Abstract

Background: Mammary carcinogenesis is a multistep process entailing the transition from normal breast to benign proliferative breast disease (ductal hyperplasia) to ductal carcinoma in situ to infiltrating ductal carcinoma.

Hypothesis: These transitions are associated with changes in the mononuclear inflammatory cell infiltrate.

Materials and methods: A total of 53 mastectomy specimens of normal breast, benign proliferative breast disease, ductal carcinoma in situ and infiltrating ductal carcinoma were evaluated for mononuclear inflammatory cell infiltrate by using immunohistological methods and monoclonal antibodies including CD20, CD68, CD3 and granzyme B, histiocytes, T cells and cytotoxic T cells.

Results: Transitions from normal breast to the subsequent tissue with lesions (normal skin v benign proliferative breast disease v ductal carcinoma in situ v infiltrating ductal carcinoma) were associated with significantly (p<0.01) increased mean (SD) density of mononuclear inflammatory cell infiltrate at the parenchyma (3.2 (1.0) v 26.4 (7.8) v 33.6 (7.9) v 39.1 (4.7) for CD20+ B cells; 2.8 (1.0) v 81.5 (14.0) v 84.0 (14.9) v103.7 (3.9) for CD3; 1.3 (2.0) v 3.8 (4.0) v 12.7 (23) v 22.1 (25.0) for CD68+ macrophages; 2.0 (1.0) v 58.3 (5.0) v 60.0 (10.0) v 74.1 (28.0) for granzyme B+ cytotoxic T cells) and at the stroma (0.7 (1.0) v 3.0 (5.0) v 13.3 (20) v 16.7 (30.0) for CD20+ B cells; 1.0 (2.06) v 4.0 (2.5) v 16.7 (5.0) v 21.7 (15) for CD68+ macrophages; 1.4 (0.6) v 4.2 (1.2) v 46.6 (16.7) v 77.0 (5.0) for CD3+ cells and 0 (0) v 0.5 (1.0) v 0.7 (1.0) v 0.7 (1.0) for granzyme B+ cytotoxic T cells).

Conclusions: The increased mononuclear inflammatory cell infiltrate during mammary carcinogenesis may reflect non-specific or specific immunological processes.