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1.
目的:研究子宫内膜癌组织中p14^ARE。和p53的表达及意义。方法:采用免疫组化LSAB法,检测118例子宫内膜癌及30例正常宫内膜组织中p14^ARE及p53的表达。结果:p14^ARE。阴性、弱阳性、中度阳性和强阳性表达率在子宫内膜癌中分别为25.4%(30/118)、38.1%(45/118)、14.4%(17/118)和22.0%(26/118),与正常内膜0(0/30)、56.7%(17/30)、33.3%(10/30)和10.0%(3/30)相比差异有统计学意义,P〈0.001,子宫内膜癌中p14^ARE。表达缺失的比例高于正常宫内膜;p14^ARE表达水平与手术病理分期、宫颈间质受累和淋巴结转移相关;与病理分级、组织学类型和肌层侵犯深度无关;不同p14^ARE表达水平患者生存率差异无统计学意义,P=0.5781。p53阴性、弱阳性、中度阳性和强阳性表达率在子宫内膜癌中分别为13.6%(16/118)、40.1%(48/118)、28.0%(33/118)和17.8%(21/118);与正常内膜相比分别为36.7%(11/30)、36.7%(11/30)、16.2%(5/30)和10.0%(3/30)差异有统计学意义,P=0.01.子宫内膜癌中p53阳性表达的比例高于正常宫内膜;p53表达与肿瘤分期、盆腔淋巴结转移和肌层侵犯深度相关,与病理分级、组织学类型和宫颈间质受累无关;不同p53表达水平患者生存率差异无统计学意义,P=0.4166;在子宫内膜癌组织中p14^ARE。与p53表达呈负相关,r=-0.243,P=0.008。结论:p14^ARE和p53异常表达与子宫内膜癌发生密切相关,但对其预后的影响有待进一步的研究。 相似文献
2.
目的探讨缺氧情况下子宫内膜癌组织血管形成的机制。方法免疫组织化学sP法检测46例子宫内膜腺癌及对照组16例子宫内膜复杂性增生伴不典型增生、12例子宫内膜单纯性增生组织中缺氧诱导因子-1α(HIF-1α)、血管内皮生长因子(VEGF)及p53的表达,同时测定微血管密度(MVD)值,分析其相关性。结果HIF-1α、VEGF、p53在子宫内膜癌组织中阳性表达率分别为52.17%(24/46)、73.90%(34/46)、47.80%(22/46)明显高于对照组,子宫内膜癌组织中HIF-1α、VEGF及p53的表达与手术病理分期和肌层浸润程度无关,而与肿瘤病理分级呈正相关(r=0.479,r=0.43,r=0.470,均P〈0.01)。子宫内膜癌组织中HIF.10I的表达与VEGF、p53表达以及MVD值之间呈正相关(r=0.734,r=0.713,r=0.831,均P=0.000)。结论子宫内膜癌组织中存在HIF-1α、p53、VEGF过表达,且与子宫内膜癌的发生、发展有关。HIF-1α通过调节VEGF的表达在子宫内膜癌组织血管形成中发挥重要作用。HIF-1α和p53缺失或突变可能协同参与了缺氧对子宫内膜癌细胞的调节。 相似文献
3.
PTEN和p53蛋白在子宫内膜癌组织中的表达及临床意义 总被引:5,自引:1,他引:4
目的:探讨PTEN和p53蛋白在子宫内膜癌组织中的表达及其在癌发生发展中的作用。方法:应用免疫组化方法检测40例子宫内膜癌组织和23例正常子宫内膜组织中PTEN和p53蛋白的表达,观察二者与子宫内膜癌临床病理学参数的关系,分析其在肿瘤发生发展中的作用。结果:40例子宫内膜癌组织中,PTEN阳性表达率为52.5%(21/40),与全部为阳性表达的正常子宫内膜相比,子宫内膜癌中PTEN表达明显下降,χ^2=15.643,P〈0.01。PTEN蛋白表达与子宫内膜癌的分化程度、临床分期、病理类型、肌层是否浸润及有无淋巴结转移均无关,P均〉0.05。在正常子宫内膜组织中未见p53阳性染色,而在内膜癌组织中17.5%(7/40)染色呈阳性。p53蛋白的表达与肿瘤分化程度有关,随着分化程度下降,表达增加。在子宫内膜癌中,PTEN和p53蛋白的表达具有相关性,χ^2=4.969,P=0.026。结论:与正常子宫内膜相比,子宫内膜癌中PTEN表达明显下降;p53则随着肿瘤细胞分化程度下降而表达增加。PTEN和p53在子宫内膜癌的发生发展过程中,发挥着重要作用。 相似文献
4.
子宫内膜增生及癌变组织中增殖细胞核抗原与p16和p53基因表达的相关性研究 总被引:1,自引:0,他引:1
目的探讨增殖细胞核抗原(PCNA)及基因p16、p53在单纯性子宫内膜增生(ESH)、子宫内膜不典型增生(EAH)和子宫内膜癌(EC)组织中表达情况。方法应用免疫组化法分别对26例EC、28例EAH、24例ESH组织进行PCNA和p16、p53基因蛋白定位及表达程度检测,并对比其差异,分析它们之间的关系。结果PCNA在ESH、EAH和EC3组病例中强阳性表达分别为16.7%、82.1%和96.2%,ESH与EAH、EC比较差异有统计学意义(P〈0.01),而EAH与EC比较差异无统计学意义(P〉0.05)。p16在ESH、EAH和EC3组病例中阳性表达分别为95.8%、46.4%和50.0%,ESH与EAH、Ec组比较差异有统计学意义(P〈0.05);EAH与EC组比较差异无统计学意义(P〉0.05)。p53在ESH组无阳性表达病例,EAH组阳性率25%,EC组阳性率65.4%,3组病例之间比较差异均有统计学意义(P〈0.01)。结论PCNA、p53表达在子宫内膜增殖性病变、细胞恶性转化的进程中呈递增趋势,而p16趋于递减,提示细胞的过度增殖和增殖-凋亡相关基因的表达失衡在子宫内膜恶性转化过程中起重要作用。PCNA、p16和p53的异常表达可作为子宫内膜增生性疾病不同发展阶段的诊断及预测其生物学行为的参考指标。 相似文献
5.
目的:探讨肿瘤坏死因子相关凋亡诱导配体(TRAIL)受体DR5、DcR1在子宫内膜癌中的表达及临床意义。方法:采用免疫组化Elivision^TM plus法检测DR5、DcR1在10例正常子宫内膜、12例增生性子宫内膜及42例子宫内膜癌中的表达。结果:子宫内膜癌中DR5的阳性表达率为36/42(85.71%),明显高于正常子宫内膜3/10(30.00%),(P〈0.01)。正常子宫内膜中DcR1的阳性表达率为100.00%,明显高于子宫内膜癌19/42(45.24%),(P〈0.01)。在子宫内膜癌中,DR5的阳性表达与病理分级及肌层浸润呈反比。结论:子宫内膜癌中DR5的高表达使TRAIL用于子宫内膜癌的治疗在理论上具有可行性;子宫内膜癌中DcR1的表达可能导致TRAIL诱导的凋亡耐受。 相似文献
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目的:研究子宫内膜组织中PTEN、p16蛋白的异常表达,探讨其与子宫内膜癌变的关系和早期诊断及评判预后的可能性。方法:应用免疫组化S—P法对20例正常子宫内膜组织、40例子宫内膜增生症组织、30例内膜腺癌组织中PTEN、p16蛋白的表达进行研究。结果:在正常增生期子宫内膜、子宫内膜增生症(单纯型增生、复杂型增生、不典型增生)、子宫内膜腺癌组织中PTENp16蛋白的阳性表达率呈递减趋势,子宫内膜腺癌与除不典型增生外的子宫内膜增生症组织及正常子宫内膜组织的glEN蛋白表达差异有显著性(P〈0.05),正常子宫内膜、单纯型增生与不典型增生组织的PTEN蛋白表达差异有显著性(P〈0.05),子宫内膜腺癌与正常子宫内膜及单纯型增生子宫内膜p16蛋白表达差异有显著性(P〈0.05),正常子宫内膜与增生症子宫内膜差异无显著性(P〉0.05)增生症子宫内膜各组间p16蛋白表达无显著性差异(P〉0.05),PTENP16蛋白的表达与子宫内膜癌的手术分期、组织学分级,肌层浸润有关(P〈0.05)。PTEN、p16蛋白表达存在正相关性(r=0.978,P〈0.05)。结论:PTEN、p16蛋白的异常表达与子宫内膜的癌变过程相关。 相似文献
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细胞周期抑制蛋白p16^INK4a在宫颈病变中的异常表达 总被引:1,自引:0,他引:1
[目的]探讨宫颈癌(UCC)、宫颈上皮内瘤变(CIN)及宫颈炎中p16^INK4a蛋白表达水平的变化及意义。[方法]应用免疫组化方法检测126例宫颈病变(UCC50例、CIN57例和宫颈炎19例)组织中p16^INK4a蛋白的表达,进行半定量分析及统计学检验。[结果]50例UCC中,p16^INK4a全部阳性表达;57例CIN中,p16^INK4a阳性表达41例,阳性表达率为71.93%,其中CIN Ⅰ,CINⅡ,CINⅢ p16^INK4a阳性表达率分别为36.84%(7/19)、81.82%(18/22)、100.00%(16/16),且三者间差异有显著性(P〈0.05)。19例宫颈炎组织中,p16^INK4a阳性表达8例,阳性表达率为42.11%。p16^INK4a蛋白在宫颈炎、CIN和UCC组织中表达水平依次升高,且差异有显著性(P〈0.05)。[结论]UCC及癌前病变中p16^INK4a阳性表达明显高于良性病变。p16^INK4a在UCC及癌前病变中过表达,提示其在UCC发生、发展中起重要作用。 相似文献
8.
目的:探讨PTEN和CyclinA在子宫内膜癌中的表达及其在癌发生发展中的作用。方法:采用免疫组化SP法检测PTEN和CyclinA蛋白在30例正常子宫内膜、30例子宫内膜增生、20例子宫内膜不典型性增生、55例子宫内膜癌组织中的表达。结果:不典型增生组和子宫内膜癌组中PTEN阳性表达率分别为55.00%(11/20)、45.45%(25/55),与全部为阳性表达的正常内膜及阳性表达率为90.00%(27/30)的子宫内膜增生组比较,不典型增生组和癌组中PTEN阳性表达均显著低于正常子宫内膜和子宫内膜增生组(P〈0.05)。CyclinA在不典型增生组和癌组中阳性表达率分别为45.00%(9/20)、67.27%(37/55),显著高于全部阴性表达的正常子宫内膜组和子宫内膜增生组(10.00%,3/30)(P〈0.05)。两者在不典型增生和子宫内膜癌组中的表达均呈显著性负相关(r=-0.5330,r=-0.5556;P〈0.001)。癌组中PTEN阳性表达的缺失与组织学分级有关(P〈0.05),但与肿瘤的浸润转移、临床分期和复发无关(P〉0.05);CyclinA的阳性表达率与组织学分级、肿瘤的浸润转移和临床分期、复发有关。结论:PTEN表达缺失和CyclinA的过度表达涉及子宫内膜癌的发生、发展过程,二者联合检测可作为子宫内膜癌早期诊断、判断肿瘤生物学行为的免疫学指标。 相似文献
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[目的]探讨宫颈癌(UCC)、宫颈上皮内瘤变(CIN)及宫颈炎中p16^INK4a蛋白表达水平的变化及意义。[方法]应用免疫组化方法检测126例宫颈病变(UCC50例、CIN57例和宫颈炎19例)组织中p16^INK4a蛋白的表达,进行半定量分析及统计学检验。[结果]50例UCC中,p16^INK4a全部阳性表达;57例CIN中,p16^INK4a阳性表达41例,阳性表达率为71.93%,其中CIN Ⅰ,CINⅡ,CINⅢ p16^INK4a阳性表达率分别为36.84%(7/19)、81.82%(18/22)、100.00%(16/16),且三者间差异有显著性(P〈0.05)。19例宫颈炎组织中,p16^INK4a阳性表达8例,阳性表达率为42.11%。p16^INK4a蛋白在宫颈炎、CIN和UCC组织中表达水平依次升高,且差异有显著性(P〈0.05)。[结论]UCC及癌前病变中p16^INK4a阳性表达明显高于良性病变。p16^INK4a在UCC及癌前病变中过表达,提示其在UCC发生、发展中起重要作用。 相似文献
10.
目的:探讨p33^ING1、p53在结直肠癌中的表达及其相互关系。方法:应用免疫组化SP法检测60例结直肠癌组织及相应正常黏膜组织中p33^ING1、p53的表达。结果:结直肠癌组织、相应正常黏膜组织中p33^ING1蛋白的阳性表达率分别为43.3%(26/60)、100%(60/60)(P〈O.01),p53蛋白分别为51.6%(31/60)、0%(0/60)。p33^ING1在无淋巴结转移组及淋巴结转移组癌组织中的阳性表达率分别为57.6%(19/33)、25.9%(7/27)(P〈0.05);在DukesA、B期、Dukes C、D期病例中分别为56.7%(17/30)、30.0%(9/30)(P〈0.05)。在p53表达阴性的29例中有12例(41.4%,12/29)p33^ING1表达缺失,而p53阳性的31例病例中有22例(71.0%,22/31)p33^ING1表达阴性(P〈0.05),在p53蛋白表达阳性的病例中p33^ING1蛋白表达明显缺失,两者表达呈负相关。结论:p33^ING1在结直肠癌组织中低表达,与p53互相协同,在结直肠癌的发生、发展中可能起重要作用。 相似文献
11.
目的:探讨p16基因家族失活与白血病发生、发展及预后的关系。方法:PCR检测p16、p15、p18、p19基因在白血病中纯合子缺失。结果:p16、p15基因外显子1在AL组纯合子缺失率分别为22.37%、17.05%,在ALL组为45.95%、32.43%,在ANLL组均为5.88%;在CML的慢性期均为0。p16、p15基因外显子2在AL组纯合子缺失率分别为12.5%、5.68%;在ALL组为24.32%、10.81%;在ANLL组为3.92%、1.96%;在CML和对照组二者均无缺失。p18、p19基因外显子1在AL组纯合子缺失率分别为1.14%、0;在ALL组分别为2.70%、0;在ANLL和对照组均无缺失。结论:p16、p15基因纯合子缺失在AL的发生频率较高,ALL缺失率明显高于ANLL,复发一LLL组基因失活率最高。p16、p15基因纯合子缺失是AL,尤其是ALL的发病重要因素之一。p18、p19基因在AL组中几乎未见纯合子缺失。在ALL中,p16纯合子缺失率高于p15纯合子缺失率。两个基因的纯合子缺失常伴随存在。在ANLL中,p16、p15基因的纯合子缺失均少见。 相似文献
12.
p29ING4 and p28ING5 bind to p53 and p300, and enhance p53 activity 总被引:21,自引:0,他引:21
Shiseki M Nagashima M Pedeux RM Kitahama-Shiseki M Miura K Okamura S Onogi H Higashimoto Y Appella E Yokota J Harris CC 《Cancer research》2003,63(10):2373-2378
We identified and characterized two new ING family genes, p29ING4 and p28ING5,coding for two proteins of 249 and 240 amino acids, respectively. Both p29ING4 and p28ING5 proteins have a plant homeodomain finger motif also found in other ING proteins, and which is common in proteins involved in chromatin remodeling. p29ING4 or p28ING5 overexpression resulted in a diminished colony-forming efficiency, a decreased cell population in S phase, and the induction of apoptosis in a p53-dependent manner. Both p29ING4 and p28ING5 activate the p21/waf1 promoter, and induce p21/WAF1 expression. p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically interact with p300, a member of histone acetyl transferase complexes, and p53 in vivo. These results indicate that p29ING4 and p28ING5 may be significant modulators of p53 function. 相似文献
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目的 研究INK4系列抑癌基因纯合子缺失、甲基化与白血病预后的关系。方法 采用聚合酶链反应(PCR)研究p16基因家族在白血病中纯合子缺失,应用甲基化敏感限制内切酶HpaⅡ结合PCR技术研究白血病患者p16、p15、p18、p19 基因甲基化状况,用单因素、多因素Logistic回归分析其基因失活与急性白血病(AL)预后的关系。结果 基因表达组治疗有效27例(84.38 %),基因失活组治疗有效11例(28.95 %),基因表达组治疗有效率明显高于基因失活组(P<0.001)。单因素、多因素Logistic回归分析结果显示p16、p15 基因失活化疗有效率明显低于基因表达组。结论 p16、p15基因失活可作为AL病程进展、复发、预后的指标之一。 相似文献
15.
NBP is the p53 homolog p63 总被引:7,自引:0,他引:7
We previously identified a non-p53, p53-responsive DNA element (p53RE)-binding protein named NBP, functionally analogous to p53, from human cervical carcinoma Hela cells. Here we report a biochemical study demonstrating that this activity is the recently cloned p53 analog p63. NBP was purified through conventional and DNA affinity chromatography to apparent homogeneity with a prominent polypeptide migrating in between the 43 and 68 kDa positions on a SDS gel. This polypeptide immunoreacted with monoclonal anti-p63 but not anti-p53 or anti-p73 antibodies. Also, NBP co-purified with p63 through each step of fractionation, as detected with anti-p63 antibodies. DNA-protein complexes formed with purified NBP and p53RE-containing oligomers derived from the p21(waf1) promoter were supershifted by anti-p63 but not anti-p53 antibodies. Thus, these results demonstrate that NBP is encoded by the p53 homolog p63 gene. 相似文献
16.
Mice lacking both p18(Ink4c) and p27(Kip1) develop a tumor spectrum similar to pRb(+/-) mice, and loss of p53 function accelerates tumorigenesis in pRb(+/-) mice. We hypothesized that codeletion of either p18 or p27 in conjunction with p53 deletion will also accelerate tumorigenesis. Mice lacking both p18 and p53 develop several tumors not reported in either single null genotype, including hepatocellular carcinoma, testicular choriocarcinoma, hemangiosarcoma, leiomyosarcoma, fibrosarcoma, and osteosarcoma. Mice lacking both p27 and p53 exhibit a decreased lifespan and develop unique tumors, including papillary carcinoma of the colon, hemangiosarcoma, and leiomyosarcoma. In both p18/p53 and p27/p53 double null genotypes, the incidence and spectra of tissues that develop lymphoma are also increased, as compared to the single null genotypes. The development of p27/p53 double null colon tumors correlates with secondary changes in cell-cycle protein expression and CDK (cyclin-dependent kinase) activity, perhaps contributing to the progression of colorectal cancer. We concluded that p18 and p27 can, not only functionally collaborate with one another, but also can independently collaborate with p53 to modulate the cell cycle and suppress tumorigenesis in a tissue-specific manner. 相似文献
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18.
Shujing Zhang Sumio Endo Hisashi Koga Tomio Ichikawa Xuelian Feng Kiyoshi Onda Kazuo Washiyama Toshiro Kumanishi 《Cancer science》1996,87(9):900-907
A total of 10 glioma cell lines were examined for alterations of the p16, p15, p53 and p21 genes, which are tumor suppressor genes or candidates with direct or indirect CDK-inhibitory functions. Genetic alterations (deletions or mutations) were frequently seen in the p16, p15 and p53 genes in these cell lines, but not in the p21 gene. When the states of the p16, p15 and p53 genes were compared among cell lines, all the cell lines showed abnormalities in at least 1 gene, often in 2 or 3 genes coincidentally, suggesting that dysfunction of these genes is closely related to glioma cell growth. Although alteration of all 3 genes was most frequent, there were cell lines having either p16/p15 or p53 or p16 and p53 gene alterations, suggesting that the time order of these genetic alterations was variable depending on the cell line. Among cell lines examined, one with homozygous p53 gene deletion seemed of particular practical value, since such a cell line might be useful in various studies, including investigation of the functions of various mutant p53 genes in the absence of heteromeric protein formation. On examination of the primary tumor tissues, the same alterations of the p16/p15 and p53 genes as detected in the cell lines were demonstrated in all 6 cases examined: p16/p15 gene deletion in 1, p16 gene mutation in 1 and p53 gene mutations in 5 cases. This suggested that the p16/p15 and the p53 gene alterations and their combinations in at least some glioma cell lines reflected those in the primary glioma tissues. 相似文献
19.
Abstract p53, mutated in over half of human cancers and about 13% of all hematological malignancies, maintains genomic integrity and triggers cellular senescence and apoptosis of damaged cells. In contrast to p53, the homologs p73 and p63 play critical roles in development of the central nervous system and skin/limbs, respectively. Moreover, dependent on the context they can exert tumor suppressor activities that cooperate with p53. Unlike p53, p73 and p63 are rarely mutated in cancers. Instead, up-regulation of the anti-apoptotic dominant-negative ΔNp73 and ΔNp63 isoforms is the most frequent abnormality in solid cancers. In hematological malignancies the most frequent p73 defect is promoter methylation and loss of expression, associated with unfavorable clinical outcomes. This suggests an essential tumor suppressor role of p73 in blood cells, also supported by genetic mouse models. Many therapeutic approaches aiming to restore p73 activity are currently being investigated. In contrast, the most frequent p63 abnormality is protein overexpression, associated with higher disease grade and poorer prognosis. Surprisingly, although available data are still scarce, the emerging picture is up-regulation of transactivation-competent TAp63 isoforms, suggesting a tumor-promoting role in this context. 相似文献
20.