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Transposon mutagenesis identifies genes and evolutionary forces driving gastrointestinal tract tumor progression.

Authors
  • 1
  • 2
  • 3
  • 4
  • 5
  • 6
  • 5
  • 4
  • 6
  • 6
  • 1 1] Division of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore. [2] Department of Oncologic Pathology, School of Medicine, Kanazawa Medical University, Ishikawa, Japan. , (Japan)
  • 2 Cancer Research Program, Houston Methodist Research Institute, Houston, Texas, USA.
  • 3 1] Division of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore. [2] Division of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan. , (Japan)
  • 4 Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, UK.
  • 5 Division of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore. , (Singapore)
  • 6 1] Division of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore. [2] Cancer Research Program, Houston Methodist Research Institute, Houston, Texas, USA. , (Singapore)
Type
Published Article
Journal
Nature Genetics
1546-1718
Publisher
Nature Publishing Group
Publication Date
Volume
47
Issue
2
Pages
142–150
Identifiers
DOI: 10.1038/ng.3175
PMID: 25559195
Source
Medline
License
Unknown

Abstract

To provide a more comprehensive understanding of the genes and evolutionary forces driving colorectal cancer (CRC) progression, we performed Sleeping Beauty (SB) transposon mutagenesis screens in mice carrying sensitizing mutations in genes that act at different stages of tumor progression. This approach allowed us to identify a set of genes that appear to be highly relevant for CRC and to provide a better understanding of the evolutionary forces and systems properties of CRC. We also identified six genes driving malignant tumor progression and a new human CRC tumor-suppressor gene, ZNF292, that might also function in other types of cancer. Our comprehensive CRC data set provides a resource with which to develop new therapies for treating CRC.

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