Effects of p53 overexpression on neoplastic cell mitosis and apoptosis in nasopharyngeal carcinoma

p53 gene alteration is an important molecular event in tumourigenesis of many malignancies.[1] However, the mutation rate of p53 gene in nasopharyngeal carcinoma (NPC) is lower.[2] The PCR-SSCP performed by FU Mao-fu et al. in the authors' lab in 1994 demonstrated that there were only 4 specimens showing aberrant shift in 18 NPCs (22.2%)--one in exon 5, three in exon 8.[3] On another aspect, the p53 overexpression rate almost reached about 80%.[4,5] It is well known that because the half…     

胸腺癌中p53蛋白过表达对癌细胞增殖和凋亡的影响

目的：探讨胸腺癌中ｐ５３蛋白过表达对癌细胞增殖和凋亡的影响。方法：收集手术切除的胸腺标本２０例,用抗ｐ５３蛋白（ＤＡＫＯ ＤＯ－７）和抗增殖细胞核抗原（ＰＣＮＡ,ＤＡＫＯ ｃｌｏｎｅ ＰＣ１０）的单抗,采用ＬｓＡＢ免疫组化法染色。以平均每１００个癌细胞中ｐ５３阳性细胞数为ｐ５３表达率,阳性ｐ５３蛋白细胞数超过２０％者称为ｐ５３蛋白过表达。以平均每１００个癌细胞中ＰＣＮＡ阳性细胞数为增殖指数（ｐｒｏ     

鼻咽癌中p53蛋白积聚对瘤细胞有丝分裂和凋亡的影响

目的：观察疗前鼻咽癌组织中Ｐ５３蛋白的积聚及其对瘤细胞有丝分裂和凋亡的影响。方法随机收集１９９７年疗前鼻咽癌活检标本４３例,采用免疫组化ＬＳＡＢ法ＤＯ－７一抗检测Ｐ５３蛋白的表达。在Ｈ＆Ｅ染色切片上位细胞死亡试剂盒检测瘤细胞凋亡,平均每个高倍视野下的凋亡瘤细胞数为凋亡指数（ＴＵＮＥＬ ｉｎｄｅｘ,Ｔ１）。比较高于位细胞死亡试剂盒检测瘤细胞凋亡,平均每个高倍视野下的细胞瘤细胞数为凋亡指数（ＴＵＮＥＬ     

p150 overexpression in gastric carcinoma: the association with p53, apoptosis and cell proliferation

To clarify the significance of p150 expression, 102 gastric carcinomas were immunohistochemically investigated and 14 fresh samples of the cancer were analyzed with the immunoblot method. Tumor cell apoptosis was assessed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-digoxigenin nick end labeling (TUNEL). Both Ki-67 antigen and p53 expression were analyzed immunohistochemically. Eighty-six out of 102 (85%) gastric cancers stained positively for p150. All 14 tumors analyzed by Western blotting overexpressed p150. Statistical analysis revealed a close association between p150 overexpression and the clinicopathologic parameters of gastric cancer. All well-differentiated cancers showed high p150 expression (p < 0.005). Furthermore, high p150 expression was more frequently seen in tumors at early invasive stages (p < 0.005), in tumors without metastases (both local and distant, p < 0.005) and in early TNM stages (p < 0.005) in general. As we have found for cervix and esophagus carcinoma, when tumors progress to high malignancy and metastasis, p150 begins to regress and then breaks down. A good correlation of p150 expression, but not p53 expression, with tumor cell apoptosis could be demonstrated (p < 0.01). The Ki-67 labeling index, i.e., the index for a proliferative marker, showed no correlation with either p150 or p53 expression. The results suggest that p150 may be a new early tumor marker for gastric carcinoma similar to that for esophagus and cervix carcinoma.     

沉默信息调节因子过表达或谷氨酰胺剥夺对肾透明细胞癌细胞凋亡、增殖的影响

背景与目的：肾透明细胞癌（clear cell renal cell carcinoma,ccRCC）是最常见的肾癌类型,它与代谢密切相关。探讨沉默信息调节因子4（silent information regulator 4,SIRT4）过表达或谷氨酰胺（glutamine,Gln）剥夺对ccRCC细胞增殖、凋亡的影响。方法：慢病毒构建SIRT4和突变体H161Y过表达的Caki-2细胞株,利用无Gln的培养基来构建Gln剥夺模型,并通过体外增殖活力实验［细胞计数试剂盒-8（cell counting kit-8,CCK-8）］和克隆形成实验来分析两者对Caki-2细胞增殖和生长能力的影响;利用DCFH-DA荧光探针检测细胞内活性氧自由基（reactive oxygen species,ROS）水平进而评估Gln代谢对细胞ROS含量的影响;进一步通过线粒体膜电位检测、凋亡检测和蛋白质印迹法（Western blot）检测凋亡相关分子,分析SIRT4过表达以及Gln剥夺对Caki-2细胞凋亡的影响。结果：过表达SIRT4可抑制Gln代谢从而抑制Caki-2细胞增殖,另外还原性物质还原型烟酰胺腺嘌呤二核苷酸磷酸（reduced nicotinamide adenine dinucleotide phostate,NADPH）的生成减少能够增加细胞内ROS含量,促进细胞凋亡。而Gln剥夺抑制细胞增殖和促进细胞凋亡的效果均比过表达SIRT4明显,但长期缺乏Gln将导致细胞无法生长。结论：无论是过表达SIRT4还是Gln剥夺均能抑制ccRCC细胞增殖,促进凋亡。     

PNCK对鼻咽癌细胞增殖和凋亡作用的研究

目的 研究妊娠上调的非泛素性钙调蛋白激酶(Pregnancy-upregulated nonubiquitous calmodulin kinase,PNCK)在鼻咽癌组织中的表达以及对鼻咽癌细胞增殖和凋亡的作用。方法 采用免疫组织化学方法检测鼻咽癌癌组织和正常组织中PNCK表达水平。构建慢病毒载体干扰PNCK基因表达,并采用Real time PCR和免疫印迹结果证实,采用MTT方法、流式细胞术、Caspase3和Caspase7活性检测鼻咽癌肿瘤细胞增殖和凋亡的变化。结果 免疫组织化学结果显示PNCK蛋白在鼻咽癌癌组织中呈特异性高表达。Real time PCR和免疫印迹结果证实慢病毒成功干扰鼻咽癌CNE-2Z细胞中PNCK表达(PNCK基因在mRNA和蛋白水平表达受到显著抑制)。MTT检测结果显示抑制PNCK表达抑制CNE-2Z细胞增殖。此外,干扰PNCK表达引起CNE-2Z细胞Caspase3和Caspase7活性上升,流式细胞术表明干扰PNCK基因表达可以促进CNE-2Z细胞凋亡。结论 干扰PNCK基因表达抑制鼻咽癌细胞增殖并诱导肿瘤细胞凋亡,可能是治疗鼻咽癌的潜在靶点。     

EFFECT OF ADENOVIRUS—MEDIATED p53 GENE TRANSFER ON APOPTOSIS AND RADIOSENSITIVITY OF HUMAN

To evaluate the effect of adenovirus-mediated p53 gene(Adp53) on apoptosis and radiosensitivity of human gastric carcinoma cell lines.Methods:Recombinant adenovirus expressing wild-type p53 lines with different p53 genetic status.p53 protein expression was detected by immunohistochemistry assay and western blot assay.Cell survival was assessed using a clonogenic assay.TUNEL assay was used in determination of apoptosis.Four human gastric carcinoma cells infected with Adp53 were irradiated with 4Gy and cell cycle distribution and Sub-G1 peak were assayed by flow cytometry.Results:G2/M arrest,apoptosis and inhibition of tumor cell proliferation were induced by infection at Adp53 at 100 MOI which caused high transfer rate of wild-type p53 and strong expression of p53 protein in four human gastric carcinoma cells.The radio-enhancement ratio of Adp53 at 4Gy were3.0 for W cell,3.6 for M cell,2.2 for neo cell and 2.5 for 823 cell in vitro.Conclusion :This study demonstrated that Adp53 transfer increased cellular apoptosis and radiosensitivity of human gastric carcinoma cell lines in vitro independently on cellular intrinsic p53 status thus supporting the combination of p53 gene therapy with radiotherapy in clinical trials.     

P33ING1、p53在膀胱移行细胞癌中的表达及与细胞凋亡的相关性

目的：探讨抑癌基因P33ING1在膀胱移行细胞癌（BTCC）中的表达及其与p53蛋白表达及细胞凋亡的相关性。方法：利用免疫组化S-P法和TUNEL法检测83例BTCC及11例正常膀胱黏膜组织P33ING1、p53的表达及细胞凋亡指数（AI）。结果：83例膀胱移行细胞癌组织中,P33ING1蛋白的阳性表达率为59.03%,而正常膀胱黏膜组织中P33ING1蛋白阳性表达率为90.9%。P33ING1蛋白表达与膀胱移行细胞癌的WHO肿瘤分级有相关性。Spearman相关分析表明P33ING1蛋白表达与p53蛋白表达正相关（P〈0.05）。AI与P33ING1及p53蛋白表达无相关性。结论：P33ING1在膀胱移行细胞癌中表达下降可能在膀胱移行细胞癌的发生、发展过程中起重要作用,P33ING1与p53基因具有协同作用,同时检测p53的状态和P33ING1表达水平,对于膀胱癌的诊断、治疗和预后判断可能具有积极意义。     

宫颈鳞癌放疗中MI、MI/AI、p53的变化与预后的关系

目的评估宫颈癌细胞的增殖、增殖和凋亡的比值以及p53在放疗前、中的变化及其与预后的关系,以评估它们在放疗中的价值。方法42例宫颈鳞癌患者,均经病理证实,其中Ⅱb期8例,Ⅲa期5例、Ⅲb期27例,Ⅳa期2例。采用外照射和腔内后装放疗相结合的方法治疗。外照射能量选6兆X线,总剂量48~50Gy/25~26次,每周5次;腔内后装放射治疗A点剂量35Gy/7次,1周2次,外照射第1周后开始,腔内放射治疗的当天不做外照射。所有患者分别在放疗前和放疗(外照射)第1周结束后(9~10Gy)的第6小时宫颈取材,采用原位末端标记法、免疫组化等方法,对增殖细胞核抗原(PCNA)、凋亡细胞及p53蛋白进行检测。结果PCNA的阳性细胞指数(MI)在无瘤生存组(noevidenceofdisease简称NED组)放疗9~10Gy后比放疗前明显下降(P<0·005);比死亡 带瘤生存组(alivewithdisease,anddiedofdisease简称AWD DOD组)放疗9~10Gy后亦下降明显(P<0·0001),而AWD DOD组放疗9~10Gy后比放疗前虽有所下降,但无显著性意义(P=0·9628)。MI/AI(凋亡指数)在放疗前NED组比AWD DOD组低,但无显著性意义(P=0·0660)。放疗后NED组比放疗前明显下降(P<0·05),亦比AWD DOD组低,但无显著性意义(P=0·0569)。p53在放疗后有明显上升(P<0·001),但在NED组和AWD DOD组之间无论放疗前、中均无显著差异。结论放疗后MI、MI/AI明显下降与好的预后有关;p53不适合做预测因素。     

番茄红素对人肝癌HepG2细胞增殖和凋亡的影响

目的 研究番茄红素(Lycopene,LP)对人肝癌HepG2细胞生长的影响并初探其机制。方法取对数生长期HepG2细胞设空白对照组、LP(5 μg/mL)组、LP(10 μg/mL)组、LP(20 μg/mL)组和顺铂(40 μg/mL)组,每组设10个复孔;各组分别给药干预48 h后,噻唑蓝(MTT)比色法测定细胞增殖抑制率,流式细胞术(FCM)检测细胞周期和细胞凋亡状况,RT-PCR法检测Bax mRNA和Bcl-2 mRNA表达,Western blot法检测Caspase-3蛋白表达。结果 与空白对照组比较,经LP(10 μg/mL、20 μg/mL)或顺铂40 μg/mL干预48 h能够显著提高HepG2细胞增殖抑制率,延长细胞周期中G₀/G₁期而缩短G₂/M期,提高细胞凋亡率,上调促凋亡Bax mRNA表达并下调抑凋亡Bcl-2 mRNA表达,提高Bax/Bcl-2比值,上调Caspase-3蛋白表达,LP上述作用具有一定的剂量依赖性。结论 LP具有抑制人肝癌HepG2细胞增殖并促进其凋亡的作用,其机制可能与LP干预细胞周期分布和调节凋亡相关基因蛋白表达有关。     

食管黏膜癌变过程中组织细胞增殖、凋亡和p53表达的变化

目的探讨食管黏膜癌变过程中增殖、凋亡和p53表达的变化及临床意义。方法对连续胃镜检查对象818例进行食管黏膜活检和病理组织学检查,并应用TUNEL法检测凋亡指数、免疫组织化学法检测增殖指数和p53表达。结果818例食管活检组织中,正常上皮694例,单纯增生39例,轻中度异型增生24例,食管鳞癌61例。在正常上皮→单纯增生→轻中度异型增生→鳞癌中,随分化程度的进展,凋亡指数（AI）等级逐渐降低,增殖指数（PI）等级和p53表达等级则逐渐增高,差异均有统计学意义。正常上皮中AI等级与PI和p53表达等级呈负相关,PI等级与p53表达等级呈正相关。单纯增生中AI等级与p53表达等级呈负相关,PI等级与p53表达等级呈正相关。轻中度异型增生和鳞癌中AI等级、PI等级及p53表达等级之间彼此均无相关性。结论AI等级降低,PI和p53表达等级升高是食管黏膜肿瘤性生长的特征,各病理类型本身凋亡增殖和p53表达的彼此相关性可能是制约或促进癌变的机制,这些变化可以作为食管上皮恶性变倾向的参考指标。     

甲基莲心碱对长春新碱抑制人胃癌细胞增殖作用的影响

目的：观察甲基莲心碱（Nef）在体外对长春新碱抑制人胃癌细胞增殖及诱导人胃癌细胞凋亡的影响。方法：采用MTT比色法、软琼脂克隆形成法检测药物的细胞毒性作用,并用流式细胞术、AO/EB荧光双染色法测定Nef对长春新碱诱导人胃癌细胞凋亡的影响。结果：2.5、5、10μmol/LNef能增强长春新碱对人胃癌细胞（SGC7901）增殖的抑制作用;10μmol/LNef能增强长春新碱（0.1、0.5、2、4μg/ml）诱导SGC7901细胞凋亡。结论：甲基莲心碱能增强长春新碱抑制人胃癌细胞增殖及诱导人胃癌细胞凋亡,为一种低毒高效的化疗增敏剂。     

BRD4抑制剂对鼻咽癌CNE-2细胞增殖、凋亡和侵袭的影响

目的 探讨溴结构域蛋白4（BRD4）抑制剂GSK525762A对鼻咽癌CNE-2细胞增殖、凋亡及侵袭的影响。方法 0、0.1、1、10、100 μmol／L GSK525762A 处理鼻咽癌CNE-2细胞 24、48、72和96 h后,采用四甲基偶氮唑盐（MTT）比色法检测细胞增殖抑制率变化,同时采用流式细胞术Annexin V-FITC／PI双染法检测不同浓度GSK525762A处理48、96 h后的CNE-2细胞凋亡情况,Transwell法检测不同浓度GSK525762A处理48、96 h后的CNE-2细胞侵袭能力,实时定量PCR检测不同浓度GSK525762A 处理48、96 h后凋亡相关基因的表达情况。结果 GSK525762A对CNE-2细胞增殖有抑制作用,增殖抑制率呈时间和浓度依赖性,差异有统计学意义（P＜0.05）;GSK525762A处理后的细胞早期、晚期及总凋亡率升高,均高于0 μmol／L,凋亡率随浓度升高而增加;穿膜细胞数均少于0 μmol／L,且随浓度升高而降低,以上差异均有统计学意义（P＜0.05）;与0 μmol／L比较,其余各浓度的Bcl-2 mRNA水平降低,Bax mRNA、Bak mRNA水平均升高,且各浓度间差异均有统计学意义（P＜0.05）;GSK525762A各浓度处理96 h的凋亡率、穿膜细胞数及凋亡相关基因mRNA均优于48 h（P＜0.05）。结论 BRD4抑制剂GSK525762A对鼻咽癌CNE-2细胞增殖有毒性作用,可诱导CNE-2细胞凋亡,恢复凋亡相关基因的表达,并降低细胞的侵袭能力。     

PSMD7基因在人食管鳞癌组织中的表达及影响癌细胞增殖、凋亡的机制研究

背景与目的：26S蛋白酶体非ATP酶调节亚基7（26S proteasome non-ATPase regulatory subunit 7,PSMD7）作为组成19S蛋白酶体盖子结构的核心成员是否参与肿瘤的发生、发展,以及具体的分子机制尚不清楚。本实验将研究PSMD7基因在人食管鳞癌组织中的表达,以及对癌细胞增殖及凋亡的影响。方法：采用实时荧光定量聚合酶链反应（real-time fluorescent quantitative polymerase chain reaction,RTFQ-PCR）和蛋白质印迹法（Western blot）检测食管鳞癌及其癌旁正常组织标本中PSMD7的mRNA及蛋白表达情况。在人食管鳞癌细胞系TE-1中,用慢病毒介导的RNA干扰技术下调PSMD7的表达,观察细胞增殖及凋亡的变化,检测线粒体膜电位的变化、细胞质中Cyt C的表达以及凋亡相关因子的表达。结果：PSMD7基因的mRNA和蛋白在食管鳞癌组织中的表达显著高于癌旁正常组织（P<0.05）,PSMD7蛋白的高表达与淋巴结转移阳性呈正相关（P<0.05）。抑制PSMD7蛋白的表达可使细胞的增殖能力降低（P<0.05）,并促进细胞的凋亡（P<0.05）,同时线粒体膜电位降低,促进Cyt C释放进入细胞质,激活caspase级联反应,说明抑制PSMD7的表达诱导细胞凋亡是通过线粒体信号通路进行的。结论：PSMD7在食管鳞癌中呈高表达,并通过线粒体依赖的方式促进TE-1细胞凋亡。     

P33ING1、p53在膀胱移行细胞癌中的表达及与细胞凋亡的相关性

目的:探讨抑癌基因P33ING1在膀胱移行细胞癌(BTCC)中的表达及其与p53蛋白表达及细胞凋亡的相关性.方法:利用免疫组化S-P法和TUNEL.法检测83例BTCC及11例正常膀胱黏膜组织P33ING1、p53的表达及细胞凋亡指数(AI).结果:83例膀胱移行细胞癌组织中,P33ING1蛋白的阳性表达率为59.03%,而正常膀胱黏膜组织中P33ING1蛋白阳性表达率为90.9%.P33ING1蛋白表达与膀胱移行细胞癌的WHO肿瘤分级有相关性.spearman相关分析表明P33ING1蛋白表达与p53蛋白表达正相关(P<0.05).AI与P33ING1及p53蛋白表达无相关性.结论:P33ING1在膀胱移行细胞癌中表达下降可能在膀胱移行细胞癌的发生、发展过程中起重要作用,P33ING1与p53基因具有协同作用,同时检测p53的状态和P33ING1表达水平,对于膀胱癌的诊断、治疗和预后判断可能具有积极意义.     

汉黄芩素对鼻咽癌CNE2细胞增殖及凋亡的影响

目的 探讨汉黄芩素对鼻咽癌CNE2细胞增殖和凋亡的影响及其可能的作用机制。方法 采用不同浓度（2.5 μmol/L、5.0 μmol/L、10.0 μmol/L、20.0 μmol/L）汉黄芩素作用鼻咽癌CNE2细胞,以溶剂为对照组。采用实时无标记细胞功能分析仪监测细胞增殖情况,双荧光法检测细胞凋亡情况,Western blot法检测PCNA、Survivin、XIAP、Bcl-2蛋白表达水平。结果 不同浓度（2.5 μmol/L、5.0 μmol/L、10.0 μmol/L、20.0 μmol/L）汉黄芩素作用24 h后CNE2细胞增殖抑制率依次为20.3%、23.7%、33.4%、40.9%,IC₅₀为42.41 μmol/L;36 h依次为18.0%、22.0%、36.1%、40.5%,IC₅₀为34.46 μmol/L;48 h依次为7.4%、20.2%、35.0%、40.9%,IC₅₀为22.81 μmol/L。与溶剂对照组比较,10.0 μmol/L、20.0 μmol/L汉黄芩素组细胞凋亡率均升高（t=23.710,P=0.001;t=43.934,P<0.001）。20.0 μmol/L汉黄芩素处理鼻咽癌CNE2细胞48 h后,与溶剂对照组比较,Bax蛋白表达水平上升（P<0.05）,Survivin、XIAP、Bcl-2蛋白表达水平下降（P<0.05）。 结论 汉黄芩素可抑制鼻咽癌CNE2细胞增殖并诱导其凋亡,可能通过促进Bax蛋白表达并抑制Survivin、XIAP、Bcl-2蛋白表达发挥作用。     

术前动脉化疗对胃癌细胞凋亡及p53表达的影响

背景与目的:区域化疗具有肿瘤局部药物浓度高、全身副作用小的特点,术前选择性区域动脉灌注化疗可明显改变胃癌患者的肿瘤组织学形态。本文旨在研究术前动脉化疗对胃癌细胞凋亡及p53表达的影响和意义。方法:对33例胃癌患者动脉化疗前胃镜活检病理标本和动脉化疗后手术切除的病理标本,应用DNA原位末端标记法、免疫组化S-P法分别检测肿瘤细胞凋亡及p53蛋白表达。结果:胃癌动脉化疗后肿瘤细胞凋亡指数为19.29±6.48,显著高于动脉化疗前的9.24±5.03(P<0.01);动脉化疗后p53表达阳性率为30.30%,显著低于动脉化疗前的54.55%(P<0.05);动脉化疗后p53表达“下降”组的生存期长于p53表达“增加”组的生存期(P<0.05)。结论:术前动脉化疗对胃癌细胞有明显的促进凋亡作用,可显著降低胃癌组织p53蛋白的表达,提高患者的生存期。     

Mesothelin regulates growth and apoptosis in pancreatic cancer cells through p53-dependent and -independent signal pathway

Mesothelin, a secreted protein, is overexpressed in some cancers, including pancreatic cancer. Rescent studies have shown that overexpression of mesothelin significantly increased tumor cell proliferation, and downregulation of mesothelin inhibited cell proliferation in pancreatic cancer cells, but its exact function and mechanism remains unclear. The aim of the present study was to evaluate the effects of mesothelin on proliferation and apoptosis in pancreatic cancer cells with different p53 status and to explore its signal pathway. Mesothelin levels were detected by western blot and RT-PCR assay in human pancreatic cancer AsPC-1, HPAC and Capan-2, Capan-1 and MIA PaCa-2 cell lines. Mesothelin was slienced by shRNA in AsPC-1, Capan-2 and Capan-1 cells with rich mesothelin level, and mesothelin was overexpressed in the HPAC and Capan-2 cells with less mesothelin level. We observed that in the AsPC-1 and Capan-1cells with mt-p53, and Capan-2 cells with wt-p53, shRNA mediated sliencing of the mesothelin significantly increased PUMA and Bax expression and caspase-3 activity, and decreased bcl-2 expression, followed by the reduced proliferation and colony forming capability and increased cell apoptosis. When PUMA was slienced by siRNA in the stable mesothelin shRNA transfected cells, proliferative capability was significantly increased, and apoptosis was decreased. However, in the Capan-2 cells with wt-p53, suppression of the mesothelin significantly increased wt-p53 levels. When p53 was blocked by siRNA in the stable mesothelin shRNA transfected Capan-2 cells, PUMA was inhibited, followed by increased proliferative capability and decreased cell apoptosis. In the HPAC and Capan-2 cells with wt-p53 and in the MIA PaCa-2 cells with mt-p53, overexpression of the mesothelin significantly decreased bax levels and increased bcl-2 levels, followed by increased proliferative and colony forming capability. Furthermore, mesothelin-shRNA-transfected cells exhibited a reduced rate of tumor growth under in vivo conditions. However, mesothelin-transfected cells exhibited a increased rate of tumor growth under in vivo conditions. Our data demonstrated that mesothelin promotes proliferation and inhibited apoptosis through p53-dependent pathway in pancreatic cancer cells with wt-p53, and p53-independent pathway in pancreatic cancer cells with mt-p53. Targeting mesothelin by shRNA is the important method for pancreatic cancer therapy.     

p53凋亡刺激蛋白在肿瘤中的研究进展

p53凋亡刺激蛋白(ASPP)是p53的重要调节蛋白,其成员有ASPP1、ASPP2、iASPP.它们与p53形成复合物后,ASPP1和ASPP2特异性促进p53的细胞凋亡功能,而iASPP则同ASPP1和ASPP2竞争性地与p53结合位点结合,从而抑制p53的抑癌功能.ASPP家族尤其是iASPP有望成为肿瘤治疗的新靶点.     

p53 overexpression impacts on the prognosis of laryngeal squamous cell carcinomas

Objectives: To investigate the prognostic implications of p53 expression in the surgical margins of laryngealsquamous cell carcinomas. Methods: Thirty one patients with T3-4N0M0 cancers with pathologically negativemargins were analyzed by immunohistochemistry (IHC) to detect expression of p53. Results: The p53 positiverates by IHC in the surgical margin were 16.1% (5/31). In the p53 positive margin group, the recurrent ratewas higher than those without (80% vs 19.2%, P = 0.006). Also, the median free of disease period in the p53positive margin group was shorter than other group (22.2 vs 47.8 months, P < 0.0001). Conclusions: We foundthat the overexpression of p53 can serve a prognostic role for both recurrence and disease-specific mortality inhead and neck squamous cell carcinoma. p53 expression could stratify patients, in an easy and inexpensive way,according to their risk of local or regional recurrence.