皮脂腺肿瘤p53及blc—2蛋白表达的研究

目的 研究ｐ５３及ｂｃｌ－２基因在此脂腺肿瘤中的作用。方法 应用免疫组化方法对皮脂腺良、恶性肿瘤上述两种基因产物的表达进行了检测。结果 ５例皮脂腺癌、２你皮脂腺痣和２例皮脂腺增生症均可不同程度表达ｂｃｌ－２蛋白，而ｐ５３蛋白仅表达于５例皮脂腺癌的癌细胞。两种蛋白表达强度无相关关系（ｒ’ｓ＝０．１０５，Ｐ〉０．０５）。结论 ｐ５３基因突变在皮脂腺癌发生中起决定性作用，而ｂｃｌ－２基因则起协同促进作用     

皮脂腺肿瘤p53及bcl-2蛋白表达的研究

目的研究ｐ５３及ｂｃｌ ２基因在皮脂腺肿瘤中的作用。方法应用免疫组化方法对皮脂腺良、恶性肿瘤上述两种基因产物的表达进行了检测。结果５例皮脂腺癌、２例皮脂腺痣和２例皮脂腺增生症均不同程度表达ｂｃｌ ２蛋白,而ｐ５３蛋白仅表达于５例皮脂腺癌的癌细胞。两种蛋白表达强度无相关关系（ｒ’ｓ＝０．１０５,Ｐ＞０．０５）。结论ｐ５３基因突变在皮脂腺癌发生中起决定性作用,而ｂｃｌ ２基因则起协同促进作用。检测ｐ５３蛋白可用于鉴别皮脂腺良、恶性肿瘤。     

光线性角化病皮损细胞Bcl—2基因表达产物的定量分析

Ｂｃｌ－２蛋白是Ｂｃｌ－２基因的表达产物，可抑制细胞凋亡，在某些恶性肿瘤细胞出现过度表达。为探讨Ｂｃｌ－２蛋白与光线性角化病（ＡＫ）的关系，作者用流式细胞免疫荧光技术，检测了２７例ＡＫ。结果显示：２７例ＡＫ及正常对照的Ｂｃｌ－２蛋白相对含量ＦＩ（ＦｌｕｏｒｅｓｃｅｎｃｅＩｎｄｅｘ）分别为１．１５０±０．１８８和０．９９６±０．０６５（Ｘ－±Ｓ），０．０５＜Ｐ＜０．０１。但其中８例不典型增生严重ＡＫ的ＦＩ为１．３３５±０．０１７６（Ｘ－±Ｓ），与正常对照相比Ｐ＜０．０２。提示该病的Ｂｃｌ－２蛋白有增高的倾向。     

Bcl—2,p53在偏平苔藓病变组织中的表达

为了探讨扁平苔藓的发平同查，采用标记抗链菌卵蛋白－生物素的方法，检测了３５例扁平苔藓Ｂｃｌ－２和Ｐ５３蛋白的表达。提示Ｂｃｌ－２Ｐ５３可能是协同参与扁平苔藓病变的重要因素。     

汗腺肿瘤P53及bcl-2蛋白的表达

目的 探讨Ｐ５３和ｂｃｌ－２蛋白在汗腺肿瘤中的表达及其意义。方法 对２２例良性,恶性汗腺肿瘤Ｐ５３及ｂｃｌ－２蛋白的表达进行了免疫组化检测。结果 １０例恶性汗腺肿瘤Ｐ５３和ｂｃｌ－２蛋白表达率率显著高于良笥肿瘤（Ｘ＾２值分别为１８．３３和８．５６,Ｐ均〈０．０５５）。Ｐ５３和ｂｃｌ－２蛋白表达强度显著正相关。结论;ｐ５３基因突变和ｂｃｌ－２蛋白表达在恶性汗腺肿瘤的发生和发展中起重要促进作用。     

蕈样肉芽肿bcl—2蛋白表达的研究

目的 探讨ｂｃｌ－２蛋白在蕈样肉芽肿（ＭＦ）中的表达及其意义，方法 对１３例ＭＦｂｃｌ－２蛋白的表达进行了免疫组织化学检测，结果 ８例肿瘤细胞表达ｂｃｌ－２（＋～２＋）不同临床分期的ＭＦｂｃｌ－２蛋白阳性率之宰无显著性差异（Ｐ均〉０．０５）肿瘤细胞ｂｃｌ－２蛋白表达强度与ＭＦ临床分期不相关（Ｐ均〈０．０５）。结论 提示ｂｃｌ－２蛋白表达与ＭＦ的发生有关。     

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。     

恶性黑素瘤和良性黑素细胞肿瘤bcl-2蛋白表达

目的探讨ｂｃｌ ２蛋白在恶性黑素瘤（ＭＭ）中的表达及其意义。方法应用免疫组化方法对２４例ＭＭ的ｂｃｌ ２蛋白表达进行了检测。结果１５／２４的ＭＭ的瘤细胞阳性,且ｂｃｌ ２蛋白表达强度与ＭＭ的病理分级呈低度正相关（ｒｓ′＝０．４７１,Ｐ＜０．０５）,而良性黑素细胞肿瘤则极少表达ｂｃｌ ２蛋白。结论ｂｃｌ ２蛋白与ＭＭ的发展有关。     

凋亡抑制蛋白Bcl—2在皮肤基底细胞癌中的表达

用免疫组化方法检测了凋亡抑制基因蛋白Ｂｃｌ－２蛋白在基底细胞癌中的表达，同时分析比较了ｐ５３蛋白、Ｐａｎ－ｒａｓ蛋白和增殖细胞核抗原（ＰＣＮＡ）的表达。结果ＢＣＣ中２１／２１例Ｂｃｌ－２蛋白阳性，且几乎所有肿瘤细胞均呈阳性胞浆反应；５／１０例ｐ５３蛋白阳性，阳性细胞率小于５０％；Ｐａｎ－ｒａｓ蛋白在１０／１０例中均阴性；ＰＣＮＡ在９／１０例中阳性，但阳性细胞率小于１０％，这些表明，ＢＣＣ是一种低增     

尖锐湿疣p53及Bcl-2蛋白表达的研究

尖锐湿疣（ＣＡ）发病中的细胞增生机制至今未明了。我们研究了ＣＡ中ｐ５３及Ｂｃｌ２两种蛋白的表达，试图从细胞凋亡角度探讨其发生机制。１一般资料实验组共３１例（男性２２例，女性９例）。年龄２０～５５岁，发病后均未用药物治疗。电灼手术时取组织活检。对照组为１０名健康男性手术切除的包皮。按病理活检常规处理标本。２实验方法：超薄切片，贴于ＡＰＥＳ预处理玻片，６０℃烘烤２ｈ，常规脱蜡，在枸橼酸缓冲液中置微波炉加热１０ｍｉｎ。按ＬＳＡＢ法常规染色。第一抗稀释度分别为ｐ５３１∶８０，Ｂｃｌ２１∶５０（均为Ｄ…     

SAg作用的银屑病T细胞对表皮c-myc bcl-2及P53蛋白的影响

目的探讨链球菌超抗原与银屑病的关系,揭示银屑病患者外周血T细胞的特殊活性。方法将银屑病患者和正常人外周血T细胞及链球菌超抗原(SAg)刺激的银屑病和正常人T细胞分别与皮肤组织共同培养,免疫组化法检测不同T细胞对表皮cmyc,bcl2及P53蛋白的影响。结果正常人皮肤、银屑病患者未受累皮肤受银屑病患者T细胞作用后,表皮cmyc,bcl2及P53蛋白与正常人T细胞作用组比较有显著性差异(P均<0.05);受SAg刺激的银屑病患者T细胞对表皮cmyc,bcl2及P53蛋白的影响与未受SAg刺激组比较差异无显著性(P均>0.05),SAg非特异性活化的正常人T细胞对表皮cmyc,bcl2及P53蛋白不能产生显著影响(P均>0.05)。结论银屑病患者T细胞在外周血已处于活化状态,其活性与链球菌超抗原多克隆激活的正常人T细胞在功能上有本质区别,这一特殊的活性,可能在诱导表皮动力学紊乱及银屑病发病中发挥重要的作用。     

Analysis of apoptosis‐associated molecules Erythroid differentiation regulator 1, bcl‐2 and p53 in actinic keratosis after treatment with ingenol mebutate

Actinic keratosis (AK) is the most common cutaneous premalignant neoplasm precursor of malignant skin tumors. The aberrant apoptotic pathway is thought to be associated with pathogenesis of AK. Ingenol mebutate has been shown to be effective and safe for treatment of AK. However, the effect of ingenol mebutate on apoptosis‐related molecules using human skin samples has not been studied well. Erythroid differentiation regulator 1 (Erdr1) was recently reported to play a crucial role in malignant skin cancers like malignant melanoma. The role of Erdr1 in premalignant actinic keratosis (AK) has not been explored. The purpose of this study was to investigate whether the expression of apoptosis‐associated molecules such as Erdr1, p53 and bcl‐2 was affected by the treatment of ingenol mebutate in AK. Nine patients with AK underwent skin biopsy at baseline and 8 weeks after treatment with ingenol mebutate for immunohistochemical evaluation with Erdr1, p53 and bcl‐2. In addition, skin samples from five control subjects were retrieved. Upregulation of Erdr1 and a significant decrease in expression of p53 and bcl‐2 were observed after treatment with ingenol mebutate. Ingenol mebutate treatment for AK resulted in the modulation of apoptosis‐associated molecules with an increase in the expression of Erdr1 and a decrease in the expression of p53 and bcl‐2.     

Use of proliferation rate, p53 staining and perforating elastic fibers in distinguishing keratoacanthoma from hypertrophic lichen planus: a pilot study

Background: Distinguishing keratoacanthoma (KA) and hypertrophic lichen planus (LP) histopathologically can be difficult, and the challenge is compounded by the tendency of KA to arise in association with hypertrophic LP. Methods: In this pilot study, we compared 18 cases each of KA and hypertrophic LP for proliferation index (MIB‐1), p53 staining and the presence of perforating elastic fibers (elastic Verhoeff‐van Gieson) to determine the utility of these staining modalities in distinguishing KA from hypertrophic LP. Results: Proliferation index in KA compared to hypertrophic LP is 88.2 (mean positive MIB‐1 cells/×100 field), SD = 56.6 and 47.3, SD = 68.4, respectively. p53 staining in KA compared to hypertrophic LP is 251 (mean positive cells/×100 field), SD = 117 and 158, SD = 119, respectively. Fifteen of eighteen (83%) keratoacanthomata demonstrate perforating elastic fibers compared to 1/18 (6%) for hypertrophic LP. Conclusion: Proliferation index is not significantly different between KA and hypertrophic LP (p = 0.059). Expression of p53 is increased in KA over hypertrophic LP (p = 0.024). The presence of perforating elastic fibers in KA is significantly different from hypertrophic LP (p < 0.0001) and suggests that elastic Verhoeff‐van Gieson staining may be of practical benefit in distinguishing KA from hypertrophic LP in difficult cases. Bowen AR, Burt L, Boucher K, Tristani‐Firouzi P, Florell SR. Use of proliferation rate, p53 staining and perforating elastic fibers in the distinction of keratoacanthoma and hypertrophic lichen planus: a pilot study.     

银屑病皮损中细胞凋亡的原位标记检测与bcl-2的表达

目的　探讨细胞凋亡与银屑病发病的关系。方法　用末端脱氧核苷酰转移酶 (Td T)介导的 d- U TP-生物素缺口末端标记技术 (TUNEL ) ,原位检测了银屑病皮损的凋亡角朊细胞 ,应用免疫过氧化酶技术研究了正常人皮肤与银屑病皮损的 p5 3蛋白、增殖细胞核抗原 (PCNA)和 bcl- 2的表达。结果银屑病表皮各层中 ,大量角朊细胞呈现出细胞凋亡的形态学和生化特征。基底层及表皮中下部各层大量角朊细胞 PCNA染色强阳性 ,基底层中 bcl- 2阳性细胞明显减少。结论　在银屑病皮损中角朊细胞凋亡增加 ,推测可能是针对细胞过度增殖的一种稳态机理     

Expression of apoptosis regulatory proteins p53, bcl-2 and bax in recurrent aphthous ulceration

Background Recurrent aphthous ulceration (RAU) is considered to be an acute inflammatory disease of unknown pathogenesis. Apoptosis may represent an important event in the control of inflammation. Objectives The aim of this study was to investigate apoptosis process in RAU using immunohistochemistry. Methods We studied the expression and location of p53, bcl‐2 and bax in ulcerated lesions clinically diagnosed as RAU (n = 12) and compared it with that of oral clinically normal mucosa (n = 6) and of other inflammatory chronic disease such as oral fibrous inflammatory hyperplasia (FIH; n = 18). Results Significant statistically differences (n < 0.05) in p53 expression were noticed in RAU when compared with normal mucosa. No significant statistically differences (P > 0.05) were noticed between FIH and RAU. Bcl‐2 and bax did not show remarkable differences between groups. Conclusions Taken together, the data suggest that RAU induces p53 immunoexpression. Therefore, the protein might be related to the aetiopathogenesis of the ulcerated oral lesions.     

皮肤鳞状细胞癌的细胞凋亡及某些凋亡相关基因产物的表达

目的观察皮肤鳞状细胞癌（ＳＣＣ）的细胞凋亡及ｐ５３、ｂｃｌ ２、Ｂａｘ和Ｆａｓ蛋白的表达。方法采用ＴＵＮＥＬ法和免疫组化染色。结果在２２例ＳＣＣ病变组织中,均可见到细胞凋亡,分化差、核分裂像多的ＳＣＣ中凋亡细胞较多,而分化好、核分裂像少的ＳＣＣ中则凋亡细胞少。在２７例ＳＣＣ中,１６例ｐ５３阳性表达,１４例ｂｃｌ ２阳性,１９例Ｂａｘ阳性,６例Ｆａｓ阳性。结论ＳＣＣ的发生与细胞凋亡及某些凋亡相关基因产物的异常表达有关。     

Analysis of p53 and bcl-2 protein expression in the non-tumorigenic, pretumorigenic, and tumorigenic keratinocytic hyperproliferative lesions

BACKGROUND: The hyperproliferative keratinocytic lesions encompass a wide range of non-tumorigenic, pretumorigenic, and tumorigenic conditions. The aim of this work was to examine the expression patterns of apoptosis-linked molecules (bcl-2 and p53) in these lesions. METHODS: Immunoperoxidase staining methods were applied to analyze p53 and bcl-2 protein expression in a total of 66 cases, including 12 squamous cell carcinomas (both in situ and invasive SCC), 11 actinic keratoses (AK), 13 psoriasis vulgaris (PV), eight verruca vulgaris (VV), six chronic dermatitis (CD), five seborrheic keratosis (SK), four lichen planus (LP), three epidermodysplasia verruciformis (EDV), two condyloma acuminata (CA), two lichen simplex chronicus (LSC), and 10 specimens from normal skin. RESULTS: As compared to normal skin (0.70 +/- 0.26), the bcl-2 average weighted scores in the non-tumorigenic (0.76 +/- 0.16), pretumorigenic (1.45 +/- 0.28), and tumorigenic lesions (2.83 +/- 0.50 and 2.92 +/- 0.50 for in situ and invasive SCC, respectively) showed significant up-regulation (p = 0.001). In the non-tumorigenic lesions, the bcl-2 expression values decreased in the following order: SK > EDV > CD > LP > CA > PV > VV (1.40 +/- 0.24 > 1.33 +/- 0.67 > 0.83 +/- 0.40 > 0.67 +/- 0.21 > 0.50 +/- 0.20 > 0.46 +/- 0.22 > 0.13 +/- 0.01, respectively). As compared to normal skin (1.10 +/- 0.23), the p53 average weighted scores in the non-tumorigenic (1.86 +/- 0.18), pretumorigenic (3.64 +/- 0.53), and tumorigenic lesions (5.00 +/- 1.00 and 5.08 +/- 0.86 for in situ and invasive SCC, respectively) showed significant up-regulation (p = 0.021). In the non-tumorigenic lesions, p53 average weighted scores decreased in the following order: SK > PV > CA > LP > CD > VV > EDV (3.20 +/- 0.49 > 2.38 +/- 0.27 > 2.0 +/- 0.0 > 1.83 +/- 0.48 > 1.0 +/- 0.37 > 1.0 +/- 0.33 > 1.0 +/- 0.0, respectively). There was a positive correlation between bcl-2 and p53 protein expression in normal skin (r = 0.966, p = 0.0001), non-tumorigenic (r = 0.775, p = 0.0001), pretumorigenic (r = 0.830, p = 0.001), and tumorigenic lesions (r = 0.757, p = 0.003). CONCLUSIONS: Bcl-2 and p53 proteins are altered in the keratinocytic hyperproliferative lesions. Determination of whether these alterations reflect underlying gene mutations will require further investigations.     

狼疮性肾炎患者肾组织bcl-2 c-myc P53的表达

为探讨凋亡相关基因产物ｂｃｌ－２、ｃ－ｍｙｃ、Ｐ５３在狼疮性肾炎患者肾组织中的表达情况，用卵白素生物素酶复合物法（ＡＢＣ法）对５例狼疮性肾炎病人和３例正常同龄对照肾组织标本进行了免疫组化检测。结果表明：ｂｃｌ ２和ｃ ｍｙｃ在狼疮性肾炎肾组织中均明显高表达（Ｐ＜０．０１），表达部位在肾小球系膜细胞和肾小管上皮细胞。Ｐ５３表达较弱，且与正常无明显差别。结果提示ｂｃｌ ２和ｃ ｍｙｃ在狼疮性肾炎肾组织中的异常高表达可能抑制肾组织细胞的正常凋亡并促进其增殖，从而参与狼疮性肾炎的发病，可能是狼疮性肾炎发病机制之一