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      Meeting report from the joint IARC–NCI international cancer seminar series: a focus on colorectal cancer

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          Despite significant progress in our understanding of the etiology, biology and genetics of colorectal cancer, as well as important clinical advances, it remains the third most frequently diagnosed cancer worldwide and is the second leading cause of cancer death. Based on demographic projections, the global burden of colorectal cancer would be expected to rise by 72% from 1.8 million new cases in 2018 to over 3 million in 2040 with substantial increases anticipated in low- and middle-income countries. In this meeting report, we summarize the content of a joint workshop led by the National Cancer Institute and the International Agency for Research on Cancer, which was held to summarize the important achievements that have been made in our understanding of colorectal cancer etiology, genetics, early detection and treatment and to identify key research questions that remain to be addressed.

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          Most cited references 121

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          Global Cancer Statistics 2018: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries

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            Comprehensive Molecular Characterization of Human Colon and Rectal Cancer

            Summary To characterize somatic alterations in colorectal carcinoma (CRC), we conducted genome-scale analysis of 276 samples, analyzing exome sequence, DNA copy number, promoter methylation, mRNA and microRNA expression. A subset (97) underwent low-depth-of-coverage whole-genome sequencing. 16% of CRC have hypermutation, three quarters of which have the expected high microsatellite instability (MSI), usually with hypermethylation and MLH1 silencing, but one quarter has somatic mismatch repair gene mutations. Excluding hypermutated cancers, colon and rectum cancers have remarkably similar patterns of genomic alteration. Twenty-four genes are significantly mutated. In addition to the expected APC, TP53, SMAD4, PIK3CA and KRAS mutations, we found frequent mutations in ARID1A, SOX9, and FAM123B/WTX. Recurrent copy number alterations include potentially drug-targetable amplifications of ERBB2 and newly discovered amplification of IGF2. Recurrent chromosomal translocations include fusion of NAV2 and WNT pathway member TCF7L1. Integrative analyses suggest new markers for aggressive CRC and important role for MYC-directed transcriptional activation and repression.
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              Cancer genome landscapes.

              Over the past decade, comprehensive sequencing efforts have revealed the genomic landscapes of common forms of human cancer. For most cancer types, this landscape consists of a small number of "mountains" (genes altered in a high percentage of tumors) and a much larger number of "hills" (genes altered infrequently). To date, these studies have revealed ~140 genes that, when altered by intragenic mutations, can promote or "drive" tumorigenesis. A typical tumor contains two to eight of these "driver gene" mutations; the remaining mutations are passengers that confer no selective growth advantage. Driver genes can be classified into 12 signaling pathways that regulate three core cellular processes: cell fate, cell survival, and genome maintenance. A better understanding of these pathways is one of the most pressing needs in basic cancer research. Even now, however, our knowledge of cancer genomes is sufficient to guide the development of more effective approaches for reducing cancer morbidity and mortality.

                Author and article information

                Ann Oncol
                Ann. Oncol
                Annals of Oncology
                Oxford University Press
                April 2019
                05 February 2019
                05 February 2019
                : 30
                : 4 , Evidence for an early, on-therapy biomarker of response in patients with advanced melanoma treated with anti-PD-1
                : 510-519
                [1 ]Section of Nutrition and Metabolism, International Agency for Research on Cancer, Lyon, France
                [2 ]King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia
                [3 ]Section of Cancer Surveillance, International Agency for Research on Cancer, Lyon, France
                [4 ]Division of Clinical Epidemiology and Aging Research, Division of Preventive Oncology and German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg
                [5 ]National Center for Tumor Diseases (NCT), Heidelberg, Germany
                [6 ]Institute of Genetic Medicine, Newcastle University, Newcastle, UK
                [7 ]Center for Public Health Genomics, University of Virginia, Charlottesville
                [8 ]Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, USA
                [9 ]School of Public Health, Imperial College London, London, UK
                [10 ]Harvard T.H. Chan School of Public Health, Boston
                [11 ]Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, USA
                [12 ]Division of Genetics and Epidemiology, Institute of Cancer Research, London, UK
                [13 ]Centre for Epidemiology and Biostatistics, University of Melbourne, Melbourne, Australia
                [14 ]SIRIC CARPEM, APHP European Georges Pompidou Hospital Paris, Universite Paris Descartes, Paris, France
                [15 ]Public Health Science Division, Fred Hutchinson Cancer Research Center, Seattle
                [16 ]Lineberger Comprehensive Cancer Center, UNC School of Medicine, University of North Carolina, Chapel Hill
                [17 ]Memorial Sloan Kettering Cancer Center, New York, USA
                [18 ]Section of Genetics, International Agency for Research on Cancer, Lyon, France
                Author notes
                Correspondence to: Dr Marc J. Gunter, Section of Nutrition and Metabolism, International Agency for Research on Cancer, 150 cours Albert Thomas, 69372 Lyon cedex 08, France. Tel: +33-4-7273-8094; E-mail: GunterM@
                © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (, which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact

                Pages: 10
                Funded by: International Agency for Research on Cancer 10.13039/100008700
                Funded by: IARC 10.13039/100005921
                Funded by: Division of Cancer Epidemiology and Genetics
                Funded by: DCEG 10.13039/100011541
                Funded by: US National Cancer Institute Intramural Research Program
                Special Article

                Oncology & Radiotherapy

                prevention, colorectal cancer, screening, etiology, genetics, therapy


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