Development of carcinoma in cases of ulcerative colitis is initiated out of regions of dysplasia. Dysplasia may present as single or multiple flat lesions, or as polypoid dysplasia (DALM-lesion). Dysplasia in DALM lesions may not be readily differentiated from that of sporadic adenomas by light microscopy. Such distinction, however, dictates therapeutic strategies. Since colectomy is treatment of choice in DALM lesions but removal of a sporadic adenoma is sufficient therapy, several attempts have been made to find markers to differentiate the two lesions. In recent years molecular genetic studies have demonstrated different genetic alterations in the dysplasia-carcinoma event in ulcerative colitis versus sporadic colorectal carcinoma, which may in fact help to differentiate the two entities. The diagnostic tools to differentiate DALM from sporadic adenomas are briefly described and a specific emphasis is given to the molecular genetic studies which may help in defining the specific entities.

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