Expressions of cyclin D1 and p27^(kip1) in carcinogenesis of stomach mucosa

Objective： To evaluate the relationship between the expressions of cyclin D1 and p27^kip1 in the canceration course of the stomach. Methods： The immunohistochemical staining technique （SP method） was used to detect the expressions of cyclin D1, p27^kip1 in chronic superficial gastritis （CSG）, chronic atrophic gastritis （CAG）, intestinal metaplasia （IM）, dysplasia （DYS）, gastric carcinoma （GCA） biopsy specimens. Results： The positive cyclin D1 expression rates increased with the progressing from CAG--,IM--,DYS--,GCA respectively, and those in IM, DYS and GCA were different from those in CSG, P 〈 0.05, while DYS group was indifferent from GCA group, P 〉 0.05. The positive p27^kip1 expression rates decreased with the mucosa progressing from CAG→IM→DYS→GCA. There was a negative correlation between the expression cyclin D1 and p27^kip1 （y = -0.53, P = 0.000）. Conclusion： Expression rates of cyclin D1 in the canceration course of the stomach mucosa trend were increased and those of p27^kip1 were decreased; the abnormal expressions of them were found in the early term of the canceration course of the stomach mucosa, and the inverse expression suggests there may be a negative feedback regulatory loop between cyclin D1 and p27^kip1.

Expression and hypermethylation of p27^(kip1) in hepatocarcinogenesis

AIM： To study the expressions of p27^kip1 protein and p27mRNA, the hypermethylation of p27^kip1 and the relation between them in various stages of hepatocarcinogenesis. METHODS： p27 protein and p27mRNA were detected by immunohistochemical staining and in situ hybridization respectively in 68 cases of normal liver, liver cirrhosis, pericancerous cirrhosis and hepatocellular carcinoma （HCC）. The hypermethylation of p27^kip1 was detected by methylation-specific PCR （MSP） in 44 cases of normal liver, liver cirrhosis, and HCC. RESULTS： The positive rate of p27 protein was 66.7% （4/6） in normal liver, 60.0% （6/10） in liver cirrhosis, 50.0% （12/24） in pericancerous cirrhosis and 21.4% （6/28） in HCC. There were no statistical differences in normal liver, liver cirrhosis and pericancerous cirrhosis, but the positive rate of p27 protein significantly decreased in HCC compared to that in the other groups （P = 0.006, %2 = 7.664）. The positive rate of p27^kip1 mRNA was 83.3% （5/6） in normal liver, 70.0% （7/10） in liver cirrhosis, 75.0% （18/24） in pericancerous cirrhosis and 25.0% （7/28） in HCC. There were no statistical differences in normal liver, liver cirrhosis and pericancerous cirrhosis, but the positive rate of p27^kip1 mRNA also significantly decreased in HCC compared to that in the other groups （P = 0.000, %2 = 16.600）. In addition, there was a significant correlation between the expression of p27 protein and p27mRNA in the integrated group of normal liver and liver cirrhosis. However, no significant correlation was found between pericancerous cirrhosis and HCC. Using MSP, we found that 1 HCC in 44 cases （including 6 cases of normal liver, 10 cases of liver cirrhosis and 28 cases of HCC） was methylated, whose p27 protein and p27mRNA were negative. CONCLUSION： The reduction or loss of p27 protein and p27mRNA are potentially involved in hepatocarcinogenesis. The hypermethylation of p27 might lead to the loss of p27mRNA transcription.

Role of p53 suppression in the pathogenesis of hepatocellular carcinoma

In the world,hepatocellular carcinoma(HCC)is among the top 10 most prevalent malignancies.HCC formation has indeed been linked to numerous etiological factors,including alcohol usage,hepatitis viruses and liver cirrhosis.Among the most prevalent defects in a wide range of tumours,notably HCC,is the silencing of the p53 tumour suppressor gene.The control of the cell cycle and the preservation of gene function are both critically important functions of p53.In order to pinpoint the core mechanisms of HCC and find more efficient treatments,molecular research employing HCC tissues has been the main focus.Stimulated p53 triggers necessary reactions that achieve cell cycle arrest,genetic stability,DNA repair and the elimination of DNA-damaged cells’responses to biological stressors(like oncogenes or DNA damage).To the contrary hand,the oncogene protein of the murine double minute 2(MDM2)is a significant biological inhibitor of p53.MDM2 causes p53 protein degradation,which in turn adversely controls p53 function.Despite carrying wt-p53,the majority of HCCs show abnormalities in the p53-expressed apoptotic pathway.High p53 in-vivo expression might have two clinical impacts on HCC:(1)Increased levels of exogenous p53 protein cause tumour cells to undergo apoptosis by preventing cell growth through a number of biological pathways;and(2)Exogenous p53 makes HCC susceptible to various anticancer drugs.This review describes the functions and primary mechanisms of p53 in pathological mechanism,chemoresistance and therapeutic mechanisms of HCC.

Study of pathogenic genes in a pedigree with familial dilated cardiomyopathy

BACKGROUND Dilated cardiomyopathy(DCM)is a genetically heterogeneous cardiac disorder characterized by left ventricular dilation and contractile dysfunction.The substantial genetic heterogeneity evident in patients with DCM contributes to variable disease severity and complicates overall prognosis,which can be very poor.AIM To identify pathogenic genes in DCM through pedigree analysis.METHODS Our research team identified a patient with DCM in the clinic.Through invest-igation,we found that the family of this patient has a typical DCM pedigree.High-throughput sequencing technology,next-generation sequencing,was used to sequence the whole exomes of seven samples in the pedigree.RESULTS A novel and potentially pathogenic gene mutation-ANK2p.F3067L-was discovered.The mutation was completely consistent with the clinical information for this DCM pedigree.Sanger sequencing was used to further verify the locus of the mutation in pedigree samples.These results were consistent with those of high-throughput sequencing.CONCLUSIONS ANK2p.F3067L is considered a novel and potentially pathogenic gene mutation in DCM.

Changes of p53 and Waf1p21 and cell proliferation in esophageal carcinogenesis

AIM To study the correlationship between the changes of p53, Waf1p21 and the cell proliferation determined by PCNA at different stages of human esophageal carcinogenesis. METHODS Biopsied and resected esophageal tissues from a high risk population for esophageal cancer in northern China were used in this study. All the specimens were fixed with 85% alcohol and further processed with routine histology. The avidin biotin peroxidase complex (ABC) method was used for the detection of p53, Waf1p21 and PCNA. RESULTS The strong nuclear staining for p53, Waf1p21 and PCNA was observed in the normal esophageal epithelium and the epithelia with different severities of lesions. As the lesions progressed to dysplasia (DYS) and to esophageal squamons cell carcinoma (SCC), the percentage of Waf1p21 immunoreactivity decreased. The number of Waf1p21 immunostaining positive cells increased slightly from normal to basal cell hyperplasia (BCH), but there was no further increase in DYS and in SCC. The total number of positive cells for Waf1p21 stain appeared to be lower than that of p53 in normal and BCH esophageal epithelia and much lower in DYS and SCC. The Waf1p21 positive immunostaining cells were located at the third and forth cell layers in half of the samples examined, which was 2～4 cell layers higher than that of PCNA and p53 in the same histological categories of normal, BCH and DYS. CLNCLUSION The low levels of Waf1p21 at the stage of DYS may be related to a functional loss of p53. Other mechanisms may also be responsible to the lack of Waf1p21 expression in DYS and SCC.

Genes for RNA-binding proteins involved in neuralspecific functions and diseases are downregulated in Rubinstein-Taybi iNeurons

Taking advantage of the fast-growing knowledge of RNA-binding proteins(RBPs)we review the signature of downregulated genes for RBPs in the transcriptome of induced pluripotent stem cell neurons(iNeurons)modelling the neurodevelopmental Rubinstein Taybi Syndrome(RSTS)caused by mutations in the genes encoding CBP/p300 acetyltransferases.We discuss top and functionally connected downregulated genes sorted to“RNA processing”and“Ribonucleoprotein complex biogenesis”Gene Ontology clusters.The first set of downregulated RBPs includes members of hnRNHP(A1,A2B1,D,G,H2-H1,MAGOHB,PAPBC),core subunits of U small nuclear ribonucleoproteins and Serine-Arginine splicing regulators families,acting in precursor messenger RNA alternative splicing and processing.Consistent with literature findings on reduced transcript levels of serine/arginine repetitive matrix 4(SRRM4)protein,the main regulator of the neural-specific microexons splicing program upon depletion of Ep300 and Crebbp in mouse neurons,RSTS iNeurons show downregulated genes for proteins impacting this network.We link downregulated genes to neurological disorders including the new HNRNPH1-related intellectual disability syndrome with clinical overlap to RSTS.The set of downregulated genes for Ribosome biogenesis includes several components of ribosomal subunits and nucleolar proteins,such NOP58 and fibrillarin that form complexes with snoRNAs with a central role in guiding post-transcriptional modifications needed for rRNA maturation.These nucleolar proteins are“dual”players as fibrillarin is also required for epigenetic regulation of ribosomal genes and conversely NOP58-associated snoRNA levels are under the control of NOP58 interactor BMAL1,a transcriptional regulator of the circadian rhythm.Additional downregulated genes for“dual specificity”RBPs such as RUVBL1 and METTL1 highlight the links between chromatin and the RBP-ome and the contribution of perturbations in their cross-talk to RSTS.We underline the hub position of CBP/p300 in chromatin regulation,the impact of its defect on neurons’post-transcriptional regulation of gene expression and the potential use of epidrugs in therapeutics of RBP-caused neurodevelopmental disorders.

Study on the Function of ORF Genes of Porcine Circovirus-like Virus P1

[Objectives]This study was conducted to determine the functions of eight ORF genes of porcine circovirus-like virus P1.[Methods]The double-copy tandem molecular cloning of porcine circovirus-like virus P1 genome was used to construct molecular clones with eight ORFs deleted by DNA site-directed mutagenesis technology.After transfected into PK15 cells for a certain period of time,RNA were extracted and was used to verify whether the eight ORFs were deleted or not and used for gene microarry analysis.The GO functions and KEGG pathway enrichment of differentially expressed genes were analyzed.[Results]P1 ORF1 is mainly involved in the biological processes of defense response to virus,signal transduction,regulation of Rab GTPase activity,and lipid metabolic process,and involved in the molecular functions of protein phosphatase inhibitor activity,phosphatidylinositol phospholipase C activity,2 iron,2 sulfur cluster binding,phosphoric diester hydrolase activity,and Rab GTPase activator activity,and in the KEGG pathways of secretion of digestive gland and nervous system development.P1 ORF2 is mainly involved in the biological processes of positive regulation of leukocyte chemotaxis,positive regulation of cell proliferation,positive regulation of cell migration,defense response to virus,regulation of cell growth,and involved in the molecular functions of insulin-like growth factor binding,and chemokine activity,and in the KEGG pathways of cytosolic DNA-sensing pathway,RIG-I-like receptor signaling pathway,toll-like receptor signaling pathway,chemokine signaling pathway,and cytokines,cytokine-cytokine receptor interaction.The biological processes,molecular functions and related pathways involving P1 ORF3 and ORF5 are basically similar to those of ORF2.P1 ORF8 is mainly involved in the biological processes of purine ribonucleotide biosynthetic process,amino acid transport,defense response to virus,amino acid transmembrane transport,and involved in molecular functions of N6-(1,2-dicarboxyethyl)AMP AMP-lyase(fumarate-forming)activity,iron-sulfur cluster binding,amino acid transmembrane transporter activity.[Conclusions]The analysis of the ORF functions of P1 virus lays a foundation for the study of its pathogenicity and pathogenesis.

ALV-A p27基因的原核表达及其鼠源多克隆抗体的制备

试验拟通过构建A亚群禽白血病病毒(ALV-A) p27基因原核表达载体,从而制备抗p27蛋白鼠源多克隆抗体。将感染ALV-A毒株的DF-1细胞反复冻融后提取RNA并反转录为cDNA,利用PCR扩增获得ALV-A p27基因,将目的基因克隆至pColdⅠ载体,并转化入大肠杆菌BL21(DE3)菌中进行诱导表达,经镍柱纯化后免疫28～32日龄的雌性小鼠,采用间接ELISA法测定抗体效价,Western blot检测抗体特异性。试验经PCR扩增出750 bp左右的特异性条带,并成功构建pColdⅠ-ALV-A-p27原核表达载体,加入终浓度为1 mmol/L的IPTG于18℃诱导表达18～24 h成功得到重组蛋白,该蛋白主要以包涵体形式存在。间接ELISA检测显示,制备的鼠源多克隆抗体血清抗体效价为1∶3 200;Western blot检测结果表明,制备的多克隆抗体能特异性识别原核表达的p27蛋白。试验结果在ALV的抗原分析、血清学诊断等方面有着重要的应用价值。

树舌多糖对小鼠HepA P16 P27 Rb基因表达的影响

目的:探讨树舌多糖抗肿瘤作用的机制. 方法:通过免疫组化、ELISA法分别测定瘤体和血清中抑癌基因P16,P27,Rb表达蛋白的量;通过透射电镜观察凋亡小体是否存在. 结果:树舌多糖作用后P16,P27,Rb基因表达蛋白的量与盐水组有差异具有统计学意义,免疫组化结果:bP<0.01, vs(1)(2);aP<0.05,vs(2)(3);dP<0.01,vs(3).ELISA结果: aP<0.05,vs(3);bP<0.01,cP<0.05,vs(4);dP<0.01,vs (3)(4);fp<0.01,vs(4);gP<0.05,hP<0.01,vs(3).且P16, P27表达的量与Rb呈负相关mr=-0.094(1),nr=-0.446 (1),再有观察到凋亡小体的存在. 结论:树舌多糖通过激活抑癌基因,抑制肿瘤的生长促进肿瘤细胞凋亡.

Effects of endotoxin on expression of ras, p53 and bcl-2 oncoprotein in hepatocarcinogenesis induced by thioacetamide in rats

AIM To evaluate the relationship between expression of ras, p53, bcl 2 gene products, and hepatocarcinogenesis since endotoxemia produced from lipopolysaccharide admi nistration and/or the hypophagocytic state of splenectomy significantly accelerated hepatocarcinogenesis induced by thioacetamide. 〖WTH4〗METHODS〓〖WTXFZ〗The hepatocarcinoma model was induced by oral intake of 0 03% thioacetamide for six months. During the induction of hepatocarcinoma model, rats were additionally treated with splenectomy and/or lipopolysaccharide administration. The techniques of flow cytometry, immunohistochemistry and immunoelectronmicroscopy were applied to quantitative analysis of the expression of oncogene proteins. RESULTS In this model system, overexpression of ras p21 protein mainly occurred on precancerous cell population or in early stage of hepatocyte transformation. And the levels of ras p21 declined when nuclear DNA aneuploid increased. Expression of bcl 2 protein slowly and steadily rose with more hepatocytes staying in S+G2M phases as the hepatocarcinoma became more malignant. P53 was moderately expressed during the hepatocarcinogenesis. There was no statistical correlation between endotoxemia levels and the changes of ras, p53 and bcl 2 gene products. CONCLUSION Over expression of oncogene ras p21 was likely to be a precursor of the premalignant hepatocytes and it might be responsible for the initiation of hepatocarcinogenesis. Bcl 2 protein expression is proportional to the severity of the malignancies. P53 may be a key pathway on the transformation and development of hepatocarcinoma. This study confirmed the hypothesis that there are multiple genes and multiple steps involved in hepatocarcinogenesis. Expressions of oncogene proteins reflected the properties of the premalignant and malignant cells, but not directly related to endotoxemia statistically.[JP]

河北省蛋鸡群ALV p27抗原ELISA检测

禽白血病（Avian Leukusis,AL）是由反转录病毒科禽白血病/肉瘤病毒群病毒引起的禽类多种肿瘤性疾病的总称,可引起感染鸡免疫抑制和多组织器官发育迟缓、萎缩以及肿瘤等,造成鸡的生产性能下降甚至死亡,由鸡分离的ALV划分为A、B、C、D、E、J六个亚群。自2002年蛋鸡群发现禽白血病以来,全国各地频发,特别是自2009年以来,湖北、山东等地鸡白血病疑似病例频发,鸡群ALV的感染率高达60%,病死率高达50%以上[1]。

SIV p27单克隆抗体的制备和鉴定

目的建立SIVp27杂交瘤细胞株，并对其分泌的SIVp27单克隆抗体进行初步鉴定。方法使用基因重组的SIVp27蛋白免疫BALB/c小鼠，采用杂交瘤技术使用半固体培养基法建立杂交瘤细胞株，制备单克隆抗体。通过染色体核型对杂交瘤细胞株进行鉴定；采用Western blot、免疫荧光法、酶联免疫吸附法确定单克隆抗体的交叉反应性、相对亲和力、抗原识别表位、免疫球蛋白的类型和亚类。对单克隆抗体进行鉴定。结果获得4株可稳定分泌SIVp27单克隆抗体的杂交瘤细胞，IC3、286为IgG1类，2E12为IgG2b类，3G3为IgG2a类。4株单抗均能识别SIV的p27蛋白，与逆转录病毒SRV、STLV无交叉反应，286、2E12与H1Vp24有交叉反应。免疫荧光法检测腹水效价为1：10240～1：40960。1C3、286、2E12、3G3染色体平均数分别为103、97、96、101。2E12与3G3识别不同的抗原表位。结论成功地制备出4株SIVp27单克隆抗体，均具有良好的特异性和亲和力，为进一步建立免疫分析方法，进行SIV／SAIDS及其艾滋病相关研究，奠定了基础。

Inhibitory effects of polysaccharides isolated from Phellinus gilvus on benzo(a)pyrene-induced forestomach carcinogenesis in mice

AIM: Although polysaccharides from Phellinus mushrooms are a well-known material with anti-tumor properties, there is no information about the effect of polysaccharides from Phellinus gilvus (PG) on tumor. The modulating effect of polysaccharides isolated from PG on the benzo(a)pyrene (BaP)-induced forestomach carcinogenesis in ICR female mice was investigated in this study.METHODS: A forestomach carcinogenesis model was established in 40 ICR female mice receiving oral administration of BaP for 4 wk. The mice were randomly assigned to 4 groups (10 each). The mice in each group were treated with sterile water or PG for 4 and 8 wk (SW4,PGW4, SW8, and PGW8 groups). Eight or 12 wk after the first dose of BaP, forestomachs were removed for histopathological and RT-PCR analysis.RESULTS: In histopathological changes and RT-PCR analysis, sterile water-treated mice showed significant hyperplasia of the gastric mucosa with a significantly increased expression of mutant p53 mRNA compared to mice treated with PG for 8 wk.CONCLUSION: Polysaccharides isolated from PG may inhibit BaP-induced forestomach carcinogenesis in mice bydown-regulating mutant p53 expression.

HIV-1 p24和SIV p27两种ELISA试剂盒检测SIV p27抗原的比较

目的由于检测SIV p27抗原试剂盒来源困难,有时不稳定,鉴于HIV-1 p24与SIVp27有较强的交叉抗原,本研究比较HIV-1 p24和SIV p27两种ELISA试剂盒检测SIV p27抗原得出的结果是否存在一定的相关性。方法 HIV-1 p24和SIV p27两种ELISA试剂盒定性和定量检测样品中SIV p27抗原,并对检测结果进行回归和相关分析。结果 HIV-1 p24和SIV p27两种ELISA试剂盒检测SIV p27抗原的灵敏度分别是150 pg/mL和62.5 pg/mL。两种试剂盒检测病毒液和血浆中SIV p27抗原的定性结果一致。定量结果的统计分析得出病毒液的直线回归决定系数R2=0.857,直线相关系数r=0.926,P<0.01,直线正相关程度较高;血浆的直线回归决定系数R2=0.512,直线相关系数r=0.716,P<0.05,直线正相关程度较低。结论 HIV-1 p24 ELISA试剂盒能够替代SIVp27 ELISA试剂盒定性检测病毒液和血浆中SIV p27抗原,但只能定量检测病毒液中SIV p27抗原。

Apoptosis mechanisms of human gastric cancer cell line MKN-45 infected with human mutant p27

AIM: To explore the inducing effect of human mutant p27 gene on the apoptosis of the human gastric cancer cell line MKN-45 and its associated mechanisms. METHODS: The recombinant adenovirus Ad-p27mt was constructed to infect the human gastric cancer cell line MKN-45. Using flow cytometry, TUNEL assay and DNA fragment analysis, we measured the apoptotic effect of Ad-p27mt on the human gastric cancer cells. RESULTS: Ad-p27mt was successfully constructed and the infection efficiency reached 100%. After 18 h of infection, we observed an apoptotic hypodiploid peak on the flow cytometer before G1-S and apoptotic characteristic bands in the DNA electrophoresis. The apoptotic rate detected by TUNEL method was significantly higher in the Ad-p27mt group (89.4±3.12%)compared to the control group (3.12±0.13%, P ＜ 0.01).CONCLUSION: Human mutant p27 can induce apoptosis of the human gastric cancer cells in vitro.

Detecting the polymorphism sites of p53 and Fas genes of Han population in Zhejiang province

BACKGROUND： It is of significance for single nucleotide polymorphisms （SNPs）, a difference of rank, which exists widely in biology, genetics and other fields. OBJECTIVE： To detect polymorphism sites in exon-4 of p53 gene, promotor of Fas gene and intron-7 of Fas gene of healthy people in Han nationality in Zhejiang province. DESIGN： Simple random sampling. SETTING： Department of Surgery of the 118 Hospital of Chinese PLA.PARTICIPANTS： A total of 80 healthy people in Han nationality were selected from hospitals in Zhejiang province from August 2005 to January 2006. There were 43 males and 37 females aged from 3 to 78 years with the mean age of 39.5 years, and all subjects were consent. DNA which was used in genetic analysis was selected from peripheral venous blood of all subjects and maintained at -20℃.METHODS： Polymorphism sites in exon-4 of p53 gene, promotor of Fas gene and intron-7 of Fas gene were detected with directly DNA sequencing technique. MAIN OUTCOME MEASURES ： Polymorphism sites in exon-4 of p53 gene, promotor of Fas gene and intron-7 of Fas gene of healthy people in Han nationality in Zhejiang province. RESULTS： A total of 80 samples were involved in the final analysis. SNPs sites were found at the 119^th base of exon-4 of p53 gene （the 72^nd codon of p53 gene）, the 670^th base of upper start codon in promotor of Fas gene （Fas-670）, and the 995^th base of intron-7 of Fas gene, especially SNPs in the 995^th base of intron-7 pf Fas gene, i.e. C→A transversion, was a new site.CONCLUSION ： One unknown SNPs site is discovered in intron-7 of Fas gene of people in Han nationality in Zhejiang province. This study also proves that the 72^nd codon exists in p53 gene and the -670 polymorphism site exists in promotor of Fas gene.

DNA methylation and carcinogenesis in digestive neoplasms

ＤＮＡｍｅｔｈｙｌａｔｉｏｎａｎｄｃａｒｃｉｎｏｇｅｎｅｓｉｓｉｎｄｉｇｅｓｔｉｖｅｎｅｏｐｌａｓｍｓＪａｖｅｄＹａｋｏｏｂ，ＦＡＮＸｕｅＧｏｎｇ，ＨＵＧｕｏＬｉｎｇａｎｄＺＨＡＮＧＺｈｅｎｇＳｕｂｊｅｃｔｈｅａｄｉｎｇｓＤＮＡｍｅｔｈｙｌａｔｉ...

The Relationship between the Expression of p27^(Kip1),p53 and the Infiltration,Metastasis and Prognosis in Gastric Carcinoma

Objective: To study the relationship between the expression of p27Kip1 and p53, and the infiltration, metastasis and prognosis in gastric carcinoma. Methods: The expression of p27Kip1 and p53 at protein level was determined by immunohistochemical assay (two-step method) in 100 cases of gastric carcinoma. Results: Of the 100 cases, the positive rate of p27Kip1 and p53 expressions were 44% and 49%, respectively. In the group of gastric carcinomas with deep infiltration (infiltration group), lymph nodes metastasis group (metastasis group) and death-within-5-years group (death group), the expression of p27Kip1 was statistically lower (_P<0.05). In the metastasis group and death group, the expression of p53 was significantly higher (P<0.05). The results of the monovariate analysis revealed that the 5-year survival rate of the high p27Kip1 expression group was 70.59%, which is higher than those of the low p27Kip1 expression group (54.55%) and the negative experession group (26%). The 5-year survival rate of the high p53 expression group was 19.23%, which was lower than those of the p53 low expression group (43.75%) and the negative group (53.19%). Cox multivariate analysis showed that p27Kip1, like p53, was an independent prognostic index. But p27Klpl protein expression was a stronger independent survival predictor (RR=3.06) than p53 expression (RR=2.33). Conclusion: The low expression of p27Kip1 and the high expression of p53 reflected the more frequent invasion and metastasis, which resulted in the reduced survival of patients. As an independent markers of the gastric carcinoma, the expression of p27Kip1 is more useful than that of p53 in the prognosis prediction of gastric carcinoma.

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.

PTEN P27 SKp2在上皮性卵巢癌中的表达及其临床意义

目的:探讨PTEN、P27和SKp2在上皮性卵巢癌中的表达及临床意义。方法:阅读国内外有关文献并进行综述。结果:PTEN、P27和SKp2基因表达异常可能在上皮性卵巢癌的发生、发展过程中起关键作用,PTEN、P27和SKp2基因可作为卵巢癌预后的重要指标。结论:PTEN、P27和SKp2可能参与上皮性卵巢癌的发生、发展,PTEN、P27和SKp2可能是卵巢癌治疗靶点。