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• SAGE Protocols  and Software

• SAGE Tag to Gene Maps

• SAGE Data

• CGAP SAGE Page

• Download Cancer SAGE data

• Saccharomyces Genome Database

• Download Yeast SAGE data

• Genzyme SAGE Site

• Compugen

• SADE site/CEA Saclay

• SAGE and RAGE site of the M. D. Anderson Cancer Center

• University of Tokyo

• University of Rochester

SAGE Publications

• Description of SAGE method

• SAGE Reviews

• Cancer studies

• Human disease

• Pathway analysis

• Plant and model organisms

• Bioinformatics and transcriptome analysis

• Technological advances 

Jansen BJ, van Ruissen F, de Jongh G, Zeeuwen PL, Schalkwijk J  Serial 

    analysis of gene expression in differentiated cultures of human epidermal

    keratinocytes. J Invest Dermatol. 2001 Jan;116(1):12-22.

Kenzelmann M, Muhlemann K.  Transcriptome analysis of fibroblast cells

    immediate-early after human cytomegalovirus infection. 

    J Mol Biol. 2000 Dec 15;304(5):741-51.

FEBS Lett 2001 Jun 1;498(1):37-41

Books, LinkOut

Identification of novel mast cell genes by serial analysis of gene expression in cord blood-derived mast cells.

Kuramasu A, Kubota Y, Matsumoto K, Nakajima T, Sun X, Watanabe T, Saito H, Ohtsu H.

The gene expression profile of human cord blood-derived mast cells (MCs) was investigated using serial analysis of gene expression (SAGE). A total of 22914 tags, representing 9181 unique transcripts, were sequenced. By selecting tags that were detected more frequently in MCs than in other tissues, genes characteristic of MCs were enriched. Reverse transcription-PCR and the high-density oligonucleotide array hybridization confirmed the validity of our SAGE result. About 70% of the selected genes were previously uncharacterized. Northern blot analysis showed the MC-specific expression of selected genes. This inventory will be useful to identify novel genes with important functions in MCs.

PMID: 11389894 [PubMed - in process]

Cancer Res 2001 Jun 1;61(11):4320-4

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Discovery of new markers of cancer through serial analysis of gene expression: prostate stem cell antigen is overexpressed in pancreatic adenocarcinoma.

Argani P, Rosty C, Reiter RE, Wilentz RE, Murugesan SR, Leach SD, Ryu B, Skinner HG, Goggins M, Jaffee EM, Yeo CJ, Cameron JL, Kern SE, Hruban RH.

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA. pargani@jhmi.edu

Serial analysis of gene expression (SAGE) can be used to quantify gene expression in human tissues. Comparison of gene expression levels in neoplastic tissues with those seen in nonneoplastic tissues can, in turn, identify novel tumor markers. Such markers are urgently needed for highly lethal cancers like pancreatic adenocarcinoma, which typically presents at an incurable, advanced stage. The results of SAGE analyses of a large number of neoplastic and nonneoplastic tissues are now available online, facilitating the rapid identification of novel tumor markers. We searched an online SAGE database to identify genes preferentially expressed in pancreatic cancers as compared with normal tissues. SAGE libraries derived from pancreatic adenocarcinomas were compared with SAGE libraries derived from nonneoplastic tissues. Three promising tags were identified. Two of these tags corresponded to genes (lipocalin and trefoil factor 2) previously shown to be overexpressed in pancreatic carcinoma, whereas the third tag corresponded to prostate stem cell antigen (PSCA), a recently discovered gene thought to be largely restricted to prostatic basal cells and prostatic adenocarcinomas. PSCA was expressed in four of the six pancreatic cancer SAGE libraries, but not in the libraries derived from normal pancreatic ductal cells. We confirmed the overexpression of the PSCA mRNA transcript in 14 of 19 pancreatic cancer cell lines by reverse transcription-PCR, and using immunohistochemistry, we demonstrated PSCA protein overexpression in 36 of 60 (60%) primary pancreatic adenocarcinomas. In 59 of 60 cases, the adjacent nonneoplastic pancreas did not label for PSCA. PSCA is a novel tumor marker for pancreatic carcinoma that has potential diagnostic and therapeutic implications. These results establish the validity of analyses of SAGE databases to identify novel tumor markers.

PMID: 11389052 [PubMed - in process]

Br J Psychiatry 2001 Jun;178(41):S137-S141

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Serial analysis of gene expression in the frontal cortex of patients with bipolar disorder.

Sun Y, Zhang L, Johnston NL, Torrey EF, Yolken RH.

Stanley Division of Developmental Neurovirology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland. Stanley Foundation Research Program, Bethesda, Maryland, USA.

Background Bipolar disorder is a serious brain disease affecting more than a million individuals living in the USA. Epidemiological studies indicate a role for both genetic and environmental factors in the pathogenesis of this disorder. Aim To identify RNA transcripts that are up- or down-regulated in the frontal cortex regions of individuals with bipolar disorder. Method Serial analysis of gene expression (SAGE) and reverse transcriptase-polymerase chain reaction were used to identify RNA transcripts which are differentially expressed in the frontal cortex of brains obtained postmortem from individuals with bipolar disorder compared with other psychiatric and control conditions. Results Levels of RNA transcripts encoding the serotonin transporter protein and components of the NF-kappaB transcription factor complex are significantly increased in individuals with bipolar disorder compared with unaffected controls. Increased levels of expression of these RNA transcripts were also detected in the brains of some individuals with schizophrenia and unipolar depression. Conclusion The SAGE technique offers promise for the characterisation of complex human brain diseases.

PMID: 11388953 [PubMed - as supplied by publisher]

J Clin Oncol 2001 Jun 1;19(11):2948-58

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Gene discovery using the serial analysis of gene expression technique: implications for cancer research.

Polyak K, Riggins GJ.

Department of Adult Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Cancer is a genetic disease. As such, our understanding of the pathobiology of tumors derives from analyses of the genes whose mutations are responsible for those tumors. The cancer phenotype, however, likely reflects the changes in the expression patterns of hundreds or even thousands of genes that occur as a consequence of the primary mutation of an oncogene or a tumor suppressor gene. Recently developed functional genomic approaches, such as DNA microarrays and serial analysis of gene expression (SAGE), have enabled researchers to determine the expression level of every gene in a given cell population, which represents that cell population's entire transcriptome. The most attractive feature of SAGE is its ability to evaluate the expression pattern of thousands of genes in a quantitative manner without prior sequence information. This feature has been exploited in three extremely powerful applications of the technology: the definition of transcriptomes, the analysis of differences between the gene expression patterns of cancer cells and their normal counterparts, and the identification of downstream targets of oncogenes and tumor suppressor genes. Comprehensive analyses of gene expression not only will further understanding of growth regulatory pathways and the processes of tumorigenesis but also may identify new diagnostic and prognostic markers as well as potential targets for therapeutic intervention.

PMID: 11387368 [PubMed - in process]

Eur J Heart Fail 2001 Jun;3(3):271-81

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Discovering altered genomic expression patterns in heart: transcriptome determination by serial analysis of gene expression.

Anisimov SV, Lakatta EG, Boheler KR.

Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA

The development of cardiovascular diseases such as heart failure involve functional changes that are beneficial short-term, but may be fatal long-term. Current therapeutic approaches are tailored to limit progression of a disease and to maintain quality of life. At a molecular level, these disease processes involve quantitative and qualitative changes in gene expression. Although some changes in mRNA abundance may not have direct protein correlates, analysis of all the mRNAs present in a cell population (the cells transcriptome) has become a focal point of genomic research. The aim is to provide information about the dynamics of total genome expression in response to environmental changes and point to candidate genes responsible for the cascade of events that result in a disease state. One way of performing these analyses utilizes the technique of Serial Analysis of Gene Expression (SAGE). This method evaluates thousands of expressed transcripts both quantitatively and qualitatively in a single assay. In the first of two reviews on transcriptome analysis, we describe the current state of genomic research for determination of the transcriptome by Serial Analysis of Gene Expression, present the first limited SAGE analysis of rodent heart gene expression, and discuss how results generated with this approach can be applied to the study and treatment of cardiovascular diseases.

PMID: 11377997 [PubMed - in process]

Cancer Res 2001 May 15;61(10):4283-6

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Identification of differentially expressed genes by serial analysis of gene expression in human prostate cancer.

Waghray A, Schober M, Feroze F, Yao F, Virgin J, Chen YQ.

Department of Pathology [A. W., M. S., F. F., F. Y., J. V., Y. Q. C.] and Center for Molecular Medicine and Genetics [Y. Q. C.], Wayne State University, Detroit, Michigan 48201.

Prostate cancer is the leading cause of cancer death in American males. To better understand the genetic bases of this disease, we have generated a comprehensive molecular profile of human prostate. The gene expression pattern in normal and prostate cancer tissues was analyzed by serial analysis of gene expression (SAGE). A total of 133,217 transcripts were analyzed, and 35,185 distinct SAGE tags were identified representing 19,287 genes. Comparison of the transcripts in normal and tumor tissue revealed 156 differentially expressed genes (P < 0.05), of which 88 genes were up-regulated and 68 genes were down-regulated in the tumor tissue. Based on SAGE data, we estimate that the transcriptome for human prostate is approximately 37,000. Several differentially expressed genes identified by SAGE were selected for confirmation using immunohistochemistry. Some genes (e.g., E2F4) were overexpressed in tumor epithelial cells and some (e.g., Daxx) were increased in tumor stroma. Further characterization of the role of E2F4 and Daxx as well as other differentially expressed genes may provide useful insights into the mechanism of prostate cancer development.

PMID: 11358857 [PubMed - in process]

Bioinformatics 2001 Apr;17(4):300-8

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A relational schema for both array-based and SAGE gene expression experiments.

Stoeckert C, Pizarro A, Manduchi E, Gibson M, Brunk B, Crabtree J, Schug J, Shen-Orr S, Overton GC.

Computational Biology and Informatics Laboratory, Center for Bioinformatics, University of Pennsylvania, 1313 Blockley Hall, 418 Guardian Drive, Philadelphia, PA 19104-6021, USA.

Motivation and RESULTS: A relational schema is described for capturing highly parallel gene expression experiments using different technologies. This schema grew out of efforts to build a database for collaborators working on different biological systems and using different types of platforms in their gene expression experiments as well as different types of image quantification software. The tables are conceptually organized into three categories of information: Platform, Experiment (which includes image scanning and quantification), and DATA: The strengths of the schema are: (i) integrating information on array elements using a gene index; (ii) describing samples using ontologies; (iii) reducing an experiment to a single RNA source for precise descriptions yet not losing the relationships between experiments done at the same time or for the same project; and (iv) maintaining both raw and processed (e.g. cleansed and normalized) data and recording how the data is processed. The result is a novel schema, which can hold both array and non-array data, is extensible for detailed experimental descriptions that are precise and consistent, and allows for meaningful comparisons of genes between experiments. AVAILABILITY: The schema is available at http://www.cbil.upenn.edu/cgi-bin/RAD2/schemaBROWSERRAD:pl. CONTACT: stoeckrt@pcbi.upenn.edu

: Exp Cell Res 2001 Apr 15;265(1):174-83

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Involvement of polyamines in B cell receptor-mediated apoptosis: spermine functions as a negative modulator.

Nitta T, Igarashi K, Yamashita A, Yamamoto M, Yamamoto N.

Department of Microbiology and Molecular Virology, Tokyo Medical and Dental University, Tokyo, Japan.

The B cell lymphoma WEHI231 has been used as a model for studying clonal deletion of B cells on the basis of its ability to undergo growth arrest and apoptosis by B cell antigen receptor (BCR) cross-linking. To comprehensively analyze the genes involved in BCR-mediated apoptosis, we applied the technique of serial analysis of gene expression (SAGE) to WEHI231. Comparison of expression patterns revealed that BCR cross-linking caused coordinate changes in the expression of genes involved in polyamine metabolism. Polyamines are ubiquitous compounds required for cell proliferation and homeostasis. The coordinate expression of the polyamine-related genes was confirmed by semiquantitative reverse transcriptase-polymerase chain reaction analysis. During apoptosis, the genes involved in polyamine biosynthesis were downregulated, whereas those involved in polyamine catabolism were upregulated, suggesting that intracellular polyamines play a role in BCR-mediated apoptosis. Levels of intracellular putrescine, spermidine, and spermine were reduced after BCR cross-linking. These effects were prevented by concurrent CD40 stimulation, which blocked BCR-mediated apoptosis. Furthermore, addition of spermine could repress the BCR-mediated apoptosis by attenuating the mitochondrial membrane potential (Deltapsim) loss and activation of caspase-7 induced by BCR signaling. These findings strongly suggest that polyamine regulation is involved in apoptosis during B cell clonal deletion. Copyright 2001 Academic Press.

PMID: 11281655 [PubMed - indexed for MEDLINE]

Am J Pathol 1999 Jun;154(6):1685-91

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High expression of the CC chemokine TARC in Reed-Sternberg cells. A possible explanation for the characteristic T-cell infiltratein Hodgkin's lymphoma.

van den Berg A, Visser L, Poppema S.

Department of Pathology and Laboratory Medicine, University Hospital Groningen, Groningen, The Netherlands.

Hodgkin's lymphoma is characterized by the combination of Reed-Sternberg (R-S) cells and a prominent inflammatory cell infiltrate. One of the intriguing questions regarding this disease is what is causing the influx of T lymphocytes into the involved tissues. We applied the serial analysis of gene expression (SAGE) technique on the Hodgkin's lymphoma-derived cell line L428 and on an Epstein-Barr virus (EBV)-transformed lymphoblastoid B-cell line. A frequently expressed tag in L428 corresponded to the T-cell-directed CC chemokine TARC. Reverse transcription polymerase chain reaction analyses demonstrated expression of TARC in nodular sclerosis (NS) and mixed cellularity (MC) classical Hodgkin's lymphomas but not in NLP Hodgkin's lymphoma, anaplastic large-cell lymphomas, and large-B-cell lymphomas with CD30 positivity. Two of five cases of T-cell-rich B-cell lymphoma (TCRBCL) were TARC positive. RNA in situ hybridization (ISH) showed a strong signal for TARC in the cytoplasm of R-S cells, and immunohistochemical staining confirmed the presence of the TARC protein in the R-S cells of NS and MC Hodgkin's lymphomas. The lymphocytic and histiocytic (L&H)-type cells of nodular lymphocyte predominance Hodgkin's lymphoma and the neoplastic cells of non-Hodgkin's lymphomas with the exception of two cases of TCRBCL did not stain for TARC. TARC is known to bind to the CCR4 receptor, which is expressed on activated Th2 lymphocytes. The immunophenotype of lymphocytes surrounding R-S cells is indeed Th2-like, and by RNA ISH these lymphocytes showed a positive signal for the chemokine receptor CCR4. The findings suggest that production of TARC by the R-S cells may explain the characteristic T-cell infiltrate in classical Hodgkin's lymphoma.

　

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