Colon cancer appears to develop as the result of dysregulation of molecular pathways that control epithelial proliferation, maturation, and apoptosis, with perturbations of both
genetic and epigenetic components. In regeneration of normal mucosa, stem cells deep within the crypt undergo mitosis,
with subsequent maturation and differentiation of daughter
cells to mature absorptive and secretory populations of the
colonic mucosa and eventual loss of aged or damaged cells
through apoptosis. Multistep accumulation of mutations
of genes in critical control pathways, coupled with changes
in epigenetic factors, is believed to allow survival of abnormal crypt epithelial cells with the potential to undergo malignant transformation.
Colon cancer appears to develop as the result of dysregulation of molecular pathways that control epithelial proliferation, maturation, and apoptosis, with perturbations of bothgenetic and epigenetic components. In regeneration of normal mucosa, stem cells deep within the crypt undergo mitosis,with subsequent maturation and differentiation of daughtercells to mature absorptive and secretory populations of thecolonic mucosa and eventual loss of aged or damaged cellsthrough apoptosis. Multistep accumulation of mutationsof genes in critical control pathways, coupled with changesin epigenetic factors, is believed to allow survival of abnormal crypt epithelial cells with the potential to undergo malignant transformation.
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