Ki-67、PCNA在银屑病和扁平苔藓皮损中的表达

目的 研究Ki-67和增殖细胞核抗原(PCNA)在银屑病和扁平苔藓皮损处表达的一致性.方法 应用免疫组化法检测扁平苔藓和银屑病患者皮损处Ki-67及PCNA表达.结果 Ki-67在扁平苔藓和银屑病皮损处呈阳性表达,PCNA在扁平苔藓和银屑病皮损处呈强阳性表达,PCNA阳性细胞百分率较Ki-67高(P<0.001),两者在银屑病和扁平苔藓皮损处表达的一致性较差(k=0.08).结论 Ki-67和PCNA在银屑病和扁平苔藓皮损处表达一致性差,可能Ki-67比PCNA更具有特异性.     

转化生长因子α和p53基因在生殖器疣与癌中的表达

目的：探讨ｐ５３、ＴＧＦα及其受体ＥＧＦＲ在生殖器癌发生发展中的作用。方法：采用免疫组化方法检测上述基因在生殖器疣与癌中的表达。结果：生殖器癌中ｐ５３、ＴＧＦα及ＥＧＦＲ的阳性表达率分别为６３．３％（１９／３０）、９３．３％（２８／３０）和９０％（２７／３０），均非常显著高于生殖器疣。同时检测２３例癌中ＴＧＦα和ｐ５３蛋白之表达，显示２例ＴＧＦα阴性的病例，ｐ５３蛋白也未检测到。５例ＴＧＦα低表达者，其中４例ｐ５３阴性。ＥＧＦＲ和ｐ５３表达情况无明显关系。结论：提示ｐ５３、ＴＧＦα可能与生殖器癌的发生相关。     

蕈样肉芽肿的bcl-2、p53和PCNA的蛋白表达

采用免疫组化技术检测３４例蕈样肉芽肿（ＭＦ）中ｂｃｌ－２、ｐ５３和增殖细胞核抗原（ＰＣＮＡ）的蛋白表达。结果发现ｂｃｌ－２蛋白表达于大部分标本;ｐ５３蛋白表达于６０％的肿瘤期ＭＦ、２１％的斑块期ＭＦ和０％的斑片期ＭＦ;１００％的肿瘤期ＭＦ、３８％的斑块期ＭＦ和０％的斑片期ＭＦ的ＰＣＮＡ呈中或强阳性表达。表明ＰＣＮＡ和ｐ５３均与ＭＦ的恶性程度有关,对评估ＭＦ的临床生物学行为有一定的意义。     

EGF－R PCNA及P53基因在银屑病皮损中的表达

用ＥＧＦ－Ｒ、ＰＣＮＡ及Ｐ５３抗体和ＬＢＳＡ方法观察了４３例寻常性银屑病患者表皮及１２例正常皮肤。结果发现ＥＧＦ－Ｒ及ＰＣＮＡ表达明显增强，除基底层细胞外，棘层及颗粒层也有明显表达，个别病例角质层仍有少量表达。提示银屑病患者皮损处细胞增殖及分化调控紊乱。还发现银屑病患者皮损及皮损周未受累皮肤中无Ｐ５３的表达。     

EGF－R PCNA及P53基因在银屑病皮损中的表达

用ＥＧＦ－Ｒ、ＰＣＮＡ及Ｐ５３抗体和ＬＢＳＡ方法观察了４３例寻常性银屑病患者表皮及１２例正常皮肤。结果发现ＥＧＦ－Ｒ及ＰＣＮＡ表达明显增强，除基底层细胞外，棘层及颗粒层也有明显表达，个别病例角质层仍有少量表达。提示银屑病患者皮损处细胞增殖及分化调控紊乱。还发现银屑病患者皮损及皮损周未受累皮肤中无Ｐ５３的表达。     

PCNA、P21和COX-2在尖锐湿疣中的表达及其意义

目的：研究尖锐湿疣组织中增殖细胞核抗原（PCNA）、P21及环氧化酶-2（COX-2）蛋白表达及其意义。方法：应用免疫组化SP法对30例尖锐湿疣组织及10例正常组织中PCNA、P21及COX-2蛋白进行检测。结果：30例尖锐湿疣组织中PCNA、P21阳性表达较正常对照组有不同程度的增加，有统计学意义；COX-2蛋白在尖锐湿疣组织中阳性表达率13．3％（4／30），正常组织无阳性表达（0／10），两者之间无显著性差异（P〉0．05）；尖锐湿疣组织中PCNA与P21表达之间无相关性（r=0．196，P〉0．05）。结论：PCNA、P21过表达与尖锐湿疣角质形成细胞自限性增殖密切相关。     

p21与p53蛋白在银屑病皮损中的表达

银屑病是一种皮肤表皮细胞良性增生性疾病,其发病机理仍不清楚。近年来发现ras基因和p53基因与肿瘤细胞的增生有关[1～3]。为探讨ras基因和p53基因与银屑病皮损发生、发展的关系,我们分别对13例银屑病患者皮损内ras基因表达的p21蛋白和p53基因表达的p53蛋白进行了免疫组化研究。一、病例和方法1.病例资料:随机选择1996年5～12月门诊就诊的13例进行期斑块状银屑病患者,其中男8例,女5例;年龄19～50岁;病程半年至10年。诊断依据临床表现及组织病理学检查。4例正常人对照来自皮肤外伤患者创口周边外观正常皮肤。2.试剂:鼠抗人多克隆p21抗体、鼠…     

皮肤鳞状细胞癌分级与p53蛋白和增殖细胞核抗原表达及与巨噬细…

免疫组织化学法检测５０例皮肤鳞状细胞癌组织标本中ｐ５３蛋白，增殖细胞核抗原（ＰＣＮＡ）的表达及其癌间质中巨噬细胞反应，在原位客观地观察癌细胞增殖活性，间质巨噬细胞反应与癌分化、分级的关系。结果表明本组病例ｐ５３蛋白检出率为５６％，各级癌中ｐ５３蛋白阳性检出率无显著性差异，但ｐ５３蛋白阳性这细胞数与癌分级呈正相关。癌中ＰＣＮＡ阳性率为１００％，阳性细胞数与癌分级也呈正相关。癌中ｐ５３蛋白表达与ＰＣＮ     

生殖器上皮HPV感染皮损中p53蛋白过度表达的检测

采用免疫组化方法对６例鲍温样丘疹病和９例尖锐湿疣生殖器上皮人类乳头瘤病毒（ＨＰＶ）感染皮损进行了ｐ５３蛋白、ｐ２１蛋白和增殖细胞核抗原（ＰＣＮＡ）表达的检测。结果ｐ５３阳性率为：鲍温样丘疹病（３／６）、尖锐湿疣（６／９），ｐ５３阳性细胞多位于基底层以及棘细胞层的中下层，同时发现受ＨＰＶ感染的空泡样变性细胞核中有ｐ５３蛋白和ＰＣＮＡ的过度表达，说明ｐ５３蛋白表达与ＨＰＶ感染及角朊细胞异常增生有关。     

P53 PCNA K-i67 bcl-2在尖锐湿疣中的表达

目的　探讨尖锐湿疣 (CA)中P5 3、Ki 6 7、bcl 2、增殖细胞核抗原 (PCNA)表达与人乳头瘤病毒 (HPV )感染的关系。方法　用免疫组化方法对 40例CA和 10例正常包皮进行检测。结果　 40例CA中P5 3、Ki 6 7、bcl 2、PCNA阳性标本分别为 33例 ( 82 .5 % )、37例 ( 92 .5 % )、2 0例 ( 5 0 .0 % )、35例 ( 87.5 % )。CA组各种蛋白的表达强度均明显高于对照组 (P <0 .0 5 )。HPV感染的空泡细胞核中同时有P5 3、Ki 6 7、PCNA过度表达者 2 5例。P5 3、bcl 2阳性细胞多分布于基底层、棘细胞中下层。结论　CA中存在P5 3、Ki 6 7、PCNA、bcl 2过度表达 ,提示角质形成细胞异常增生与HPV感染有关。     

绞股蓝皂苷对光损伤BALB/c小鼠皮肤p53、p21蛋白表达的影响

目的 探讨绞股蓝皂苷（GP）抗光损伤的作用机制。方法 80只雌性BALB/c小鼠随机分为8组,每组10只,分别为：空白对照组（未加任何处理）、UVB模型组、GP组Ⅰ（先涂GP后照UVB）、GP组Ⅱ（先照UVB后涂GP）、维生素E组Ⅰ（先涂维生素E乳膏后照UVB）、维生素E组Ⅱ（先照UVB后涂维生素E乳膏）、基质组Ⅰ（先涂基质后照UVB）、基质组Ⅱ（先照UVB后涂基质）。中波紫外线（UVB）照射BALB/c小鼠建立光损伤模型,根据以上分组对光损伤小鼠皮肤进行干预。运用蛋白Western印迹法检测各组小鼠表皮中p53蛋白、p21蛋白的表达。结果 BALB/c小鼠表皮p53蛋白的表达：空白组p53蛋白（0.11 ± 0.08）与UVB模型组（0.22 ± 0.12）相比低表达,GP组Ⅰ（0.44 ± 0.23）高于空白组（P < 0.01）,GP组Ⅱ（0.48 ± 0.24）高于空白组（P < 0.01）及UVB模型组（P < 0.05）,维生素E组Ⅰ（0.49 ± 0.29）及维生素E组Ⅱ（0.50 ± 0.27）均与GP组作用相似。小鼠表皮p21蛋白的表达各组间差异无统计学意义。结论 1.5% GP乳膏抗光损伤的作用机制之一可能与上调表皮细胞中p53蛋白表达量有关。     

The effect of ultraviolet (UV) A1, UVB and solar-simulated radiation on p53 activation and p21

BACKGROUND: High-dose ultraviolet (UV) A1 therapy (doses in the order of 130 J cm(-2)) is effective for atopic dermatitis and scleroderma. UVA1 has been shown to induce a dose-dependent increase in p53 expression in keratinocytes. OBJECTIVES: To examine the effect of UVA1 on the activation of p53 by phosphorylation, which has not yet been studied. METHODS: Five adult volunteers were exposed to dose series of UVA1 (10-100 J cm(-2)) and, for comparison, narrowband UVB (TL-01) (25-550 mJ cm(-2)) and solar-simulated radiation (SSR) (5.6-30 J cm(-2)) on photoprotected buttock skin and the minimal erythema dose (MED) for each was determined at 24 h. Separate sites on the buttock were subsequently irradiated with a 3-MED dose of UVA1, TL-01 and SSR. At 24 h, punch biopsies (4 mm) were taken from each irradiated site and from an adjacent unirradiated control site, and immunohistochemical staining for p53 (Do-1), activation of p53 (assessed by phosphorylation at serine 15 and serine 392) and p21 was performed. Cell staining was expressed as the mean number of cells stained per three high-power fields (HPFs) and as a percentage of 1000 cells. Sunburn cells (SBCs) were also counted per HPF. RESULTS: UVA1 produced negligible numbers of SBCs, relatively little p53 (Do-1) staining (mean +/- SD cell count per HPF 16 +/- 10), no p53 activation and very little evidence of p21 expression (mean +/- SD cell count per HPF 5.3 +/- 7), in contrast to TL-01 (mean +/- SD cell count per HPF of 11.83 +/- 2.1 SBCs, 146.3 +/- 38 for Do-1, 26.6 +/- 15 for serine 15, 14.9 +/- 12 for serine 392 and 77.9 +/- 30 for p21) or SSR irradiation (mean +/- SD cell count per HPF of 3.5 +/- 1.2 SBCs, 147.5 +/- 62 for Do-1, 54 +/- 50 for serine 15, 38.9 +/- 18 for serine 392 and 56.7 +/- 30 for p21). CONCLUSIONS: These data indicate that there are fundamental differences in the effects of UVA1 on p53 and its activation pathways compared with TL-01 and SSR, and may in part explain the differential effects of these phototherapies.     

p53、增殖细胞核抗原和Bcl-2在皮肤外毛根鞘癌中的表达

目的 探索外毛根鞘癌的临床病理学特征及p53、增殖细胞核抗原(PCNA)和Bcl-2的表达与意义。方法 应用HE染色观察和免疫组化S-P方法检测22例外毛根鞘癌p53、PCNA和Bcl-2蛋白表达。结果 22例外毛根鞘癌患者中女15例,男7例,年龄40~79岁,发生于头顶枕部皮肤16例。免疫组化标记结果显示:p53阳性表达为72%(16/22),阳性分布广泛;PCNA全部阳性,但阳性细胞在高中低分化中呈递增趋势;Bcl-2阳性为63%,在各级之间表达差异有显著性(P<0.01)。结论 分叶状结构和骤然角化是外毛根鞘癌的组织学特征;p53、PCNA、Bcl-2在外毛根鞘癌均有不同程度的表达,参与肿瘤发生发展和生长调控。     

Expression of PCNA is associated with the presence of HPV DNA in skin warts

A series of 90 excised cutaneous warts (verrucae vulgaris) were studied for the presence of HPV (human papillomavirus) DNA using in situ hybridization (ISH) with biotinylated full genomic DNA probes of HPV types 1, 2, 3 and 4. The expression of PCNA (proliferating cell nuclear antigen) was examined using conventional immunohistochemistry. The aim was to test the hypothesis that HPV can reactivate PCNA, including in the host replication machinery. HPV DNA of the above types was detected in 60 of 90 verruca biopsies studied (66.7%): HPV 2 in 56 cases, HPV 1 in 2 cases, and HPV 3 in 2 cases. PCNA was expressed in all samples except two. The signal distribution of HPV DNA markedly differed from that of PCNA expression. ISH revealed strong HPV DNA signals in both the granular and the upper spinous cell layers, the most intense signals being detected in the upper epidermis. On the other hand, nuclear PCNA staining was present in the majority of parabasal and basal cells. Although strong PCNA signals within the wart lesions were found in the areas where HPV DNA was present, the PCNA positivity was almost invariably localized in the differentiated cells of the spinous cell layers, just below the HPV DNA-expressing cells. At the margins of the lesions, PCNA expression was still strong but disappeared abruptly towards the normal epidermis. HPV DNA-positive warts showed more intense expression of PCNA than did the HPV DNA-negative ones in this study. Our results indicate that PCNA induction is associated with the presence of HPV DNA, suggesting that HPV can reactivate PCNA, thus interfering with the host cell DNA replication machinery. Received: 8 May 1996