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      Identification of differentially expressed genes according to chemosensitivity in advanced ovarian serous adenocarcinomas: expression of GRIA2 predicts better survival

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          Abstract

          Background:

          The purpose of this study was to identify genes that are differentially expressed in chemosensitive serous papillary ovarian carcinomas relative to those expressed in chemoresistant tumours.

          Methods:

          To identify novel candidate biomarkers, differences in gene expression were analysed in 26 stage IIIC/IV serous ovarian adenocarcinomas (12 chemosensitive tumours and 14 chemoresistant tumours). We subsequently investigated the immunohistochemical expression of GRIA2 in 48 independent sets of advanced ovarian serous carcinomas.

          Results:

          Microarray analysis revealed a total of 57 genes that were differentially expressed in chemoresistant and chemosensitive tumours. Of the 57 genes, 39 genes were upregulated and 18 genes were downregulated in chemosensitive tumours. Five differentially expressed genes ( CD36, LIFR, CHL1, GRIA2, and FCGBP) were validated by quantitative real-time PCR. The expression of GRIA2 was validated at the protein level by immunohistochemistry, and patients with GRIA2 expression showed a longer progression-free and overall survival ( P=0.051 and P=0.031 respectively).

          Conclusions:

          We found 57 differentially expressed genes to distinguish between chemosensitive and chemoresistant tumours. We also demonstrated that the expression of GRIA2 among the differentially expressed genes provides better prognosis of patients with advanced serous papillary ovarian adenocarcinoma.

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          Most cited references33

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          Cloned glutamate receptors.

          S. Heinemann, M Hollmann (1994)
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            Critical review of published microarray studies for cancer outcome and guidelines on statistical analysis and reporting.

            Alain Dupuy, Richard M Simon (2007)
            Both the validity and the reproducibility of microarray-based clinical research have been challenged. There is a need for critical review of the statistical analysis and reporting in published microarray studies that focus on cancer-related clinical outcomes. Studies published through 2004 in which microarray-based gene expression profiles were analyzed for their relation to a clinical cancer outcome were identified through a Medline search followed by hand screening of abstracts and full text articles. Studies that were eligible for our analysis addressed one or more outcomes that were either an event occurring during follow-up, such as death or relapse, or a therapeutic response. We recorded descriptive characteristics for all the selected studies. A critical review of outcome-related statistical analyses was undertaken for the articles published in 2004. Ninety studies were identified, and their descriptive characteristics are presented. Sixty-eight (76%) were published in journals of impact factor greater than 6. A detailed account of the 42 studies (47%) published in 2004 is reported. Twenty-one (50%) of them contained at least one of the following three basic flaws: 1) in outcome-related gene finding, an unstated, unclear, or inadequate control for multiple testing; 2) in class discovery, a spurious claim of correlation between clusters and clinical outcome, made after clustering samples using a selection of outcome-related differentially expressed genes; or 3) in supervised prediction, a biased estimation of the prediction accuracy through an incorrect cross-validation procedure. The most common and serious mistakes and misunderstandings recorded in published studies are described and illustrated. Based on this analysis, a proposal of guidelines for statistical analysis and reporting for clinical microarray studies, presented as a checklist of "Do's and Don'ts," is provided.
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              Epigenetic-aging-signature to determine age in different tissues

              Carmen Koch, Wolfgang Wagner (2011)
              All tissues of the organism are affected by aging. This process is associated with epigenetic modifications such as methylation changes at specific cytosine residues in the DNA (CpG sites). Here, we have identified an Epigenetic-Aging-Signature which is applicable for many tissues to predict donor age. DNA-methylation profiles of various cell types were retrieved from public data depositories - all using the HumanMethylation27 BeadChip platform which represents 27,578 CpG sites. Five datasets from dermis, epidermis, cervical smear, T-cells and monocytes were used for Pavlidis Template Matching to identify 19 CpG sites that are continuously hypermethylated upon aging (R > 0.6; p-value <10−13). Four of these CpG sites (associated with the genes NPTX2, TRIM58, GRIA2 and KCNQ1DN) and an additional hypomethylated CpG site (BIRC4BP) were implemented in a model to predict donor age. This Epigenetic-Aging-Signature was tested on a validation group of eight independent datasets corresponding to several cell types from different tissues. Overall, the five CpG sites revealed age-associated DNA-methylation changes in all tissues. The average absolute difference between predicted and real chronological age was about 11 years. This method can be used to predict donor age in various cell preparations - for example in forensic analysis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Br J Cancer
                Journal ID (iso-abbrev): Br. J. Cancer
                Title: British Journal of Cancer
                Publisher: Nature Publishing Group
                ISSN (Print): 0007-0920
                ISSN (Electronic): 1532-1827
                Publication date (Print): 26 June 2012
                Publication date (Electronic): 29 May 2012
                Volume: 107
                Issue: 1
                Pages: 91-99
                Affiliations
                [1 ]Department of Obstetrics & Gynecology, Samsung Medical Center, Sungkyunkwan University School of Medicine , 50 Irwon-dong, Gangnam-gu, Seoul 135-710, Korea
                [2 ]Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul 135-710, Korea
                [3 ]Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine , Seoul, Korea
                [4 ]Department of Obstetrics and Gynecology, Gangnam CHA Medical Center, CHA University , Seoul, Korea
                [5 ]Department of Obstetrics & Gynecology, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine , Seoul 135-710, Korea
                Author notes
                Article
                Publisher Item ID: bjc2012217
                DOI: 10.1038/bjc.2012.217
                PMC ID: 3389416
                PubMed ID: 22644307
                SO-VID: b805ea24-bb0b-46ee-a0f1-911a8dfb4c33
                Copyright © Copyright © 2012 Cancer Research UK
                License:

                From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

                History
                Date received : 01 November 2011
                Date revision received : 12 April 2012
                Date accepted : 17 April 2012
                Categories
                Subject: Molecular Diagnostics

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gene expression profiling,microarray,ovarian serous adenocarcinoma,gria2,survival
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gene expression profiling, microarray, ovarian serous adenocarcinoma, gria2, survival

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