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      International cancer seminars: a focus on esophageal squamous cell carcinoma

      1 , 2 , 3 , 4 , 1 , 5 , 1 , 1 , 6 , 7 , 1 , 1 , 8 , 1 , 9 , 1 , 1 , 8 , 10 , 9 , 11 , 12 , 13 , 8 , 14 , 15 , 1 , 16 , 17 , 18 , 2 , 19 , 20 , 1 , 21 , 1 , 16 , 16 , 22 , 16 , 1 , 1 , 3
      Annals of Oncology
      Oxford University Press (OUP)

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          Abstract

          <p id="d7496644e529">The International Agency for Research on Cancer (IARC) and the US National Cancer Institute (NCI) have initiated a series of cancer-focused seminars [Scelo G, Hofmann JN, Banks RE et al. International cancer seminars: a focus on kidney cancer. Ann Oncol 2016; 27(8): 1382–1385]. In this, the second seminar, IARC and NCI convened a workshop in order to examine the state of the current science on esophageal squamous cell carcinoma etiology, genetics, early detection, treatment, and palliation, was reviewed to identify the most critical open research questions. The results of these discussions were summarized by formulating a series of ‘difficult questions’, which should inform and prioritize future research efforts. </p>

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          Most cited references81

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          TP53 Variations in Human Cancers: New Lessons from the IARC TP53 Database and Genomics Data.

          TP53 gene mutations are one of the most frequent somatic events in cancer. The IARC TP53 Database (http://p53.iarc.fr) is a popular resource that compiles occurrence and phenotype data on TP53 germline and somatic variations linked to human cancer. The deluge of data coming from cancer genomic studies generates new data on TP53 variations and attracts a growing number of database users for the interpretation of TP53 variants. Here, we present the current contents and functionalities of the IARC TP53 Database and perform a systematic analysis of TP53 somatic mutation data extracted from this database and from genomic data repositories. This analysis showed that IARC has more TP53 somatic mutation data than genomic repositories (29,000 vs. 4,000). However, the more complete screening achieved by genomic studies highlighted some overlooked facts about TP53 mutations, such as the presence of a significant number of mutations occurring outside the DNA-binding domain in specific cancer types. We also provide an update on TP53 inherited variants including the ones that should be considered as neutral frequent variations. We thus provide an update of current knowledge on TP53 variations in human cancer as well as inform users on the efficient use of the IARC TP53 Database.
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            Genomic and molecular characterization of esophageal squamous cell carcinoma

            Esophageal squamous cell carcinoma (ESCC) is a world-wide prevalent cancer, which is particularly common in certain regions of Asia. Here we report the whole-exome or targeted deep sequencing of 139 paired ESCC cases, and analysis of somatic copy number variations (SCNV) of over 180 ESCCs. We identified novel significantly mutated genes such as FAT1, FAT2, ZNF750 and KMT2D, in addition to previously discovered ones (TP53, PIK3CA and NOTCH1). Further SCNV evaluation, immunohistochemistry and biological analysis suggested their functional relevance in ESCC. Notably, RTK-MAPK-PI3K pathways, cell cycle and epigenetic regulation are frequently dysregulated by multiple molecular mechanisms in this cancer. Moreover, our approaches uncovered many novel druggable candidates, and XPO1 was further explored as a therapeutic target because of its mutation and protein overexpression. Together, our integrated study unmasks a number of novel genetic lesions in ESCC and provides an important molecular foundation for understanding esophageal tumors and developing therapeutic targets.
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              Signatures of mutation and selection in the cancer genome.

              The cancer genome is moulded by the dual processes of somatic mutation and selection. Homozygous deletions in cancer genomes occur over recessive cancer genes, where they can confer selective growth advantage, and over fragile sites, where they are thought to reflect an increased local rate of DNA breakage. However, most homozygous deletions in cancer genomes are unexplained. Here we identified 2,428 somatic homozygous deletions in 746 cancer cell lines. These overlie 11% of protein-coding genes that, therefore, are not mandatory for survival of human cells. We derived structural signatures that distinguish between homozygous deletions over recessive cancer genes and fragile sites. Application to clusters of unexplained homozygous deletions suggests that many are in regions of inherent fragility, whereas a small subset overlies recessive cancer genes. The results illustrate how structural signatures can be used to distinguish between the influences of mutation and selection in cancer genomes. The extensive copy number, genotyping, sequence and expression data available for this large series of publicly available cancer cell lines renders them informative reagents for future studies of cancer biology and drug discovery.
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                Author and article information

                Journal
                Annals of Oncology
                Oxford University Press (OUP)
                0923-7534
                1569-8041
                September 2017
                September 01 2017
                June 14 2017
                September 2017
                September 01 2017
                June 14 2017
                : 28
                : 9
                : 2086-2093
                Affiliations
                [1 ] Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA;
                [2 ]Section of Environment and Radiation;
                [3 ] Section of Genetics;
                [4 ] Cancer Surveillance, International Agency for Research on Cancer, Lyon, France;
                [5 ] Department of Biochemistry, University of Kashmir, Hazratbal, Srinagar, Jammu and Kashmir, India;
                [6 ] MRC Cancer Unit, Hutchison-MRC Research Centre, University of Cambridge, Cambridge, UK;
                [7 ] Department of Internal Medicine, Mayo Clinic, Scottsdale, Arizona, USA;
                [8 ] University of North Carolina Project-Malawi, Lilongwe, Malawi;
                [9 ] Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran;
                [10 ] Department of Public Health Analysis, School of Community Health and Policy, Morgan State University, Baltimore, Maryland, USA;
                [11 ] Department of Medical and Molecular Genetics, Kings College London;
                [12 ] Sydney Brenner Institute for Molecular Bioscience, University of Witwatersrand, Johannesburg, South Africa;
                [13 ] School of Public Health, Moi University, Eldoret, Kenya;
                [14 ] Tenwek Hospital, Bomet, Kenya;
                [15 ] Kilimanjaro Christian Medical Centre, Moshi, Tanzania;
                [16 ] Department of Etiology and Carcinogenesis & Department of Cancer Epidemiology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China;
                [17 ] Molecular Carcinogenesis Program, Institute Nacional de Cancer, Sao Paulo, Brazil;
                [18 ] National Cancer Institute, Center for Global Health, National Institutes of Health, Bethesda, Maryland, USA;
                [19 ] School of Public Health, University of Sydney, New South Wales, Australia;
                [20 ] School of Public Health & Community Medicine, University of New South Wales, Sydney, Australia
                [21 ] Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California, USA
                [22 ] Director's office, International Agency for Research on Cancer, Lyon, France
                Article
                10.1093/annonc/mdx279
                5834011
                28911061
                34454043-3c06-4887-8e71-078b28e0f86c
                © 2017
                History

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