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Letter
Integrin a6 loss promotes colitis-associated colorectal cancer. Response to: “Integrin a6 variants and colorectal cancer” by Beaulieu JF
  1. Adèle De Arcangelis1,2,3,4,
  2. Mathias Chamaillard5,
  3. Patricia Simon-Assmann4,6,
  4. Michel Labouesse7
  1. 1 Department of Development and Stem Cells, IGBMC (Institut de Génétique et de Biologie Moléculaire et Cellulaire), Université de Strasbourg, Illkirch, France
  2. 2 Inserm, U964, Illkirch, France
  3. 3 CNRS, UMR 7104, Illkirch, France
  4. 4 Université de Strasbourg, Strasbourg, France
  5. 5 U1019 - UMR 8204 - CIIL - Centre d’Infection et d’Immunité de Lille, Université de Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, Lille, France
  6. 6 MNT3 team, INSERM U1109, Strasbourg, France
  7. 7 UMR7622, IBPS, UPMC, Paris, France
  1. Correspondence to Dr Adèle De Arcangelis, Department of Development and Stem Cells, IGBMC (Institut de Génétique et de Biologie Moléculaire et Cellulaire), Université de Strasbourg, Illkirch 67400, France; adele{at}igbmc.fr

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In a recently published letter,1 Dr Beaulieu questions our recent publication suggesting that α6 integrin acts as a tumour suppressor gene in colorectal cancer (CRC),2 given the apparent antagonistic role of α6A and α6B integrin isoforms in the intestine. We thank him for raising this important issue and welcome the opportunity of clarifying the topic. We showed that mice failing to express the α6 integrin (both α6A and α6B isoforms) specifically in intestinal epithelial cells (α6ΔIEC) spontaneously develop fully penetrant colitis and adenocarcinoma afterwards.2 These mice display epithelium detachment from the basement membrane, followed …

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Footnotes

  • Contributors ADA wrote the first draft, MC and ML edited it, and PS-A revised it.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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