前列腺增生（ＢＰＨ）和１２例正常前列腺组织标本中胰岛素样生长因子－Ｉ－（ＩＧＦ－Ｉ）ｍＲＮＡ的表达情况进行了研究。ＲＴ－ＰＣＲ的方法可自所有标本中检出ＩＧＦ－ＩｍＲＮＡ的表达，并用电泳和Ｓｏｕｔｈｅｒｎ杂交证实了结果的可靠性。原位杂交表明１３／１５的ＢＰＨ和９／１２的正常前列腺标本中有ＩＧＦ－ＩｍＲＮＡ表达，ＩＧＦ－Ｉ在上皮的表达强于间质，尤以基底细胞表达最明显。ＩＧＦ－ＩｍＲＮＡ在ＢＰＨ组织中的量多于正常前列腺。     

ALTERATIONS IN GAP JUNCTION PROTEIN EXPRESSION IN HUMAN BENIGN PROSTATIC HYPERPLASIA AND PROSTATE CANCER

PURPOSE: Gap junctions composed of connexin proteins have an essential role in intercellular communication and differentiation. Dysregulation of connexin expression is believed to have a role in carcinogenesis. The human prostate has been reported to express connexin 32 and 43. However, the expression pattern in prostate cancer is controversial, while to our knowledge connexin expression has not been reported in benign prostatic hyperplasia (BPH). To understand the potential involvement in prostate disease connexin 32 and 43 expression was evaluated in a series of normal prostate, BPH and prostate cancer specimens that were surgically removed due to bladder outlet obstruction. MATERIALS AND METHODS: Frozen sections of 23 normal, 43 BPH and 40 cancer involved prostates were evaluated for the presence, staining intensity and pattern of connexin 32 and 43 by immunocytochemical testing. RESULTS: In all specimens examined connexin 43 stain was punctate along the borders of the basal epithelial cells, whereas connexin 32 immunolocalized to luminal epithelial cells. In normal prostate connexin 43 and 32 were present in 87% and 65% of specimens, respectively, at low to moderate stain intensity. Importantly none of the normal samples were negative foreach connexin. In BPH specimens there was a marked increase in the incidence and intensity of connexin 43 and 32 immunostaining within epithelial cells. In addition, 23% of BPH samples showed strong connexin 43 expression in stromal cells. In contrast, connexin was decreased in prostate cancer specimens, of which 65% and 38% were negative for connexin 43 and 32, respectively, and 28% were negative for each type. In poorly differentiated tumors connexin 43 and 32 were present in only 10% and 40% of tumors, respectively, at low immunostaining intensity. CONCLUSIONS: In normal human prostate basal cells communicate via connexin 43 gap junctions, whereas luminal cells communicate via connexin 32 gap junctions. In BPH gap junctional intercellular communication is increased in epithelial and stromal cells, which may have a role in BPH pathogenesis. In prostate cancer gap junctional intercellular communication is decreased, is as indicated by decreased expression of connexin 43 and 32 with severe loss in poorly differentiated prostate cancer. These alterations in connexin expression may have a role in dedifferentiation and tumor progression.