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1.
探讨大肠腺癌突变型P53基因蛋白表达与P53基因cDNA突变间的相互关系和意义。方法对100例新鲜大肠腺癌组织采用PAb240单克隆抗体免疫组织化学染色检测突变型P53基因蛋白表达、RT-PCR-SSCP检测P53基因cDNA突变,并比较它们间相互关系。 相似文献
2.
p53基因蛋白在大肠腺癌中表达的病理学意义*1季晨阳2季丹3DuncanRSmith3Hak-SuGoh野生型p53基因蛋白是抑癌基因蛋白,可以调控细胞生长、分化和DNA修复并促进凋亡〔1,2〕。在发生肿瘤时,p53基因失活(突变、杂合性丢失),不但... 相似文献
3.
应用一非同位素PCR-SSCP方法检测常规石蜡包埋乳腺癌组织中p53基因点突变。结果显示60例乳腺癌中,14例有异常电泳带,表明这些病例相应DNA片段中发生了点突变,其中4例位于第5~6外显子,3例位于第7外显子,7例位于第8外显子。免疫组化法检测突变型p53蛋白的表达,13例为阳性,其中11例SSCP检测到异常电泳带,另2例突变可能发生在所检测的基因片段以外。而5例SSCP分析发现基因突变者,免疫染色却为阴性,主要可能由于石蜡包埋组织中p53抗原性减弱或消失所致,因此,SSCP法检测p53基因点突变更为准确、可靠,而且可初步将突变定位在基因某一片段。本研究结果表明非同位素PCR-SSCP是一简便、快速、有效的检测基因点突变的方法,特别适用于对大量标本基因点突变的筛选;p53基因点突变与突变型p53蛋白免疫染色阳性呈相关关系,但并不完全吻合。 相似文献
4.
免疫组化和PCR—SSCP检测p53基因异常的一致性探讨 总被引:1,自引:0,他引:1
目的:探讨免疫组化检测p53蛋白表达和PCR-SSCP检测p53基因突变的一致性。方法:单克隆抗体DO-7检测85例非小细胞肺癌(NSCLC)的p53蛋白表达,PCR-SSCP检测其中31例腺癌的p53基因突变。结果:85例NSCLC中p53蛋白表达阳性率为68%(58/85),31例腺癌中p53蛋白表达阳性率为61%(19/31),14例(46%)出现p53基因5~8外显子突变,p53蛋白免疫组化和PCR-SSCP检测p53基因突变无显著相关(χ2=0.1,P=0.76),其一致率为52%。结论:p53蛋白表达并不能很好地反映p53基因突变。 相似文献
5.
肺癌中MTS1/p16和p53基因产物的表达与细胞增殖的关系 总被引:3,自引:0,他引:3
目的:研究肺癌中MTS1/p16和p53基因产物的表达与细胞增殖的关系。方法:应用S-P免疫组织化学方法研究62例肺癌组织中p16蛋白和p53蛋白的表达情况,并进行增殖细胞核抗原(PCNA)检测,计算细胞增殖指数(proliferationindex,PI)。结果:62例肺癌组织中p16蛋白和p53蛋白阳性率分别为58.1%和59.7%。腺癌p16蛋白的阳性率明显高于小细胞癌(P<0.05);淋巴结转移阳性组p16蛋白的表达显著低于阴性组(P<0.05);PI分级为Ⅱ级的p16蛋白表达显著高于Ⅳ级(P<0.05)。不同组织类型肺癌中p53蛋白的表达未见明显差异,淋巴结转移阳性组p53蛋白的表达高于阴性组(P<0.01);不同PI分级中p53蛋白的表达,Ⅳ级明显高于Ⅰ级(P<0.05)和Ⅱ级(P<0.05),Ⅲ级明显高于Ⅰ级(P<0.05)和Ⅱ级(P<0.01)。p16蛋白低表达和p53蛋白过表达之间未见明显相关。结论:p16蛋白低表达和p53蛋白过表达均有促进肺癌细胞增殖的作用,p16蛋白的表达与肺癌的细胞分化有关,p53蛋白过表达对肺癌细胞的转移起重要作用。抑癌基因p53对MTS1/p16基因无明显调控作 相似文献
6.
DukesC期大肠癌原发灶与淋巴结转移灶中p53基因突变的比较 总被引:3,自引:0,他引:3
目的探讨大肠癌转移与p53基因突变的关系。方法用PCR-SSCP检测73例DukesC期大肠癌及40例相应的淋巴结转移灶p53基因第5至第9外显子的突变。结果73例原发灶有27例(37%),40例淋巴结转移灶中有19例(47.5%)检测到p53基因突变,总突变率为44%。在原发灶和转移灶同时检测的40例中,有21例(52.5%)两者均未见p53突变;另12例(30%)两者均可见完全相同的突变条带;余下的7例(17.5%)两者PCR-SSCP的结果不一致。这7例经DNA直接测序确定了p53基因突变位点。其中5例原发灶未见p53突变,而转移灶p53有明确突变;7例中2例转移灶可见p53有二个外显子突变,而原发灶仅一个或无突变点。结论多数p53基因突变发生在转移之前并持续存在于大肠癌进展至转移的整个时期,大肠癌的转移可伴有p53基因的新突变,或转移对p53基因突变有一定选择,提示p53基因突变可能与大肠癌转移相关。 相似文献
7.
用免疫组化方法观察45例大肠腺瘤和61例大肠腺癌中bc1-2和p53蛋白的表达。结果显示:正常大肠粘膜中bc1-2和p53均未见表达,而大肠腺瘤及大肠腺癌阳性率均较正常组织明显增加(P<0.01).大肠腺瘤中bc1-2表达位于不典型增生较重区域。大肠腺瘤p53表达随腺瘤直径增加而增加,其中≥20mm组阳性率显著高于<10mm组(p<0.05)。p53蛋白阳性率也随不典型增生程度增加而增高。p53表达与大肠腺癌分化程度及Dukes分期有关。大肠腺瘤中bc1-2和p53蛋白的表达呈负相关。结果表明,bc1-2蛋白表达对大肠腺瘤的增殖有一定意义,p53在大肠腺瘤癌变和大肠腺癌进展中起重要作用。 相似文献
8.
c-erbB-2、p53、bcl-2和nm23-H1在肺癌中的表达 总被引:5,自引:0,他引:5
目的:探讨cerbB2、p53、bcl2和nm23H1基因在肺癌发生发展过程中的作用。方法:用免疫组化ABC法对原发性肺癌组织中4种基因的表达和突变进行检测。结果:58例肺癌中,31例(5345%)p53过度表达,18例(3103%)bcl2过度表达。cerbB2与nm23H1在10例小细胞肺癌(SCLC)中未见表达。而在48例非小细胞肺癌(NSCLCs)中两者过度表达率均为50%。cerbB2与nm23H1表达呈正相关(P<005)。腺癌nm23H1的表达明显高于鳞癌(P<005)。p53、bcl2蛋白表达在肺癌分化程度中呈负相关(P<005)。nm23H1、p53和bcl2的表达与患者的生存率有关(P<005)。结论:cerbB2、p53、bcl2和nm23H1基因蛋白产物的检测对肺癌患者的诊治和预后评估有积极意义。 相似文献
9.
目的探讨p53基因与化学致癌剂诱发小鼠皮肤肿瘤的关系。方法运用PCRSSCP和直接DNA测序法,检测37例DMBATPAMNNG诱发的小鼠皮肤肿瘤[包括6例乳头状瘤,15例高分化鳞状细胞癌(SCCI)和16例中分化鳞状细胞癌(SCCⅡ)]中,p53基因第5~8外显子的序列改变。结果乳头状瘤均未见p53基因突变,而258%(8/31例)SCC测得突变,其中SCCⅠ和SCCⅡ突变率分别为266%(4/15例)和25%(4/16例)。在这8例肿瘤中共有9个突变,其中7个位于第8外显子,有7个为G→A转换。结论p53基因突变发生于该三步化学致癌法诱发的小鼠皮肤乳头状瘤向SCC恶性转化过程中。 相似文献
10.
p53基因与溃疡性结肠炎 总被引:1,自引:0,他引:1
徐三荣 《国际病理科学与临床杂志》1997,17(3):209-212
野生型p53蛋白具有抗细胞增殖功能,它可使DNA有损伤的细胞生长停止于G1/G0期。散发性结直肠癌p53基因中常见点突变发生,发生于溃疡性结肠炎基础上的结直肠癌(UCACRC)亦有很高的p53基因突变率。另一等位基因的杂合性缺失(p53LOH)的发生也增高,加强溃疡性结肠炎病人p53基因点突变和p53LOH的研究,可为监测UCACRC的形成提供新方法。 相似文献
11.
L. Kaklamanis K. C. Gatter N. Mortensen R. J. Baigrie A. Heryet D. P. Lane A. L. Harris 《The American journal of pathology》1993,142(1):87-93
To assess the expression of p53 in premalignant lesions, we examined by immunohistochemistry benign colorectal adenomas (n = 72, measuring more than 6 mm and less than 95 mm in diameter) from patients without (group I, n = 23) or with (group II, n = 49) concurrent sporadic colorectal carcinomas. Using a panel of three monoclonal antibodies (PAb 240, PAb 421, PAb 1801) and two polyclonal antibodies (CM1, C19) immunohistological staining was demonstrated in 26% of the cases (19 of 72 adenomas, 7 of 23 from group I and 12 of 49 from group II). In the majority of the cases, p53 positive foci in the adenomas occurred in the most dysplastic areas, although focal positivity was detected in glands that were histologically normal. Expression of p53 protein was also detected in 21 of 30 (70%) colorectal carcinomas of group II. In two cases focal positive staining was observed in the polyps but not in the concurrent carcinomas. Non-neoplastic colonic mucosa and stromal lymphoid cells were negative in all cases examined. Over-expression of p53 in neoplastic tissues detected by immunocytochemistry is generally believed to correlate with the presence of mutation in the gene. This may not be an absolute rule, because in some hemopoietic malignancies, there is evidence that p53 protein may be detectable in the absence of an underlying mutation. These findings therefore represent the highest incidence in colorectal adenomas of abnormalities in the p53 protein expression, probably largely due to underlying mutations. This study also suggests that immunocytochemical demonstration of p53 protein may be a suitable method for the routine detection of subpopulations of cells which, by clonal expansion, could acquire a growth advantage within an adenoma during the neoplastic process. 相似文献
12.
Ten cases of hepatoblastoma were studies for overexpression of p53 protein by immunohistochemistry and for possible p53 gene mutation by single strand conformation polymorphism (SSCP) analysis and direct DNA sequencing of the polymerase chain reaction products. Only one case of the macrotrabecular type at stage IV showed overexpression of p53 protein. No DNA mobility shift was found in any of the cases studies by SSCP analysis. DNA sequencing performed on the case showing overexpression of p53 protein revealed no mutation within exons 5 to 8. The associated adrenal cortical carcinoma of the same case also showed overexpression of p53 protein, but no mutation of the p53 gene. These results indicate that mutation of the p53 gene is infrequent in hepatoblastoma. This observation supports the view that mutation of the p53 gene is not as important in the oncogenesis of childhood neoplasms as in adult cancers. 相似文献
13.
骨肉瘤患者p53基因的改变及其与预后的关系 总被引:3,自引:0,他引:3
目的:研究人骨肉瘤中p53蛋白表达及P53基因突变及其与预后的关系。方法:免疫组织化学染色观察人骨肉瘤中P53蛋白表达,银染PCR-SSC民埋从瘤中P53基因5-8外显子点突变状态。预后分析用Kaplan-Meier生存曲线及Logrank时序检验。结果:人骨肉瘤中P53蛋白阳性率为29.17%,SSCP检测P53基因5-8外显子占突变率为23.96%,P53蛋主SSC生患者与其阴性患者间总和生存 相似文献
14.
G. Chemeris A. Rempel P. Bannasch A. Loktinov M. Schwarz 《Virchows Archiv : an international journal of pathology》1995,426(6):563-569
P53 tumour suppressor gene expression was estimated immunohistochemically using DO-1 monoclonal antibody (recognising both wild-type and mutant p53) in 88 human renal tumours. Single strand conformation polymorphism (SSCP) analysis of possible mutations within exons 4–8 of the p53 gene was performed in 29 of the tumours (mostly immunostaining-positive cases). Obviously elevated p53 content was detected with DO-1 antibody in chromophobic cell carcinomas and most clear/chromophilic cell tumours (in chromophilic cell populations). In contrast, clear cell carcinomas demonstrated either complete absence of p53 expression or the presence of single immunopositive nuclei. Oncocytomas were completely negative. Additional immunostaining of the positive samples with mutant p53-specific Pab240 monoclonal antibody failed to detect immunopositive material. No p53 mutation was found in any of the samples analysed by SSCP. Our results suggest that the elevated p53 content in human renal cell carcinomas does not result from gene mutation and that p53 gene alterations are probably not an important mechanism in the development of human renal cell carcinomas. Accumulation of the wild-type p53 protein may be a useful prognostic marker indicating neoplastic progression and malignancy. 相似文献
15.
目的:观察大肠癌组织p14ARF基因遗 传和表观遗传变化及p53基因突变状况,探讨两者改变的关系及p14ARF-p53通路功能 破坏在大肠癌发生中的作用。方法:应用PCR、直接测序、甲基化特异PC R和RT-PCR分别检测56例原发性大肠癌及相应癌旁正常组织p14ARF基因纯合性缺失、 突变、5′CpG岛甲基化、mRNA表达及p53基因突变状况。结果:①大肠 癌组织p14ARF总变异率为27% (15/56),其中1例纯合性缺失,14例5′CpG岛甲基化,未见突变发生。②15例p14ARF基因变异的大肠癌组织其相应mRNA表达阴性(13例)或 低水平表达(2例),41例未发生基因变异的大肠癌组织和所有癌旁正常组织p14ARF mRNA均显示明显表达。③大肠癌组织p53突变率为48% (27/56)。④56例大肠癌组织中,12例 仅发生p14ARF变异,24例仅显示p53突变,3例同时有p14ARF 5′CpG岛甲基化 和p53突变,17例p14ARF和p53均无变异,p14ARF-p53通路总变异率为70%(39/ 56),p14ARF 5′CpG岛高甲基化与野生型p53状态有关(P<0.05)。⑤低分化 腺癌组p14ARF变异率(44%,7/16)明显高于高中分化腺癌组(20%,8/40)(P< 0.05),但两组间p53突变率无显著差异(P>0.05)。结论:①大肠癌p14ARF基因5′ CpG岛高甲基化是其表达失活的主要机制;②大肠癌p14 ARF基因高甲基化与p53基因突变可能是相互独立的事件,两者的失活可能各自出现于不同 的大肠癌亚组中;③p14ARF高甲基化或p53突变引起的p14ARF-p53通路功能 破坏在大肠癌的发生中具有重要作用。 相似文献
16.
Takashi Oka Ashit Baran Sarker Norihiro Teramoto Tadashi Yoshino Tadaatsu Akagi 《Pathology international》1998,48(1):15-21
Accumulation of the p53 protein has been found In several types of lymphomas. However, p53 gene mutations have been infrequently demonstrated in some specific types of lymphomas. In the present study, a correlation between p53 immunoreactivity and p53 gene mutations in a large panel of non-Hodgkin's lymphoma (NHL) cases is attempted. A panel of 202 cases of NHL was evaluated by immuno-hlstochemical staining for p53 protein. All cases that were immunohistochemically positive for p53 protein were analyzed by the polymerase chain reaction (PCR) single strand conformation polymorphism (SSCP) method to identify mutations within the pS3 gene. In order to confirm the mutation, sequencing of PCR-amplified p53 gene segments was performed. Overexpression of p53 protein was found in 59 of the 202 cases of NHL, but only four of these 59 cases showed a shift on SSCP analysis, and point mutations were detected in three of them by the subsequent sequencing. p53 Immunoreactivity was generally greater in high-grade lymphoma. The results of this study suggest that Immunohistochemlcal reactivity for p53 protein is not a reliable Indicator of the presence of their structural alterations of p53 gene exons 4–9 in NHL. 相似文献
17.
18.
The relationship between the mutation of the p53 gene and the expression of the p53 protein and the Ki-67 antigen has been investigated in 115 cases with non-Hodgkin's lymphoma, using the immunohistochemical double staining technique, single-strand conformational polymorphism and DNA sequencing methods. Eighteen cases showed more than 10% of p53+ cells and the others showed a few p53+ cells presented sporadically. Alterations in the p53 gene were detected in six cases with B cell type, consisting of five cases with point mutation and one case with point mutation and 15 base pairs deletion. These six cases showed a high percentage of p53+ cells and five cases revealed that the percentage of p53+ cells was higher than that of Ki-67+ cells (p53+ cells > Ki-67+ cells). Excluding the six cases with mutation of the p53 gene, all cases revealed that the percentage of p53+ cells was less than that of Ki-67+ cells (p53+ cells < Ki-67+ cells). Moreover, there was a positive correlation between expression of the p53 protein and of the Ki-67 antigen in histologic types of B cell lymphomas and of T cell lymphomas, respectively, except in small non-cleaved (Burkitt's) and lymphoblastic types. Therefore, sporadic cases showing p53+ cells > Ki-67+ cells revealed alteration of the p53 gene, and expressed abnormal p53 protein (mutant form). Most cases showing p53+ cells < Ki-67+ cells expressed normal p53 protein (wild type), and may reflect the rapid proliferation rate. 相似文献
19.
Five antibodies directed against the whole or part of p53 protein have been used to detect the protein immunohistochemically in 70 infiltrating breast carcinomas and 10 ductal carcinomas in situ. Mutations are known to occur in different conserved domains, and the antibodies employed spanned the expected sites. p53 protein was identified in 53 per cent of infiltrating carcinomas using the antibodies PAb 240, PAb 1801, C19, and JG8. The antibody PAb 421 detected the protein in 31.5 per cent; all positive with the other antibodies. Well-differentiated oestrogen receptor-positive tumours had a low incidence of p53 detection. Variation in the percentage of reactivity was seen between carcinomas and in some cases between different antibodies in the same cancer. Those carcinomas with a high percentage of positive cells with all antibodies were more likely to have metastasized to nodes, be at an advanced stage, and be oestrogen receptor-negative/epidermal growth factor receptor-positive. There was no significant correlation with c-erbB-2 protein expression or retinoblastoma protein loss. p53 protein was detected in a high proportion of cells in three of the six comedo ductal carcinomas in situ studied but either not at all or at a lower level in tumours of the cribriform type. p53 mutations are common in breast carcinomas, but heterogeneity within individual tumours is frequent. Marked expression of p53 appears to relate to tumour progression. 相似文献
20.
Ⅲ期鼻咽癌p53蛋白表达与生物学行为及预后的关系及其与p53基因突变、潜伏膜蛋白-1表达的相关研究 总被引:16,自引:0,他引:16
目的:探讨Ⅲ期鼻咽分化型非角化性鳞癌中P53蛋白的表达与生物学行为及预后的关系,以及P53蛋白表达与P53基因突变和潜伏膜蛋白(LMP)-1蛋白表达的关系。方法:应用免疫组织化学EnVison法和聚合酶链反应-单链构象多态性分析(PCR-SSCP)检测58Ⅲ例鼻咽分化型非角化性鳞癌标本。结果:58份Ⅲ期鼻咽分化型非角化性鳞癌中,P53蛋白总阳性率为65.5%(3858),生存期在5年以下的患者阳性率为82.1%(32/39),5年以上患者31.6%(6/19),两组间P53蛋白表达差异有显著性意义(P<0.05),P53蛋白表达在有预底侵袭组为74.4%(29/39),无颅底侵袭组为47.4%(919),两组间差异有显著性意义(P<0.05),PCR-SSCP检测15例P53蛋白阳性的病例,P53基因5-8外显子突变率为0(0/15),LMP-1蛋白免疫组织化学总阳性率为72.4%(42/58),与P53蛋白表达呈正相关关系(r=0.504)。结论:本组Ⅲ期鼻咽分化型非角化性鳞癌患者中P53蛋白表达与P53基因突变无相关关系。与LMP-1蛋白的表达相关,P53蛋白的表达阳性率随着患者生存期的延长而降低,有颅底侵袭组P53蛋白表达阳性率高于无颅底侵袭组。 相似文献