Journal of nucleic acids investigation最新文献_第3页

Body fluid micro(mi)RNAs as biomarkers for human cancer 体液微rna作为人类癌症的生物标志物

Journal of nucleic acids investigation Pub Date : 2011-01-17 DOI: 10.4081/JNAI.2011.E1

E. Sauter, N. Patel

{"title":"Body fluid micro(mi)RNAs as biomarkers for human cancer","authors":"E. Sauter, N. Patel","doi":"10.4081/JNAI.2011.E1","DOIUrl":"https://doi.org/10.4081/JNAI.2011.E1","url":null,"abstract":"Accepted tools for early cancer detection run the gamut from Pap staining to detect cervical cancer detection to colonoscopy and biopsy for colorectal cancer detection to imaging (mammogram and, in high risk women, magnetic resonance imaging) and biopsy for breast cancer detection. These modalities use standard cytopathologic assessment to determine if disease is present. There are few biologic (DNA, RNA, protein or carbohydrate) markers (biomarkers) that are in general use for the detection of any cancer, or to identify individuals at increased cancer risk. Biomarkers have been identified that provide information to physicians on disease prognosis. Panels of biomarkers are being developed to predict response to treatment in individuals with known cancer, and some are currently in use. Nonethless, there is a great need to identify accurate biomarkers for the early detection of a new cancer, to identify individuals at increased cancer risk, and among those with cancer, to determine their likelihood of responding to a given treatment, risk of disease relapse and death. Micro (mi)RNAs hold promise as biomarkers for determining at risk individuals, for early cancer detection, and among those with cancer, to assess how likely a person is to respond a given treatment, their risk of disease recurrence and death.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"2 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2011-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/JNAI.2011.E1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70281499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 23

MicroRNAs as biomarkers for the diagnosis and prognosis of human cancer microrna作为人类癌症诊断和预后的生物标志物

Journal of nucleic acids investigation Pub Date : 2010-12-13 DOI: 10.4081/JNAI.2010.2130

D. Asslaber, J. P. Hofbauer, R. Greil, A. Egle

引用次数: 2

Development of network inference among LexA/ RecA-dependent manner genes in the SOS response SOS反应中LexA/ reca依赖方式基因的网络推理研究进展

Journal of nucleic acids investigation Pub Date : 2010-11-25 DOI: 10.4081/JNAI.2010.1871

S. Aburatani

{"title":"Development of network inference among LexA/ RecA-dependent manner genes in the SOS response","authors":"S. Aburatani","doi":"10.4081/JNAI.2010.1871","DOIUrl":"https://doi.org/10.4081/JNAI.2010.1871","url":null,"abstract":"The expression of many genes varies under different conditions. The relationships among genes can be identified from DNA microarray data. To better understand the SOS response, I developed a network model of whole LexA/RecA-dependent manner genes in two genotypes of Escherichia coli from expression data after ultraviolet (UV) irradiation. First, all LexA/RecA-dependent manner genes were estimated by a combination of the Mann-Whitney U test and hierarchical clustering. Second, the relationships between genes were inferred from a graphical Gaussian model (GGM) combined with hierarchical clustering. Here, I incorporate a step-by-step procedure of the method developed in my previous study to identify interactions within larger clusters. The analysis suggested the presence of a sequential relationship between LexA/RecA-dependent manner gene groups in which the association between neighboring groups was positive while that between non-neighboring groups was negative. I suggest the inferred network provides information on the functional role of poorly defined genes whose expression patterns change according to LexA/RecA. Although relationships in the network require biological validation, the model presented here provides insights into potential LexA/RecA regulation following UV irradiation.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"13"},"PeriodicalIF":0.0,"publicationDate":"2010-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/JNAI.2010.1871","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of microRNA during bovine adipogenesis 牛脂肪形成过程中microRNA的表达

Journal of nucleic acids investigation Pub Date : 2010-11-11 DOI: 10.4081/JNAI.2010.1872

S. L. Pratt, T. Burns, E. Curry, S. Duckett

{"title":"Expression of microRNA during bovine adipogenesis","authors":"S. L. Pratt, T. Burns, E. Curry, S. Duckett","doi":"10.4081/JNAI.2010.1872","DOIUrl":"https://doi.org/10.4081/JNAI.2010.1872","url":null,"abstract":"Studies have recently indicated that the adipogenic process and the expression of genes involved in lipid metabolism may be regulated in part at the post-transcriptional level by a class of small RNA called microRNA (miRNA). The objectives of this study were to i) determine if miRNAs are differentially expressed, and ii) evaluate expression of known miRNA targets in bovine adipocytes. Bovine adipose samples were collected from castrated males fattened on a high concentrate diet (C) or pasture (PA) and were frozen in liquid nitrogen and stored at -80°C, or used to generate primary stromal-vascular cells (SV). SV cells were cultured to confluence (Control) or differentiated at confluence and harvested 2 (D2), 6 (D6), or 12 (D12) days post-confluence. A 3x3 microarray analysis was performed comparing Control and differentiated samples. miR-21, -221, and -222 (P less than 0.05) were differentially expressed. qRT-PCR was conducted using the in vitro samples, and all three miRNAs were down regulated on D2 (P less than 0.05). miR-221 and -222 were decreased on D6 compared to Control (P less than 0.05), but only miR-222 expression was decreased at D12 (P less than 0.05) compared to Control. miR-21 increased in expression compared to Control on D12 (P less than 0.05). In vivo , only miR-21 expression was affected and it was reduced in PA compared to C fat samples (P less than 0.05). Two targets of miR-21 are Programmed Cell Death Protein 4 (PDCD4) and Phosphatase and Tensin Homolog (PTEN), and neither messenger RNA was differentially expressed in vitro (P greater than 0.05), but both messenger RNAs were elevated for PA compared to C (P less than 0.05). These data show that miRNAs are differentially expressed in adipose cells and tissue, and that miR-21 may be involved in adipocyte function by regulating the translation of PDCD4 and PTEN.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"12"},"PeriodicalIF":0.0,"publicationDate":"2010-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

Molecular markers for prediction of risk of radiation-related injury to normal tissue 用于预测正常组织辐射相关损伤风险的分子标记

Journal of nucleic acids investigation Pub Date : 2010-10-11 DOI: 10.4081/JNAI.2010.E11

M. Ghilotti, M. Pierotti, M. Gariboldi

{"title":"Molecular markers for prediction of risk of radiation-related injury to normal tissue","authors":"M. Ghilotti, M. Pierotti, M. Gariboldi","doi":"10.4081/JNAI.2010.E11","DOIUrl":"https://doi.org/10.4081/JNAI.2010.E11","url":null,"abstract":"Radiotherapy is one of the most effective methods for the treatment of cancer, but occurrence of adverse reactions developing in the co-irradiated normal tissue can be a threat for patients. Identification of individuals at risk of severe reaction is very difficult and considerable efforts have been made to correlate normal tissue toxicity with cellular responses to ionizing radiation. Genetic markers enabling to identify hyper-sensitive patients prior to treatment would considerably improve its outcome. Gene association studies should help to identify such markers. Expression levels of specific transcripts could be putative markers; in fact different studies found associations between gene expression profiles in normal cells and the reaction of normal tissues to radiation therapy. The finding that ionizing radiation induces the deregulation of a high number of genes suggests that also microRNAs that affect the expression of a large number of target genes may be involved. This review briefly introduces the mechanisms of radiation-induced normal tissue toxicity and summarizes clinical research focused on the evaluation of molecular biomarkers for predicting risk of injury to normal tissue, mainly describing gene transcripts alterations.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2010-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Predictive molecular markers for EGFR-TKI in non-small cell lung cancer patients: new insights and critical aspects 非小细胞肺癌患者EGFR-TKI的预测性分子标记:新的见解和关键方面

Journal of nucleic acids investigation Pub Date : 2010-07-15 DOI: 10.4081/JNAI.2010.E10

P. Ulivi, D. Calistri, W. Zoli, D. Amadori

{"title":"Predictive molecular markers for EGFR-TKI in non-small cell lung cancer patients: new insights and critical aspects","authors":"P. Ulivi, D. Calistri, W. Zoli, D. Amadori","doi":"10.4081/JNAI.2010.E10","DOIUrl":"https://doi.org/10.4081/JNAI.2010.E10","url":null,"abstract":"In recent years, a number of novel agents have been investigated that target specific molecular pathways in non-small cell lung cancer (NSCLC). A great deal of effort has been focused on identifying specific markers that predict treatment response, given that a tailored approach would maximize both the therapeutic index and the cost-effectiveness. The epidermal growth factor receptor (EGFR) pathway has emerged as a key regulator of cancer cell proliferation and invasion, and several specific EGFR inhibitors have been examined. Gefitinib and erlotinib are selective EGFR tyrosine kinase inhibitors (EGFR-TKIs), demonstrating good results in selected cases both in terms of objective response rate and of overall survival. At present, EGFR gene mutations are the best positive predictive factors for TKI therapy, and a number of other potential biomarkers are being investigated as additional positive or negative predictors of response. The correct selection of patients that could benefit from these innovative therapies, based on an accurate molecular characterization, is mandatory to provide the best clinical management. Currently, the main factor limiting the characterization of metastatic NSCLC patients is the small quantity of tumor cells available for molecular analysis. In this paper we provide an overview of the most important molecular predictive markers for EGFR-TKIs therapy in NSCLC patients, and focus attention on biological samples suitable for analysis and alternative sampling approaches such as plasma- or serum-derived DNA.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2010-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

A novel detection method for heteroduplex DNA using carbodiimide-induced interrupted primer extension 一种利用碳二亚胺诱导的中断引物延伸检测异双工DNA的新方法

Journal of nucleic acids investigation Pub Date : 2010-06-03 DOI: 10.4081/JNAI.2010.1577

T. Tabone, R. Cotton, Ninan Mathew, J. Parkin, J. Savige

{"title":"A novel detection method for heteroduplex DNA using carbodiimide-induced interrupted primer extension","authors":"T. Tabone, R. Cotton, Ninan Mathew, J. Parkin, J. Savige","doi":"10.4081/JNAI.2010.1577","DOIUrl":"https://doi.org/10.4081/JNAI.2010.1577","url":null,"abstract":"Direct sequencing may be problematic in demonstrating mutations where inherited disease results from multiple different heterozygous variants in large genes. We describe here a novel mutation screening method based on the ability of carbodiimide to bind mismatched DNA and interrupt primer extension thereby identifying both a heterozygous variant and its location. This assay detected all four classes of DNA mismatch in 550 bp engineered plasmid fragments and in two dominantly inherited renal diseases. In patients with thin basement membrane nephropathy, the method demonstrated multiple variants within a single amplicon including some close to the primer binding site. This method also detected a complex mutation in medullary cystic kidney disease type 2 (c.278-289 del/insCCGGCTCCT) as multiple termination events and, furthermore, correctly identified five affected and 28 unaffected family members. Carbodiimide-induced interrupted primer extension identifies heterozygous variants in large or multiexonic genes, where the variants differ in each family, their locations are unknown, and even if there are multiple known non-pathogenic variants within the same amplicon. This assay incorporates a “universal” protocol that detects all types of mutations without the need for further optimization, and potentially detects mutations where the proportion of heteroduplex is less than 50%.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2010-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/JNAI.2010.1577","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Survival of the fittest or best adapted: HLA-dependent tumor development 适者生存或最佳适应:hla依赖的肿瘤发展

Journal of nucleic acids investigation Pub Date : 2010-05-27 DOI: 10.4081/JNAI.2010.1654

G. Masucci, E. Andersson, L. Villabona, H. Helgadottir, K. Bergfeldt, F. Cavallo, G. Forni, S. Ferrone, A. Choudhury, B. Seliger, R. Kiessling

引用次数: 10

FHIT suppresses inflammatory carcinogenic activity by inducing apoptosis in esophageal epithelial cells FHIT通过诱导食管上皮细胞凋亡抑制炎性致癌活性

Journal of nucleic acids investigation Pub Date : 2010-05-20 DOI: 10.4081/JNAI.2010.E7

K. Mimori, T. Yokobori, M. Iwatsuki, T. Sudo, F. Tanaka, K. Shibata, H. Ishii, M. Mori

{"title":"FHIT suppresses inflammatory carcinogenic activity by inducing apoptosis in esophageal epithelial cells","authors":"K. Mimori, T. Yokobori, M. Iwatsuki, T. Sudo, F. Tanaka, K. Shibata, H. Ishii, M. Mori","doi":"10.4081/JNAI.2010.E7","DOIUrl":"https://doi.org/10.4081/JNAI.2010.E7","url":null,"abstract":"We focused on the mechanism by which FHIT suppresses neoplastic transformation in normal but damaged esophageal epithelial cells exposed to inflammatory stimuli in vivo and to chemo-radiotherapy in clinical samples. For in vitro analysis, Adenoviral-FHIT (Ad-FHIT) in TE4 and TE2 were used for microarray analysis. For in vivo analysis, wild-type (WT) FHIT and FHIT-deficient (KO) C57BL/6 mice were exposed to N-nitrosomethylbenzylamine (NMBA) and to a cyclooxygenase-2 inhibitor (COXI). Considering DNA damage on clinical samples, expressions of FHIT, BAX and PCNA were evaluated by comparing between 3 cases of esophageal cancer cases of the chemo-radiotherapy responder and 7 cases of the non-responder. In in vitro analysis, we listed the down-regulated genes in Ad-FHIT that significantly control Lac-Z infected cells, such as prostaglandin E receptor 4, cyclooxygenase-1 and cyclooxygenase-2. In in vivo analysis, FHIT-KO mice were much more susceptible to tumorigenesis than were FHIT-WT mice. A significant difference in PGE2 activation was observed between FHIT-WT mice (5.2 ng/mL) and FHIT-KO mice (28.4 ng/mL) after exposure to NMBA in the absence of COXI as determined by ELISA assay (P less than 0.01). BAX expression was significantly higher in FHIT-WT (1.0±0.43) than in FHIT-KO (0.17±0.17) (P less than 0.05). The IHC score for FHIT and BAX expression was significantly higher in responders than the others (P less than 0.05). FHIT possesses tumor suppressor activity by induction of apoptosis in damaged cells after exposure to inflammatory carcinogens and DNA damaging chemo-radiotherapy.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"31-35"},"PeriodicalIF":0.0,"publicationDate":"2010-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/JNAI.2010.E7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer immunoediting and dioxin-activating aryl hydrocarbon receptor: a missing link in the shift toward tumor immunoescape? 肿瘤免疫编辑和二恶英激活芳烃受体:肿瘤免疫逃逸转变的缺失环节?

Journal of nucleic acids investigation Pub Date : 2010-05-19 DOI: 10.4081/JNAI.2010.E6

R. Ridolfi, M. Guidoboni, L. Ridolfi

{"title":"Cancer immunoediting and dioxin-activating aryl hydrocarbon receptor: a missing link in the shift toward tumor immunoescape?","authors":"R. Ridolfi, M. Guidoboni, L. Ridolfi","doi":"10.4081/JNAI.2010.E6","DOIUrl":"https://doi.org/10.4081/JNAI.2010.E6","url":null,"abstract":"The aryl hydrocarbon receptor (AhR), a member of the PAS protein family, is found in organisms as diverse as Drosophila melanogaster, nematodes, and mammals. While several reviews have reported that AhR, once activated by agonist ligands, causes long-term effects such as modification of cell growth through cell cycle control, there is also recent evidence of its decisive role in immunosuppression. The most widely studied AhR agonist is 2,3,7,8-tetrachlorodibenzo-p-dioxin, which binds AhR with the highest known affinity, leading to profound suppression of both humoral and cellular immune responses, with praecox thymus involution, consequent thymocyte loss, and induction of T-cell apoptosis. Dioxin-AhR binding causes a decline in the number of dendritic cells and enhances apoptosis following their inappropriate activation. Dioxin-mediated activation of AhR also has a direct influence on the expansion of regulatory T-cells CD4+CD25+ FoxP3+ (T-regs) and an adverse affect on CD8+ T-cell responses. Dioxin released from industrial and waste incinerators over the last few decades has caused widespread contamination of food, leading to its accumulation in fatty tissue in animals and humans. The elimination half-life of dioxin in humans (7-10 years) may favor the potentially continuous and long-lasting activation of AhR, leading to perpetual immune suppression and facilitating the onset, growth, and diffusion of tumors, especially in young people. In the cancer immunoediting hypothesis, which subdivides the relationship between tumor and immune system into three phases: elimination, equilibrium, and escape, it is thought that dioxin accumulation may cause an inevitable shift toward tumor escape.","PeriodicalId":89421,"journal":{"name":"Journal of nucleic acids investigation","volume":"1 1","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2010-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/JNAI.2010.E6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70280654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2