Comparative Oncogenomics Identifies Combinations of Driver Genes And
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Comparative Oncogenomics Identifies Tyrosine Kinase FES As a Tumor Suppressor in Melanoma
RESEARCH ARTICLE The Journal of Clinical Investigation Comparative oncogenomics identifies tyrosine kinase FES as a tumor suppressor in melanoma Michael Olvedy,1,2 Julie C. Tisserand,3 Flavie Luciani,1,2 Bram Boeckx,4,5 Jasper Wouters,6,7 Sophie Lopez,3 Florian Rambow,1,2 Sara Aibar,6,7 Bernard Thienpont,4,5 Jasmine Barra,1,2 Corinna Köhler,1,2 Enrico Radaelli,8 Sophie Tartare-Deckert,9 Stein Aerts,6,7 Patrice Dubreuil,3 Joost J. van den Oord,10 Diether Lambrechts,4,5 Paulo De Sepulveda,3 and Jean-Christophe Marine1,2 1Laboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium. 2Laboratory for Molecular Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium. 3INSERM, Aix Marseille University, CNRS, Institut Paoli-Calmettes, CRCM, Equipe Labellisée Ligue Contre le Cancer, Marseille, France. 4Laboratory for Translational Genetics, Center for Cancer Biology, VIB, Leuven, Belgium. 5Laboratory for Translational Genetics, and 6Laboratory of Computational Biology, Department of Human Genetics, KU Leuven, Leuven, Belgium. 7Laboratory of Computational Biology, and 8Mouse Histopathology Core Facility, VIB Center for Brain & Disease Research, Leuven, Belgium. 9Centre Méditerranéen de Médecine Moléculaire (C3M), INSERM, U1065, Université Côte d’Azur, Nice, France. 10Laboratory of Translational Cell and Tissue Research, Department of Pathology, KU Leuven and UZ Leuven, Leuven, Belgium. Identification and functional validation of oncogenic drivers are essential steps toward -
Journal of Carcinogenesis Biomed Central
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central Journal of Carcinogenesis BioMed Central Editorial Open Access New paradigms, new Hopes: the need for socially responsible research on carcinogenesis Gopala Kovvali* Address: Gopala Kovvali Ph.D. Editor-in-Chief, Journal of Carcinogenesis, Founder President, Carcinogenesis Foundation, 22 Heritage Drive, Edison, NJ 08820, USA Email: Gopala Kovvali* - [email protected] * Corresponding author Published: 21 November 2005 Received: 15 November 2005 Accepted: 21 November 2005 Journal of Carcinogenesis 2005, 4:22 doi:10.1186/1477-3163-4-22 This article is available from: http://www.carcinogenesis.com/content/4/1/22 © 2005 Kovvali; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. It has been three years since the publication of the first The formation of the Carcinogenesis Foundation is a his- article in the Journal of Carcinogenesis; it was the editorial toric opportunity. While its goal is to promote and that espoused the need for the launch of the journal. Hav- advance research in the field of carcinogenesis, it has a ing seen three springs and three falls, it is time to ask specialized mission of understanding the phenomenon of where we are as a journal and where we want to be in the increased cancer incidence among individuals who years to come. migrate to the western countries. -
Rare Variants in the DNA Repair Pathway and the Risk of Colorectal Cancer Marco Matejcic1, Hiba A
Author Manuscript Published OnlineFirst on February 24, 2021; DOI: 10.1158/1055-9965.EPI-20-1457 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Rare variants in the DNA repair pathway and the risk of colorectal cancer Marco Matejcic1, Hiba A. Shaban1, Melanie W. Quintana2, Fredrick R. Schumacher3,4, Christopher K. Edlund5, Leah Naghi6, Rish K. Pai7, Robert W. Haile8, A. Joan Levine8, Daniel D. Buchanan9,10,11, Mark A. Jenkins12, Jane C. Figueiredo13, Gad Rennert14, Stephen B. Gruber15, Li Li16, Graham Casey17, David V. Conti18†, Stephanie L. Schmit1,19† † These authors contributed equally to this work. Affiliations 1 Department of Cancer Epidemiology, Moffitt Cancer Center, Tampa, FL 33612, USA 2 Berry Consultants, Austin, TX, 78746, USA 3 Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH 44106, USA 4 Seidman Cancer Center, University Hospitals, Cleveland, OH 44106, USA 5 Department of Preventive Medicine, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA 6 Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, NY 10467, USA 7 Department of Laboratory Medicine and Pathology, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA 8 Department of Medicine, Research Center for Health Equity, Cedars-Sinai Samuel Oschin Comprehensive Cancer Center, Los Angeles, CA 90048, USA 9 Colorectal Oncogenomics Group, Department of Clinical Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia 10 Victorian Comprehensive Cancer Centre, University of Melbourne, Centre for Cancer Research, Parkville, Victoria 3010, Australia 1 Downloaded from cebp.aacrjournals.org on September 29, 2021. -
A Sleeping Beauty Mutagenesis Screen Reveals a Tumor Suppressor
A Sleeping Beauty mutagenesis screen reveals a tumor PNAS PLUS suppressor role for Ncoa2/Src-2 in liver cancer Kathryn A. O’Donnella,b,1,2, Vincent W. Kengc,d,e, Brian Yorkf, Erin L. Reinekef, Daekwan Seog, Danhua Fanc,h, Kevin A. T. Silversteinc,h, Christina T. Schruma,b, Wei Rose Xiea,b,3, Loris Mularonii,j, Sarah J. Wheelani,j, Michael S. Torbensonk, Bert W. O’Malleyf, David A. Largaespadac,d,e, and Jef D. Boekea,b,i,2 Departments of aMolecular Biology and Genetics, iOncology, jDivision of Biostatistics and Bioinformatics, and kPathology and bThe High Throughput Biology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; cMasonic Cancer Center, dDepartment of Genetics, Cell Biology, and Development, eCenter for Genome Engineering, and hBiostatistics and Bioinformatics Core, University of Minnesota, Minneapolis, MN 55455; fDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030; and gLaboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892 Edited by Harold Varmus, National Cancer Institute, Bethesda, MD, and approved March 23, 2012 (received for review September 21, 2011) The Sleeping Beauty (SB) transposon mutagenesis system is a pow- alterations have been documented in liver cancer, the key genetic erful tool that facilitates the discovery of mutations that accelerate alterations that drive hepatocellular transformation remain tumorigenesis. In this study, we sought to identify mutations that poorly understood. Nevertheless, a unifying feature of human cooperate with MYC, one of the most commonly dysregulated HCC is amplification or overexpression of the MYC oncogene (8, genes in human malignancy. -
Oncogenomics: Clinical Pathogenesis Approach
International Journal of Genetics, ISSN: 0975–2862, Volume 1, Issue 2, 2009, pp-25-43 Oncogenomics: Clinical pathogenesis approach Gupta G. 1, Gupta N. 2, Trivedi S. 3, Patil P. 5, Gupta M. 2, Jhadav A. 4, Vamsi K.K.6, Khairnar Y. 4, Boraste A. 4, Mujapara A.K. 7, Joshi B.8 1S.D.S.M. College Palghar, Mumbai 2Sindhu Mahavidyalaya Panchpaoli Nagpur 3V.V.P. Engineering College, Rajkot, Gujrat 4Padmashree Dr. D.Y. Patil University, Navi Mumbai, 400614, India 5Dr. D. Y. Patil ACS College, Pimpri, Pune 6Rai foundations College CBD Belapur Navi Mumbai 7Sir PP Institute of Science, Bhavnagar 8Rural College of Pharmacy, D.S Road, Bevanahalli, Banglore Abstract - Oncogenomics is new research sub-field of genomics, which applies high throughput technologies to characterize genes associated with cancer and synonymous with cancer genomics. The goal of oncogenomics is to identify new oncogenes or tumor suppressor genes that may provide new insights into cancer diagnosis, predicting clinical outcome of cancers, and new targets for cancer therapies. Oncoproteomics is the term used to describe the application of proteomic technologies in oncology and parallels the related field of oncogenomics. It is now contributing to the development of personalized management of cancer. Genomics has generated a wealth of data that is now being used to identify additional molecular alterations associated with cancer development. Mapping these alterations in the cancer genome is a critical first step in dissecting oncological pathways. Keywords - Biomarkers, Drug development, Drug resistance, Gene therapy, Oncogenomics Introduction Oncogenomics applies high throughput technologies to characterize genes associated transducing cellular signals of cell growth or with cancer and is used to identify new death. -
Mitochondrial Metabolism in Carcinogenesis and Cancer Therapy
cancers Review Mitochondrial Metabolism in Carcinogenesis and Cancer Therapy Hadia Moindjie 1,2, Sylvie Rodrigues-Ferreira 1,2,3 and Clara Nahmias 1,2,* 1 Inserm, Institut Gustave Roussy, UMR981 Biomarqueurs Prédictifs et Nouvelles Stratégies Thérapeutiques en Oncologie, 94800 Villejuif, France; [email protected] (H.M.); [email protected] (S.R.-F.) 2 LabEx LERMIT, Université Paris-Saclay, 92296 Châtenay-Malabry, France 3 Inovarion SAS, 75005 Paris, France * Correspondence: [email protected]; Tel.: +33-142-113-885 Simple Summary: Reprogramming metabolism is a hallmark of cancer. Warburg’s effect, defined as increased aerobic glycolysis at the expense of mitochondrial respiration in cancer cells, opened new avenues of research in the field of cancer. Later findings, however, have revealed that mitochondria remain functional and that they actively contribute to metabolic plasticity of cancer cells. Understand- ing the mechanisms by which mitochondrial metabolism controls tumor initiation and progression is necessary to better characterize the onset of carcinogenesis. These studies may ultimately lead to the design of novel anti-cancer strategies targeting mitochondrial functions. Abstract: Carcinogenesis is a multi-step process that refers to transformation of a normal cell into a tumoral neoplastic cell. The mechanisms that promote tumor initiation, promotion and progression are varied, complex and remain to be understood. Studies have highlighted the involvement of onco- genic mutations, genomic instability and epigenetic alterations as well as metabolic reprogramming, Citation: Moindjie, H.; in different processes of oncogenesis. However, the underlying mechanisms still have to be clarified. Rodrigues-Ferreira, S.; Nahmias, C. Mitochondria are central organelles at the crossroad of various energetic metabolisms. -
Oncogenomics
Oncogene (2002) 21, 7901 – 7911 ª 2002 Nature Publishing Group All rights reserved 0950 – 9232/02 $25.00 www.nature.com/onc Groups of p53 target genes involved in specific p53 downstream effects cluster into different classes of DNA binding sites Hua Qian1,4, Ting Wang1, Louie Naumovski2, Charles D Lopez3 and Rainer K Brachmann*,1,5 1Division of Oncology, Department of Medicine, Washington University School of Medicine, 660 S Euclid Avenue, Box 8069, St Louis, Missouri, MO 63110, USA; 2Division of Hematology, Oncology and Stem Cell Transplantation, Stanford University, 269 Campus Drive, CCSR Room 1215, Stanford, California, CA 94305, USA; 3Division of Hematology and Medical Oncology, Department of Medicine, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road, Baird Hall Room 3030, Portland, Oregon, OR 97201, USA The tumor suppressor protein p53, once activated, can and/or apoptosis (Prives and Hall, 1999; Vogelstein et cause either cell cycle arrest or apoptosis through al., 2000). Direct target genes of p53 have one or more transactivation of target genes with p53 DNA binding p53 DNA binding site(s) (DBS) very similar to the p53 sites (DBS). To investigate the role of p53 DBS in the consensus DBS that consists of two copies of the 10 regulation of this profound, yet poorly understood base pair (bp) motif 5’-PuPuPuC(A/T)(T/A)GPyPyPy- decision of life versus death, we systematically studied 3’ separated by 0 – 13 bp (el-Deiry et al., 1992; Funk et all known and potential p53 DBS. We analysed the DBS al., 1992). However, only one p53 DBS, Type IV separated from surrounding promoter regions in yeast Collagenase, is a perfect match for the p53 consensus and mammalian assays with and without DNA damage. -
Domain Segregated 3D Chromatin Structure and Segmented DNA
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.13.903963; this version posted January 14, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Domain segregated 3D chromatin structure and segmented DNA methylation in carcinogenesis Yue Xue1, Ying Yang1, Hao Tian1, Hui Quan1, Sirui Liu1, Ling Zhang1, Yi Qin Gao1,2,3,* 1 Beijing National Laboratory for Molecular Sciences, College of Chemistry and Molecular Engineering, Peking University, Beijing 100871, China 2 Biomedical Pioneering Innovation Center (BIOPIC), Peking University, Beijing 100871, China 3 Beijing Advanced Innovation Center for Genomics (ICG), Peking University, Beijing 100871, China *Corresponding author. E-mail: [email protected] Abstract The three-dimensional (3D) chromatin structure, together with DNA methylation and other epigenetic marks, profoundly affects gene expression and displays abnormal behaviors in cancer cells. We elucidated the chromatin architecture remodeling in carcinogenesis from the perspective of spatial interactions between CGI forest and prairie domains, which are two types of megabase-sized domains defined by different sequence features but show distinct epigenetic and transcriptional patterns. DNA sequence strongly affects chromosome spatial interaction, DNA methylation and gene expression. Globally, forests and prairies show enhanced spatial segregation in cancer cells and such structural changes are accordant with the alteration of CGI interactions and domain boundary insulation, which could affect vital cancer-related properties. As the cancer progresses, a gradual increase of the DNA methylation difference between the two types of DNA domains is also observed for many different types of cancers. -
BRCA1, BRCA2 and Beyond: an Update on Hereditary Cancer Keynote Speaker and Basser Global Prize Awardee: Steven Narod, MD, FRCPC, FRSC
5TH ANNUAL SCIENTIFIC SYMPOSIUM BRCA1, BRCA2 and Beyond: An Update on Hereditary Cancer Keynote Speaker and Basser Global Prize Awardee: Steven Narod, MD, FRCPC, FRSC THURSDAY, MAY 4, 2017 FRIDAY, MAY 5, 2017 Smilow Center for Translational Research Auditorium/Commons (enter through Perelman Center for Advanced Medicine) Program Overview This symposium is designed to educate researchers, scientists, and health care providers in cancer genetics by presenting cutting-edge data from renowned BRCA1/2 researchers. This symposium will provide new information on the basic biology of known cancer susceptibility genes. In addition, progress in cancer screening and prevention as well as ongoing work in targeted therapy for BRCA1/2 mutation carriers will be discussed through a series of lectures and panel discussions. Attendees will have the opportunity to network with colleagues working in the field. PROGRAM OBJECTIVES At the completion of this symposium, attendees should be able to: • Discuss new research on the basic biology of BRCA1 and BRCA2 and other homologous repair deficiency genes. • Describe the current clinical management strategies for individuals with genetic risk of breast, ovarian and pancreatic cancer. • Review new approaches to screening and prevention of hereditary breast and ovarian cancer. • Discuss new advances in cancer treatment for BRCA1/2 mutation carriers. WHO SHOULD ATTEND Healthcare providers including medical oncology, surgical oncology, gynecology oncology, ob-gyn, genetic counselors, primary care physicians and nurses/nurse practitioners who are interested in the genetics of BRCA1/2 related cancers. KEYNOTE SPEAKER AND BASSER GLOBAL PRIZE AWARDEE Steven Narod, MD, FRCPC, FRSC Women’s College Research Institute, University of Toronto Women with mutations in BRCA1 and BRCA2 have a high risk of breast or ovarian cancer. -
Epigenetic Regulation (DNA Methylation, Histone Modifications
Oncogene (2007) 26, 6566–6576 & 2007 Nature Publishing Group All rights reserved 0950-9232/07 $30.00 www.nature.com/onc ONCOGENOMICS Epigenetic regulation (DNA methylation, histone modifications) ofthe 11p15 mucin genes (MUC2, MUC5AC, MUC5B, MUC6) in epithelial cancer cells A Vincent, M Perrais, J-L Desseyn, J-P Aubert, P Pigny and I Van Seuningen Inserm, U560, Place de Verdun, Lille cedex, France The human genes MUC2, MUC5AC, MUC5B and Introduction MUC6 are clustered on chromosome 11 and encode large secreted gel-forming mucins. The frequent occurrence of DNA methylation, associated with histone deacetyla- their silencing in cancers and the GC-rich structure of tion, is a common mechanism used by cancer cells to their promoters led us to study the influence ofepigenetics inhibit the expression of tumour suppressor genes on their expression. Pre- and post-confluent cells were (Herman and Baylin, 2003) and genes involved in treated with demethylating agent 5-aza-20-deoxycytidine tumour formation (Momparler, 2003). Recent works and histone deacetylase (HDAC) inhibitor, trichostatin aimed at studying the importance of epigenetics in A. Mapping ofmethylated cytosines was performed by cancer opened the way to a host of innovative diagnostic bisulfite-treated genomic DNA sequencing. Histone modi- and therapeutic strategies, attesting that DNA methyla- fication status at the promoters was assessed by chromatin tion is a powerful tool in the clinic (Laird, 2003). Hence, immunoprecipitation assays. Our results indicate that discovery of new methylated genes in cancer will help MUC2 was regulated by site-specific DNA methylation both in the classification of tumours and the identifica- associated with establishment ofa repressive histone code, tion of genes influencing tumour progression. -
Comparative Oncogenomics Identifies Novel Regulators and Clinical Relevance of Neural Crest Identities in Melanoma
University of Massachusetts Medical School eScholarship@UMMS GSBS Dissertations and Theses Graduate School of Biomedical Sciences 2017-12-01 Comparative Oncogenomics Identifies Novel Regulators and Clinical Relevance of Neural Crest Identities in Melanoma Arvind M. Venkatesan University of Massachusetts Medical School Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/gsbs_diss Part of the Bioinformatics Commons, Cancer Biology Commons, Developmental Biology Commons, Genomics Commons, and the Integrative Biology Commons Repository Citation Venkatesan AM. (2017). Comparative Oncogenomics Identifies Novel Regulators and Clinical Relevance of Neural Crest Identities in Melanoma. GSBS Dissertations and Theses. https://doi.org/10.13028/ M20386. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/939 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in GSBS Dissertations and Theses by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. COMPARATIVE ONCOGENOMICS IDENTIFIES NOVEL REGULATORS AND CLINICAL RELEVANCE OF NEURAL CREST IDENTITIES IN MELANOMA A Dissertation Presented By Arvind Murali Venkatesan Submitted to the faculty of the University of Massachusetts Medical School, Worcester in partial fulfillment of the of the requirements for the degree of DOCTORATE OF PHILOSOPHY December 1, 2017 Interdisciplinary Graduate Program COMPARATIVE ONCOGENOMICS IDENTIFIES NOVEL -
Open Access Medical Journals: Promises, Perils and Pitfalls
Open Access Medical Journals: Promises, Perils and Pitfalls • Kenneth V. Iserson, M.D., MBA, FACEP, FAAEM, FIFEM • Professor Emeritus, Emergency Medicine • The University of Arizona, Tucson “OPEN ACCESS” Designed at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org LEARNING OBJECTIVES. At the end of this talk, attendees will be able to: Identify Use Describe Identify the various Use several Describe the types and methods to professional and requirements for differentiate ethical problems legitimate open- legitimate from associated with access (OA) predatory OA publishing in OA journals. journals. journals. • What is the problem? Problem • Why is it important? • How common is it? Number of print and open access (OA) journals increasing dramatically over ~15 years—as are the scientific papers they are publishing Electronic availability of information on the Internet offers great potential for information sharing Procedure & Guidelines from informational professional videos organizations Free articles (e.g., Easier collaboration— through Pub med, worldwide & across ResearchGate) academic disciplines Internet also facilitates illegitimate and “predatory” journals OA: While a laudable development, it . • Provided breeding ground for unacceptable & unethical publishing practices • Is an ever-growing system with little to no regulation Ethical Issues: Predatory OA Publishing • Misrepresent who they are & what services they offer • Lack editorial/publishing standards & practices • Academics misrepresent their accomplishments by publishing in predatory journals • Waste research effort & funding • Lack of archived content for others to access • Undermine confidence in research literature “An emerging Wild West in academic publishing” • “From humble and idealistic beginnings a decade ago, open-access scientific journals have mushroomed into a global industry, driven by author publication fees rather than traditional subscriptions.