Histological sections of 65 surgical specimens from patients with inflammatory colonic disease (ICD) and a colorectal carcinoma, were reviewed. Twenty-five specimens had ulcerative colitis, 35 Crohn's colitis and 2 indeterminate colitis. The presence of neoplastic glands at the tumour front having: a) retained mucin, inflammatory cells and/or necrotic material, b) neoplastic glands with a thin layer of tumour cells, c) neoplastic glands lacking a group of tumour cells (i.e. glandular pore formation) and d) neoplastic glands in which the intraglandular retained mucin, inflammatory cells and/or necrotic material were seen discharged through the glandular pores into the juxtaposed matrix, were recorded. Of the 58 specimens with gland-forming adenocarcinomas, 17 (29.3%) had at the invading front neoplastic glands with a thin layer of tumour cells and 56 (96.6%) neoplastic glands with pores. The material discharged through those pores into the surrounding matrix was mucin (n = 46), inflammatory cells -mainly granulocytes- and/or necrotic material (n = 10). It was assumed that the thin layer of tumour cells in neoplastic glands antedated glandular "pore" formation. Through those "pores" mucin, inflammatory cells and/or necrotic material were subsequently released into the surrounding host tissues. Those products, rich in proteolytic enzymes, would encourage the degradation of the juxtaposed normal tissues, thus facilitating local tumour growth. To restore the continuity of those incomplete glands, new cancer cells would grow around mucin "lakes" or inflammatory-necrotic aggregates in the stroma. This mechanism will guarantee a life-long tumour progression in untreated patients.