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Tytuł pozycji:

Integrative clinical transcriptome analysis reveals TMPRSS2-ERG dependency of prognostic biomarkers in prostate adenocarcinoma.

Tytuł:
Integrative clinical transcriptome analysis reveals TMPRSS2-ERG dependency of prognostic biomarkers in prostate adenocarcinoma.
Autorzy:
Gerke JS; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Orth MF; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Tolkach Y; Institute of Pathology, University Hospital Bonn, Bonn, Germany.
Romero-Pérez L; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Wehweck FS; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Stein S; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Musa J; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Knott MML; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.; Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Hölting TLB; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Li J; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Sannino G; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Marchetto A; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Ohmura S; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Cidre-Aranaz F; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.
Müller-Nurasyid M; Institute of Genetic Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany.; Chair of Genetic Epidemiology, IBE, Faculty of Medicine, LMU Munich, Munich, Germany.; Department of Internal Medicine I (Cardiology), Hospital of the LMU Munich, Munich, Germany.
Strauch K; Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Stief C; Urologic Clinic und Polyclinic, Clinical Center of the University of Munich, Munich, Germany.
Kristiansen G; Institute of Pathology, University Hospital Bonn, Bonn, Germany.
Kirchner T; Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.; German Cancer Consortium (DKTK), partner site Munich, Munich, Germany.; German Cancer Research Center (DKFZ), Heidelberg, Germany.
Buchner A; Department of Internal Medicine I (Cardiology), Hospital of the LMU Munich, Munich, Germany.
Grünewald TGP; Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.; Institute of Pathology, Faculty of Medicine, LMU Munich, Munich, Germany.; German Cancer Consortium (DKTK), partner site Munich, Munich, Germany.; German Cancer Research Center (DKFZ), Heidelberg, Germany.
Źródło:
International journal of cancer [Int J Cancer] 2020 Apr 01; Vol. 146 (7), pp. 2036-2046. Date of Electronic Publication: 2019 Nov 29.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: 1995- : New York, NY : Wiley-Liss
Original Publication: 1966-1984 : Genève : International Union Against Cancer
MeSH Terms:
Biomarkers, Tumor*
Adenocarcinoma/*genetics
Adenocarcinoma/*mortality
Oncogene Proteins, Fusion/*genetics
Prostatic Neoplasms/*genetics
Prostatic Neoplasms/*mortality
Adenocarcinoma/diagnosis ; Computational Biology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Male ; Neoplasm Grading ; Neoplasm Metastasis ; Neoplasm Staging ; Prognosis ; Prostatic Neoplasms/diagnosis
References:
Sathianathen NJ, Konety BR, Crook J, et al. Landmarks in prostate cancer. Nat Rev Urol 2018;15:627-42.
Cancer Research UK. Cancer Research UK, prostate cancer. 2018. Available from: http://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/prostate-cancer/survival#heading-Four. Accessed January 14, 2018.
Schapira MM, Lawrence WF, Katz DA, et al. Effect of treatment on quality of life among men with clinically localized prostate cancer. Med Care 2001;39:243-53.
Wiklund F. Prostate cancer genomics: can we distinguish between indolent and fatal disease using genetic markers? Genome medicine. BioMed Central 2010;2:45.
Torre LA, Siegel RL, Ward EM, et al. Global cancer incidence and mortality rates and trends-an update. Cancer Epidemiol Biomarkers Prev 2016;25:16-27.
Daskivich TJ, Lai J, Dick AW, et al. Variation in treatment associated with life expectancy in a population-based cohort of men with early-stage prostate cancer. Cancer 2014;120:3642-50.
Tomlins SA, Bjartell A, Chinnaiyan AM, et al. ETS gene fusions in prostate cancer: from discovery to daily clinical practice. Eur Urol 2009;56:275-86.
Abeshouse A, Ahn J, Akbani R, et al. The molecular taxonomy of primary prostate cancer. Cell 2015;163:1011-25.
Penney KL, Pettersson A, Shui IM, et al. Association of Prostate Cancer Risk Variants with TMPRSS2:ERG status: evidence for distinct molecular subtypes. Cancer Epidemiol Biomarkers Prev 2016;25:745-9.
He Z, Tang F, Lu Z, et al. Analysis of differentially expressed genes, clinical value and biological pathways in prostate cancer. Am J Transl Res 2018;10:1444-56.
Erho N, Crisan A, Vergara IA, et al. Discovery and validation of a prostate cancer genomic classifier that predicts early metastasis following radical prostatectomy. PLoS One 2013;8:e66855.
Piccolo SR, Sun Y, Campbell JD, et al. A single-sample microarray normalization method to facilitate personalized-medicine workflows. Genomics 2012;100:337-44.
Carvalho B. pd.huex.1.0.st.v2: Platform Design Info for Affymetrix HuEx-1_0-st-v2. 2015.
Dai M, Wang P, Boyd AD, et al. Evolving gene/transcript definitions significantly alter the interpretation of GeneChip data. Nucleic Acids Res 2005;33:e175.
Torres-García W, Zheng S, Sivachenko A, et al. PRADA: pipeline for RNA sequencing data analysis. Bioinformatics (Oxford, England) 2014;30:2224-6.
Perner S, Rupp NJ, Braun M, et al. Loss of SLC45A3 protein (prostein) expression in prostate cancer is associated with SLC45A3-ERG gene rearrangement and an unfavorable clinical course. Int J Cancer 2013;132:807-12.
Yoshihara K, Shahmoradgoli M, Martínez E, et al. Inferring tumour purity and stromal and immune cell admixture from expression data. Nat Commun 2013;4:2612.
Gentleman R, Carey V, Huber W. genefilter: methods for filtering genes from high-throughput experiments. 2017.
Subramanian A, Tamayo P, Mootha VK. et al. Gene set enrichment analysis: A knowledge-based approach for interpreting genome-wide expression profiles. 2005; 102:15545-50.
R Core Team. R: a language and environment for statistical computing. Austria: Vienna, 2016.
Sboner A, Demichelis F, Calza S, et al. Molecular sampling of prostate cancer: a dilemma for predicting disease progression. BMC Med Genomics 2010;3:8-8.
Therneau TM. A package for survival analysis in S version 2.38. Available at https://CRAN.R-project.org/package=survival; 2015.
Uhl B, Gevensleben H, Tolkach Y, et al. PITX2 DNA methylation as biomarker for individualized risk assessment of prostate cancer in Core biopsies. J Mol Diagn 2017;19:107-14.
Barbieri CE, Baca SC, Lawrence MS, et al. Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer. Nat Genet 2012;44:685-9.
Pierorazio PM, Walsh PC, Partin AW, et al. Prognostic Gleason grade grouping: data based on the modified Gleason scoring system: prognostic Gleason grade grouping. BJU Int 2013;111:753-60.
Egevad L, Granfors T, Karlberg L, et al. Prognostic value of the Gleason score in prostate cancer. BJU Int 2002;89:538-42.
Andrén O, Fall K, Franzén L, et al. How well does the Gleason score predict prostate cancer death? A 20-year followup of a population based cohort in Sweden. J Urol 2006;175:1337-40.
Shariat SF, Karakiewicz PI, Roehrborn CG, et al. An updated catalog of prostate cancer predictive tools. Cancer 2008;113:3075-99.
Capitanio U, Briganti A, Gallina A, et al. Predictive models before and after radical prostatectomy. Prostate 2010;70:1371-8.
O'Leary NA, Wright MW, Brister JR, et al. Reference sequence (RefSeq) database at NCBI: current status, taxonomic expansion, and functional annotation. Nucleic Acids Res 2016;44:D733-45.
Rochette A, Boufaied N, Scarlata E, et al. Asporin is a stromally expressed marker associated with prostate cancer progression. Br J Cancer 2017;116:775-84.
Jacobsen F, Kraft J, Schroeder C, et al. Up-regulation of Biglycan is associated with poor prognosis and PTEN deletion in patients with prostate cancer. Neoplasia 2017;19:707-15.
Zhou BS, Tsai P, Ker R, et al. Overexpression of transfected human ribonucleotide reductase M2 subunit in human cancer cells enhances their invasive potential. Clin Exp Metastasis 1998;16:43-9.
Burdelski C, Strauss C, Tsourlakis MC, et al. Overexpression of thymidylate synthase (TYMS) is associated with aggressive tumor features and early PSA recurrence in prostate cancer. Oncotarget 2015;6:8377-87.
Goltz D, Montani M, Braun M, et al. Prognostic relevance of proliferation markers (Ki-67, PHH3) within the cross-relation of ERG translocation and androgen receptor expression in prostate cancer. Pathology 2015;47:629-36.
Karnes RJ, Cheville JC, Ida CM, et al. The ability of biomarkers to predict systemic progression in men with high-risk prostate cancer treated surgically is dependent on ERG status. Cancer Res 2010;70:8994-9002.
Karnes RJ, Bergstralh EJ, Davicioni E, et al. Validation of a genomic classifier that predicts metastasis following radical prostatectomy in an at risk patient population. J Urol 2013;190:2047-53.
Karnes RJ, Choeurng V, Ross AE, et al. Validation of a genomic risk classifier to predict prostate cancer-specific mortality in men with adverse pathologic features. Eur Urol 2018;73:168-75.
Dalela D, Santiago-Jiménez M, Yousefi K, et al. Genomic classifier augments the role of pathological features in identifying optimal candidates for adjuvant radiation therapy in patients with prostate cancer: development and internal validation of a multivariable prognostic model. J Clin Oncol 2017;35:1982-90.
Klein EA, Haddad Z, Yousefi K, et al. Decipher genomic classifier measured on prostate biopsy predicts metastasis risk. Urology 2016;90:148-52.
Cuzick J, Swanson GP, Fisher G, et al. Prognostic value of an RNA expression signature derived from cell cycle proliferation genes in patients with prostate cancer: a retrospective study. Lancet Oncol 2011;12:245-55.
Knezevic D, Goddard AD, Natraj N, et al. Analytical validation of the Oncotype DX prostate cancer assay-a clinical RT-PCR assay optimized for prostate needle biopsies. BMC Genomics 2013;14:690.
Contributed Indexing:
Keywords: TMPRSS2-ERG; metastasis; personalized medicine; prognostic biomarker; prostate adenocarcinoma
Substance Nomenclature:
0 (Biomarkers, Tumor)
0 (Oncogene Proteins, Fusion)
0 (TMPRSS2-ERG fusion protein, human)
Entry Date(s):
Date Created: 20191117 Date Completed: 20200219 Latest Revision: 20200219
Update Code:
20240104
DOI:
10.1002/ijc.32792
PMID:
31732966
Czasopismo naukowe
In prostate adenocarcinoma (PCa), distinction between indolent and aggressive disease is challenging. Around 50% of PCa are characterized by TMPRSS2-ERG (T2E)-fusion oncoproteins defining two molecular subtypes (T2E-positive/negative). However, current prognostic tests do not differ between both molecular subtypes, which might affect outcome prediction. To investigate gene-signatures associated with metastasis in T2E-positive and T2E-negative PCa independently, we integrated tumor transcriptomes and clinicopathological data of two cohorts (total n = 783), and analyzed metastasis-associated gene-signatures regarding the T2E-status. Here, we show that the prognostic value of biomarkers in PCa critically depends on the T2E-status. Using gene-set enrichment analyses, we uncovered that metastatic T2E-positive and T2E-negative PCa are characterized by distinct gene-signatures. In addition, by testing genes shared by several functional gene-signatures for their association with event-free survival in a validation cohort (n = 272), we identified five genes (ASPN, BGN, COL1A1, RRM2 and TYMS)-three of which are included in commercially available prognostic tests-whose high expression was significantly associated with worse outcome exclusively in T2E-negative PCa. Among these genes, RRM2 and TYMS were validated by immunohistochemistry in another validation cohort (n = 135), and several of them proved to add prognostic information to current clinicopathological predictors, such as Gleason score, exclusively for T2E-negative patients. No prognostic biomarkers were identified exclusively for T2E-positive tumors. Collectively, our study discovers that the T2E-status, which is per se not a strong prognostic biomarker, crucially determines the prognostic value of other biomarkers. Our data suggest that the molecular subtype needs to be considered when applying prognostic biomarkers for outcome prediction in PCa.
(© 2019 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

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