Editorial
Copyright ©The Author(s) 2015.
World J Gastroenterol. Apr 7, 2015; 21(13): 3763-3772
Published online Apr 7, 2015. doi: 10.3748/wjg.v21.i13.3763
Figure 1
Figure 1 Schematic representation of proposed mechanisms for formation of field defect. A: A mutation or epigenetic alteration in a stem cell (depicted in red) is inherited by all cells within the crypt through niche succession. Crypt fission results in several crypts becoming biologically altered creating a patch defect. Further mutation within this field of altered mucosa leads to malignant transformation; B: Tumour secretes chemical signals that alter the adjacent mucosa resulting in a field defect; C: Malignant cells shed from a tumour travel in the bloodstream and seed in a distant site rendering the mucosa susceptible to malignant transformation.
Figure 2
Figure 2 Changes in crypt morphology, cellular ultrastructure and epigenetic modulation in the field defect. A, B: Changes in crypt morphology characterised by increased branching and distension of crypts, increased cell division and a change in proportion of cells with increase in goblet cells; C, D: Changes in the cell cytoskeleton, organelles and nuclear composition; E, F: Epigenetic modulation of DNA leading to transcriptional silencing of certain genes involved in regulation of cell division, apoptosis and DNA repair.