Expressions of oncogenes c-fos and c-myc in skin lesion of cutaneous squamous cell carcinoma

Objective:To explore the expressions of c-fos and c-myc in skin lesion of cutaneous squamous cell carcinoma(CSCC).Methods:Using retrospective analysis.73 cases of CSCC were selected from Department of Dermatology,the Second Affiliated Hospital of Xi'an Jiaotong University.which were removed between January 2000 and January 2012.It was considered as experimental group.Meanwhile.11 cases of normal skin specimens of non tumor patients were selected as control group.The expression level of c-fos and c-myc was compared in the two groups.Results:The expressions of c-fos[72.60%(53/73)]and c-myc[83.56%(61/73)]in experimental group were statistically significant(P≤0.05)compared with control group(0%).Expression of c-myc protein was negatively related to differentiation of CSCC.The difference was statistically significant(X^2=7.26.P=0.001<0.05).While expression of c-fos protein was positively related to differentiation of CSCC.which was statistically significant(X^2=7.47,P=0.0012<0.025).Conclusions:The expression level of c-fos and c-myc can be used as an importan indicator of CSCC differentiation,and it has closely connection with the differentiated degree,which can guide clinical prognosis.

THE EXPRESSIONS OF HBV X GENE AND ets-2, IGF-Ⅰ, c-myc AND N-ras ONCOGENES IN HUMAN HEPATOCELLULAR CARCINOMA AND TUMOR-ADJACENT TISSUES

The expressions of HBV X gene and ets-2, IGF-I, c-myc and N-ras were studied in 7 pairs of human primary hepatocellular carcinoma (PHC) and tumor-adjacent tissues, using RNA hybridization and im-munoblot methods. The results showed that specific 17 and 28 kD HBV X gene products (HBxAg) were existed in a portion of PHC and tumor-adjacent tissues. The 17 kD HBxAg was detected in the sera of 3 patients who also had 17 kD HBxAg in their liver tissues. Multiple expressions of oncogenes such as ets-2, c-myc and N-ras were observed in PHC and tumor-adjacent tissues that had HBxAg expressed, indicating HBxAg might function as a transactivator in the course of intracellular proto-oncogene activation. It is also observed that in some tumor-adjacnet tissues the expressions of ets-2, c-myc and N-ras were higher than those in corresponding PHC. The relationship of HBxAg to the expression of est-2, IGF-Ⅱ, c-myc and their possible roles in the carcinogenesis of PHC are discussed.

ANTIBODY TO ONCOGENE PROTEIN PRODUCT AND ITS CONJUGATE WITH RICIN A-CHAIN

The proteins encoded by oncogene were thought to be tumor associated antigen. The protein P110 in MGC803, a human gastric cancer cell line, was purified as immunogen. The IgY to the gastric cancer was extracted from eggs laid by immunized hen. The IgY could react immunohistochemically with gastric cancers. Positive staining rates of PAF were 80% in gastric cancers and markedly higher than in cancers of other organs and normal gastric tissue. The IgY-Ricin A was synthesized by the IgY conjugated with Ricin A- chain. TCID50 of MGC803 treated by the IgY-Ricin A was 0. 01 mg/ml and markedly lower than other cell. These results showed the IgY-Ricin A were able to react with gastric cancers selectively.

Function of apoptosis and expression of the proteins Bcl-2,p53 and C-myc in the development of gastric cancer

INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer .

PDRG1 at the interface between intermediary metabolism and oncogenesis

PDRG1 is a small oncogenic protein of 133 residues. In normal human tissues, the p53 and DNA damageregulated gene 1(PDRG1) gene exhibits maximal expression in the testis and minimal levels in the liver. Increased expression has been detected in several tumor cells and in response to genotoxic stress. High-throughput studies identified the PDRG1 protein in a variety of macromolecular complexes involved in processes that are altered in cancer cells. For example, this oncogene has been found as part of the RNA polymerase Ⅱ complex, the splicing machinery and nutrient sensing machinery, although its role in these complexes remains unclear. More recently, the PDRG1 protein was found as an interaction target for the catalytic subunits of methionine adenosyltransferases. These enzymes synthesize S-adenosylmethionine, the methyl donor for, among others, epigenetic methylations that occur on the DNA and histones. In fact, downregulation of S-adenosylmethionine synthesis is the first functional effect directly ascribed to PDRG1. The existence of global DNA hypomethylation, together with increased PDRG1 expression, in many tumor cells highlights the importance of this interaction as one of the putative underlying causes for cell transformation. Here, we will review the accumulated knowledge on this oncogene, emphasizing the numerous aspects that remain to be explored.

Expressions of beta-catenin, APC Protein, C-myc and Cyclin D1 in Ovarian Epithelial Tumor and Their Implication

Objective： To investigate the expressions of beta-catenin, protein APC （adenomatous polyposis coil protein）, c-myc and cyclin D1 and their implication in ovarian epithelial tumor. Methods： Immunohistochemical staining with SP method was conducted to identify the expressions of beta-catenin, APC protein, c-myc and cyclin D1 in ovarian epithelial tumor in 48 cases. Results： The abnormal expression rate of beta-catenin in malignant and borderline ovarian epithelial tumors was higher than that in benign epithelial tumors （P〈0.01）. The expression rates of c-myc and cyclin-D1 in ovarian malignant and borderline epithelial tumors were higher than those in benign epithelial tumors too（P〈0.05）. The prevalence of APC protein positive expression in benign epithelial tumors were significantly greater than that in malignant epithelial tumors （P〈0.05）. A significant negative correlation was found between beta-catenin and APC protein in ovarian epithelial tumors; while a significant positive correlation was found between beta-catenin, c-myc and cyclin-D1 in ovarian epithelial tumor （P〈0.05）. Conclusion： The abnormal expressions of Beta-catenin, APC protein, c-myc and cyclin-D1 might be used to indicate the malignance transform of ovarian epithelial tumors.

EFFECT OF ACTIVE COMPOUNDS ISOLATED FROM PTERIS SEMIPINNATA L ON DNA TOPOISOMERASES AND TYROSINE PROTEIN KINASE AND EXPRESSION OF C-MYC IN LUNG ADENOCARCINOMA CELLS

Objective: To study the effect of active compound 6F and A from Pteris semipinnata L.(PsL) on the activities of DNA topoisomerase (TOPO) I and II, activities of cytosolic and membrane TPK, and expression of oncogene c-myc in lung adenocarcinoma cells. Methods: The effect of compound 6F and A on activities of cytosolic and membrane TPK was measured by scintillation counting; the effect of compound A on expression of oncogene c-myc was determined by flow cytometry indirect fluorimetry. Results: compound 6F and A could inhibit the activities of TOPO I, and they strongly inhibited the TOPO II in 0.01 mg/L and 10.0 mg/L respectively. Compound A slightly inhibited the activities of membrane TPK, but not the cytosolic one. Compound A could inhibit the expression of oncogene c-myc. Conclusion: Topoisomerases are target of compound 6F and A. Compound A could slightly inhibit the activities of TPK, and showed an inhibitory effect on the expression of oncogene c-myc.

Effects of Okadaic Acid, Retinoic Acid, and Phorbol Myristate Acetate Tumor Promoter on Oncogene Expression

The effect of okadaic acid (OA) on proto-oncogene protein expression of c-neu, c-myc, v-rasH, EGFR, and phosphotyrosine-containing phosphoproteins (P-Tyr) was investigated in rapidly growing (RG) normal human keratinocytes (NHK) and in SV-40 virally-transformed keratinocytes (SVK) cultured in a growth factor supplemented serum-free medium as assessed by indirect immunofluorescence microscopy. P-Tyr positively stains cell surface antigens (cytoplasm) diffusely at monopolar sites in RG NHK cultures. OA-treatment intensifies cytoplasmic P-Tyr staining at localized monopolar intercellular focal adhesion (IFA) sites with reduced cytoplasmic staining. P-Tyr expression was predominate at IFA sites with little cytoplasmic staining in RG SVK cultures. OA-treatment increased monopolar P-Tyr staining and cytoplasmic staining. OA-treatment in RG NHK cultures intensified cytoplasmic staining of c-myc and EGFR (epidermal growth factor receptor) expression. OA-treatment in RG NHK and SVK cultures intensified c-neu staining at monopolar IFA sites and intensified c-neu staining at both cytoplasmic and bipolar IFA sites in RG SVK cells. OA was especially cytotoxic for SVK cells. RA treatment decreased c-neu expression in RG NHK cultures while TPA treatment has a lesser effect on both cytoplasmic and IFA sites. RA treatment also decreased P-Tyr staining in both NHK and SVK cells. Again, TPA had a lesser inhibitory effect on P-Tyr staining pattern. RA-treatment had a similar effect on P-Tyr staining of RG cultures of a mouse fibroblast cell line. These results confirm the generality of OA, RA and TPA on the regulation of oncogene expression in both normal and malignantly transformed keratinocytes.

Reactive oxygen species-induced activation of Yes-associated protein-1 through the c-Myc pathway is a therapeutic target in hepatocellular carcinoma

BACKGROUND The Hippo signaling pathway regulates organ size by regulating cell proliferation and apoptosis with terminal effectors including Yes-associated protein-1(YAP-1).Dysregulation in Hippo pathway has been proposed as one of the therapeutic targets in hepatocarcinogenesis.The levels of reactive oxygen species(ROS)increase during the progression from early to advanced hepatocellular carcinoma(HCC).AIM To study the activation of YAP-1 by ROS-induced damage in HCC and the involved signaling pathway.METHODS The expression of YAP-1 in HCC cells(Huh-7,HepG2,and SNU-761)was quantified using real-time polymerase chain reaction and immunoblotting.Human HCC cells were treated with H2O2,which is a major component of ROS in living organisms,and with either YAP-1 small interfering RNA(siRNA)or control siRNA.To investigate the role of YAP-1 in HCC cells under oxidative stress,MTS assays were performed.Immunoblotting was performed to evaluate the signaling pathway responsible for the activation of YAP-1.Eighty-eight surgically resected frozen HCC tissue samples and 88 nontumor liver tissue samples were used for gene expression analyses.RESULTS H2O2 treatment increased the mRNA and protein expression of YAP-1 in HCC cells(Huh-7,HepG2,and SNU-761).Suppression of YAP-1 using siRNA transfection resulted in a significant decrease in tumor proliferation during H2O2 treatment both in vitro and in vivo(both P<0.05).The oncogenic action of YAP-1 occurred via the activation of the c-Myc pathway,leading to the upregulation of components of the unfolded protein response(UPR),including 78-kDa glucoseregulated protein and activating transcription factor-6(ATF-6).The YAP-1 mRNA levels in human HCC tissues were upregulated by 2.6-fold compared with those in nontumor tissues(P<0.05)and were positively correlated with the ATF-6 Levels(Pearson’s coefficient=0.299;P<0.05).CONCLUSION This study shows a novel connection between YAP-1 and the UPR through the c-Myc pathway during oxidative stress in HCC.The ROS-induced activation of YAP-1 via the c-Myc pathway,which leads to the activation of the UPR pathway,might be a therapeutic target in HCC.

Downregulation of the Spi-1/PU.1 oncogene induces the expression of TRIM10/HERF1, a key factor required for terminal erythroid cell differentiation and survival

Spi-1/PU.1 和 Fli-1 oncoproteins 的持续表示在老鼠 erythroleukemia 房间堵住 globin 基因激活；然而，仅仅 Spi-1/PU.1 表示禁止 exon 的包括 16 在成熟 4.1R mRNA。这个拼接的事件为红血房间膜正直为功能的 4.1R 蛋白质并且，因此是关键的。这份报告证明 Spi-1/PU.1 downregulation 导致 TRIM10/hematopoietic 戒指手指 1 的激活(HERF1 ) ，分成三部分的主题(修剪) 的一个成员为 globin 基因抄写需要的 /RBCC 蛋白质家庭。另外，我们证明 TRIM10/HERF1 为 exon 拼接调整被要求 16 在迟了的 erythroid 区别期间。用可诱导的 overexpression 和 silencing 途径，我们发现了那：(1 ) TRIM10/HERF1 击倒在导致的 dimethylsulfoxide (DMSO ) 禁止拼接的血红素生产和 exon 和扳机房间 apoptosis 房间；(2 ) TRIM10/HERF1 upregulation 被要求，但是在它的自己上是不够的激活 exon 保留；(3 ) Fli-1 没在 TRIM10/HERF1 表示上有效果，而也导致 DMSO 的 downregulation 或 Spi-1/PU.1 shRNA 击倒表示是足够的激活 TRIM10/HERF1 表示；并且(4 ) Spi-1/PU.1 击倒的扳机抄写和拼接的事件独立于化学正式就职。总的来说，这些数据显示主要 Spi-1/PU.1 downregulation 通过至少二条小径，其一条要求 TRIM10/HERF1 upregulation 和平行对迟了的 erythroid 区别起作用 Spi-1/PU.1-induced Fli-1 用以遮闭之物规章的串联。

Polymerase chain reaction-single strand conformational polymorphism analysis of rearranged during transfection proto-oncogene in Chinese familial hirschsprung's disease

AIM: To investigate the relationship between mutations of rearranged during transfection (RET) proto-oncogene and Chinese patients with Hirschsprung's disease (HD), and to elucidate the genetic mechanism of familial HD patient at the molecular level.METHODS: Genomic DNA was extracted from venous blood of probands and their relatives in two genealogies.Polymerase chain reaction (PCR) products, which were amplified using specific primers (RET, exons 11, 13, 15and 17), were electrophoresed to analyze the single-strand conformational polymorphism (SSCP) patterns. The positive amplified products were sequenced. Forty-eight sporadic HD patients and 30 normal children were screened for mutations of RET proto-oncogene simultaneously.RESULTS: Three cases with HD in one family were found to have a G heterozygous insertion at nucleotide 18 974 in exon 13 of RET cDNA (18 974insG), which resulted in a frameshift mutation. In another family, a heterozygosity for T to G transition at nucleotide 18 888 in the same exon which resulted in a synonymous mutation of Leu at codon 745 was detected in the proband and his father. Eight RET mutations were confirmed in 48 sporadic HD patients.CONCLUSION: Mutations of RET proto-oncogene may play an important role in the pathogenesis of Chinese patients with HD. Detection of mutated RET proto-oncogene carriers may be used for genetic counseling of potential risk for HD in the affected families.

Disorder structural predictions of the native EWS and its oncogenic fusion proteins in rapport with the function

The Intrinsic structural disorder (ISD) of native EWS and its fusion oncogenic proteins, including EWS/FliI, EWS/ATF1 and EWS/ZSG, was estimated by different Predictors. The ISD difference between the wild type and the oncogenic fusions found in the CTD is due to the fusion partner, usually a transcription factor (TF). A disordered region was found in the sequence (AA 132 - 156) of the NTD (EAD) of EWS, consisting of the longest region free of Y motifs. The IQ domain (AA 258 - 280), a Y-free region, flanked by two Y-boxes, is also disordered by all used Predictors. The EWS functional regions RGG1, RGG2 and RGG3 are predominantly disordered. A strong dependence was found between the structure of EWS protein and its oncogenic fusions, and their estimated ISD. The oncogenic function of the fusions is related to a decreased ISD in the CTD, due to the fused TF. The Predictors shown that the different isoforms have similar profiles, shifted with some amino acids, due to the translocations. On the bases of the prediction results, an analysis was made of the EWS sequence and its functional regions with increased ISD to make a relationship sequence-disorder-function that could be helpful in the design of antitumor agents against the corresponding malignances.

Eosinophil MBP Extract Modulates Oncogene Expression in Prostate Tumor Cells: A Preliminary Study with Monolayer Cultures

Prostate cancer is the second leading cause of cancer deaths in the United States and remains a significant health concern for men throughout the world. Despite the discovery of promising immunotherapeutic strategies, curative outcomes remain elusive. We have investigated eosinophils as potential anti-cancer effector cells, and have reported the ability of their toxic granular proteins (MBP, EPO, ECP, EDN) to inhibit prostate tumor cell growth?in vitro. This study investigates the effect of eosinophil MBP extract on the expression of oncogenes p53, bcl-xl, bax, and c-myc, which modulate tumor growth, proliferation, and apoptosis. Briefly, granular proteins were differentially extracted from GRC.014.22 and GRC.014.24, eosinophilic cell lines established in our laboratory from a patient with moderate asthma. Protein extracts were fractionated on Sephadex G-50 columns, and prostate tumor cell lines DU-145, LNCaP, PC-3, and HPC8L (established in our laboratory from a tumor resected from an African American patient) were treated with MBP extracts from the pooled third peaks. Colony formation and monolayer cell growth inhibition assays were used to evaluate the protein’s growth inhibitory activity against prostate tumor cells;and gene expression analyses, to determine p53, bcl-xl, bax, and c-myc oncogene expression. We show that the granular proteins were potent in their action on HPC8L, inhibiting colony formation in a dose-dependent manner. Treated prostate tumor cell lines trended toward apoptosis-induction, as evident in bcl-xl/bax ratios < 1, increased p53 expression, and up or downregulation of c-myc. These preliminary results demonstrate the growth inhibitory potential of eosinophil granular proteins and strongly support the hypothesis that eosinophils modulate the expression of oncogenes associated with prostate tumor proliferation and apoptosis. More importantly, this study offers insights into possible applications of eosinophilic mediators in oncogenic-targeted prostate cancer treatment strategies and demonstrates the potential therapeutic implications of enhancing eosinophilic activity in prostate cancer.

VARIATION AND SIGNIFICANCE OF C-MYC PROTEIN IN RAT CARDIAC VOLUME-OVERLOAD HYPERTROPHY

Objective To investigate the change of c-myc protein, which was chosen as the response indicator to volume-overload. Methods The time and spatial course of c-myc protein expression on the model of rat cardiac volume-overload hypertrophy was examined by immunohistochemical study. Results The immunohistochemical study indicated the expression of c-myc protein was increased obviously at 4-6 hours (62.73%) than that of control (45.41%, P<0.01) after the volume-overload, then decreased gradually along with development of volume-overload hypertrophy and was decreased extremely at 5 months(r=-0.514,P<0.01).Conclusion There are disorders in the signal transduction pathways governing the hypertrophic response of cardiomyocytes in hypertrophic myocardium. C-myc gene and the product of it may be only the promoter gene of myocardial hypertrophy. Once switching on,c-myc gene and the product of it do not act anymore;While it may be that c-myc gene and the product of it increased following with myocardial hypertrophy, and have not direct relation to the occurrence and development of myocardial hypertrophy.

虎杖苷调节Akt/MDM2/p53信号通路对胆囊癌细胞增殖、迁移和细胞周期的影响

目的探讨虎杖苷(PD)调节蛋白激酶B/原癌基因MDM2/抑癌基因p53信号通路对胆囊癌细胞增殖、迁移和细胞周期的影响。方法以人胆囊癌细胞株(GBC-SD)为研究对象,体外培养人胆囊癌细胞株(GBC-SD),使用浓度为10~160 mmol/L的虎杖苷处理细胞24、48、72 h,采用CCK-8法检测细胞的增殖能力,确定最佳实验浓度。将GBC-SD细胞分为对照组(Control组)、虎杖苷低、中、高浓度组(PD-L组、PD-M组、PD-H组)、虎杖苷+Akt激活剂组(PD+SC79组),Transwell小室法评价细胞的迁移能力,Hoechst染色观察细胞的凋亡,流式细胞术检测细胞周期与细胞凋亡,Western blot检测Akt、MDM2、p53磷酸化水平,建立荷瘤小鼠模型评价虎杖苷对胆囊癌肿瘤生长的影响。结果浓度为10~160 mmol/L的虎杖苷处理细胞24 h,可显著抑制GBC-SD细胞的增殖活性,选择10、20、40 mmol/L的虎杖苷进行后续实验;与Control组比较,PD-L组、PD-M组、PD-H组GBC-SD细胞的迁移数、细胞凋亡率、G2/M期细胞比例及S期细胞比例、P-Akt、P-MDM2蛋白表达显著降低,G0/G1期细胞比例、P-p53蛋白表达显著升高,且呈浓度依赖性(P<0.05);与PD-H组比较,PD+SC79组GBC-SD细胞的迁移数、细胞凋亡率、G2/M期细胞比例及S期细胞比例、P-Akt、P-MDM2蛋白表达显著升高,G0/G1期细胞比例、P-p53蛋白表达显著降低(P<0.05);虎杖苷干预治疗后,小鼠移植瘤的生长速度显著降低(P<0.05)。结论虎杖苷可以通过调节Akt/MDM2/p53信号通路使细胞周期阻滞,抑制胆囊癌细胞增殖、迁移。

西藏地区结直肠癌免疫治疗和靶向治疗相关分子标志物的检测及意义

目的研究西藏地区结直肠癌中SWI/SNF相关、基质相关、肌动蛋白依赖性染色质调节因子A亚科成员4(SMARCA4)/Brahma相关基因1、V-raf鼠类肉瘤病毒癌基因同源物B(BRAF)、P53、程序性死亡受体1(PD-1)及程序性死亡配体1(PD-L1)免疫组织化学表达和BRAF、神经营养因子酪氨酸受体激酶(NTRK)基因改变情况,为西藏地区结直肠癌患者的靶向治疗及免疫治疗提供依据。方法收集2015年1月至2021年7月西藏自治区人民医院经手术切除病理确诊为结直肠癌病例64例,全部病例均进行SMARCA4、BRAF、P53、PD-1、PD-L1免疫组织化学染色和NTRK1、NTRK2、NTRK3融合基因荧光原位杂交检测及BRAF V600E基因突变PCR检测。结果64例结直肠癌病例男女比例1.21∶1,平均年龄(56.59±13.27)岁;46例(71.88%)位于结肠,18例(28.12%)位于直肠;60例(93.75%)为腺癌,4例(6.25%)为其他类型;11例(17.19%)为T1或T2期,53例(82.81%)为T3或T4期;24例(37.50%)出现淋巴结转移。免疫组织化学方面,64例中1例(1.56%)SMARCA4部分肿瘤细胞表达减弱或缺失,4例(6.25%)BRAF肿瘤细胞阳性表达,35例(54.69%)P53为突变型表达;45例(70.31%)PD-1肿瘤相关免疫细胞阳性比例分数<10%,19例(29.69%)≥10%;52例(81.25%)PD-L1联合阳性分数<10,12例(18.75%)≥10。64例NTRK1、NTRK2、NTRK3融合基因检测均为阴性;4例(6.25%)检测到BRAF V600E基因突变;1例SMARCA4表达缺失病例未检测到SMARCA4基因改变。PD-L1的表达与错配修复缺陷/高度微卫星不稳定和PD-1的高表达呈显著正相关(χ^(2)=10.223,P=0.001;χ^(2)=11.979,P=0.001)。结论西藏地区结直肠癌中较少出现SMARCA4表达减弱或缺失及NTRK融合基因改变,少数病例有BRAF V600E基因突变,Pan-TRK和BRAF免疫组织化学可作为NTRK融合基因及BRAF基因突变的初筛方法。错配修复缺陷/高度微卫星不稳定的病例中更容易出现PD-L1蛋白高表达,这部分患者有望获益于免疫治疗。P53突变与PD-L1表达无相关性,PD-1的高表达和PD-L1的高表达呈正相关。

非小细胞肺癌组织中NF-kB和c-myc及p73的表达与意义

目的:探讨NF-κB(p65)、c-myc和p73蛋白在非小细胞肺癌(non-small cell lung cancer,NSCLC)组织中的表达及相互关系。方法:用免疫组化二步法检测60例NSCLC组织标本中p65、c-myc和p73蛋白的表达,并进行相关分析。结果:p65、c-myc和p73蛋白在肺癌组织中的表达分别与在肺支气管上皮组织的表达比较差异有统计学意义,P<0.05。p65和c-myc蛋白在淋巴结转移癌组织中的表达与肺支气管上皮组织中的表达差异无统计学意义,P>0.05;p73蛋白在上述两组的表达差异有统计学意义,P<0.05。p65、c-myc和p73蛋白在肺癌高、中与低分化阳性表达的比较,差异均无统计学意义,P>0.05。伴有淋巴结转移的肺癌组织中蛋白阳性表达与无淋巴结转移比较:p65和c-myc差异无统计学意义,P>0.05;p73差异有统计学意义,P<0.05。肺癌组织中p65与c-myc具有相关性,R=0.5514,P<0.01;c-myc与p73具有相关性,R=0.6537,P<0.01;未发现p65与p73有明显相关性,R=0.1735,P>0.05。结论:p65、c-myc和p73表达上调均可能是NSCLC发生的重要因素;在肺癌发生发展中p65与c-myc、c-myc和p73可能在诱导细胞增生与抑制细胞凋亡中起协同作用;p73上调可能促进肺癌的侵袭与转移,可作为肺癌恶化进展及癌转移的动态监控标志。

膀胱癌中p53、c-myc和bcl-2的表达及意义

目的 :研究癌基因和抗癌基因蛋白产物在膀胱移行细胞癌组织中异常表达与病理分级、临床分期间关系。方法 :应用免疫组化S P法检测 96例膀胱移行细胞癌中 p5 3、c myc和bcl 2的表达水平。 结果 :96例膀胱移行细胞癌中 p5 3、c myc和bcl 2的阳性表达率分别为 6 0 4%、6 8 8%和 81 3 %。结果表明p5 3、c myc和bcl 2异常表达与膀胱移行细胞癌的分级和分期间差异有统计学意义。结论 :p5 3、c myc和bcl 2表达在膀胱癌的发生发展中起重要作用。在膀胱癌变过程中 。

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。

p53、rasp21及C-myc癌基因蛋白在胃癌中的表达及分布特征

目的通过对胃癌标本中p53、rasp21及Cmyc癌基因蛋白的表达分析,探讨其在胃癌发生中的作用。方法用免疫组化方法检测了60例胃癌标本中p53、rasp21及Cmyc的表达及分布。结果p53、rasp21及Cmyc在胃癌中的阳性表达分别为51.7%、40.0%、66.7%;胃癌旁正常黏膜上皮的阳性率分别为1.6%、13.3%、15.0%,与肿瘤区相比较有显著差异(P<0.01)。rasp21及Cmyc在肿瘤区与肿瘤移行区、癌旁正常黏膜区染色强度比较有差异(P<0.05)。p53及Cmyc阳性表达与肿瘤的分化程度有关,即分化越差,其阳性表达越高。结论p53、rasp21及Cmyc与胃癌的发生、发展密切相关,p53及Cmyc在肿瘤分化过程中可能起重要作用。