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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Possible mechanism pertinent to mucosal invasion in sporadic colonic adenomas
1Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and Hospital, Stockholm, Sweden. Carlos.Rubio@onkpat.ki.se
Abstract:
Colorectal adenomas are foci of dysplastic mucosa that may antedate the development of a colorectal cancer. In this work we investigated 62 colonic polyps. A close examination revealed that in some adenomatous glands facing the muscularis mucosa a group of dysplastic cells were missing. Those glandular defects were connoted as glandular pores. Many glands with pores were dilated and had retained mucin, inflammatory cells and/or necrotic material. Those products were often released through the pores into the surrounding lamina propria. Glandular pores were recorded in 25% (3/12) of the tubular adenomas, in 33% (2/6) of the serrated adenomas, in 50% (4/8) of the tubulo-villous adenomas and in 67% (14/21) of the villous adenomas. None of the 14 hyperplastic polyps had glandular pores. While cell locomotion is considered to be the most important parameter accountable for the local progression of tumors, the present results may offer an alternative view to the cell-migration theory (as the sole pathway of invasion). The release of proteolytic secretions through glandular pores in some colonic adenomas disrupt the surrounding matrix, a mechanism that would facilitate neoplastic cell penetration into the lamina propria.
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