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STEM CELL IN GASTROINTESTINAL STRUCTURE AND NEOPLASTIC DEVELOPMENT
  1. M Brittan1,
  2. N A Wright2
  1. 1Histopathology Unit, Cancer Research UK, Lincoln’s Inn Fields, London, UK
  2. 2Histopathology Unit, Cancer Research UK, Lincoln’s Inn Fields, London, UK and Molecular Pathology Centre, Institute of Cell and Molecular Medicine, Barts and the London, Queen Mary’s School of Medicine and Dentistry, London, UK
  1. Correspondence to:
    M Brittan
    Histopathology Unit, Cancer Research UK, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK; mairi.brittancancer.org.uk

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Stem cells are primitive cells located in a specialised mesenchymal “niche” that lack expression of any definitive markers of lineage commitment and are therefore difficult to define and identify. Stem cells maintain their capacity for limitless self replication throughout the lifetime of their host, and can also divide to produce daughter cells, committed to the formation of every adult cell lineage within their tissue of origin. The stem cells of the gastrointestinal tract remain unidentified which has led to many conflicting hypotheses as to their precise nature and function. For example, the numbers and location of stem cells in the intestinal crypts and gastric glands have never been conclusively proven and, consequently, the clonal origins of these structures under normal circumstances and in neoplasia are clouded issues. The morphological events of gastrointestinal carcinoma formation are hotly debated, with two main conflicting hypotheses of the mechanisms of expansion of a mutated stem cell clone. However, with the emergence of the molecular pathways governing gastrointestinal stem cell function, and the identification of putative intestinal molecular stem cell markers, such as Musashi-1, comes a clearer insight into the properties of the gastrointestinal stem cell. Adult stem cells from several tissues can leave their niche and engraft into extraneous tissues, including the gastrointestinal mucosa and underlying mesenchyme, and transform to produce adult cell lineages common to these foreign environments. This process is optimal when the requirement for regeneration is enhanced (that is, in diseased or damaged tissue) and indeed, the contribution of transplanted bone marrow stem cells to intestinal myofibroblasts is significantly upregulated in colitis. However, adult stem cell plasticity has recently been disparaged by reports suggesting that stem cells spontaneously fuse with indigenous adult cells to form a diploid cell with an aberrant karyotype, and it is important to investigate if bone marrow …

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