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. 2001 May;48(5):594–595. doi: 10.1136/gut.48.5.594

Landscaper seeks remunerative position

R PLAYFORD 1
PMCID: PMC1728305  PMID: 11302952

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Figure 1  .

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Schematic representation of colonic mucosa, divided into stroma and overlying epithelium. Regions with functionally relevant genetic defects are shown in light and dark grey. Adenoca., adenocarcinoma. (A) Sporadic colonic tumours acquire initial functional genetic defects in specific regions of the epithelium, causing dysplastic polyps that may progress to carcinoma. (B) In patients with conditions such as familial adenomatous polyposis, the whole of the epithelium is affected by a defect in a tumour suppressor gene, resulting in the development of multiple dysplastic polyps. Some of these polyps will subsequently progress to carcinoma. A defect in a tumour suppressor gene resulting in multiple polyps can be considered a loss of control of gatekeeper function. (C) Patients with juvenile polyposis syndrome (JPS) initially develop hamartomas that were thought to have functional genetic defects (that is, loss of the second functional allele of SMAD4) only affecting the stroma. The overlying epithelium was considered to be still under functional genetic control of the remaining normal SMAD4 allele. According to the landscaper hypothesis, this abnormality of the stroma subsequently induced the overlying epithelium to progress to carcinoma. The recent paper by Woodford-Richens et al casts doubt on the relevance of this model in patients with JPS as they have identical genetic defects affecting the overlying epithelium.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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