Pathomorphological features of inflammatory infiltrate in colorectal cancer

Abstract

Aim: to investigate the pathomorphological features and severity of inflammatory infiltration in colorectal cancers.

Materials and methods. A morphological study of surgical and biopsy material of patients with colon adenocarcinoma of various degrees of differentiation (n = 38) and mucinous adenocarcinoma (n = 7) was performed. Histological specimens were examined morphologically with morphometric analysis. The results were processed by descriptive statistics by calculating the median (Me) for quantitative variables. The statistical significance of the difference between the parameters was evaluated based on the Mann–Whitney U test.

Results. It was found that intestinal carcinoma developed on the background of chronic inflammation. Dysplasia was often detected in the glands, gradually increasing with an approach to the tumor tissue. In the tumor’s microenvironment, there were cells of the immune system: lymphocytes, macrophages, plasma cells, and cells of the myeloid lineage. In the absence of destructive changes in the tumor tissue, lymphocytes and macrophages predominated in the inflammatory microenvironment. In the conditionally standardized field of view of 100 × 100 μm (CSFV), the number of cells was 77.50 (72.25; 84.25), in the edges of the resection – 12.50 (9.00; 16.00). The development of necrotic changes led to a change in cellular representation with a significant increase in myeloid cells. In 3 cases, a significant number of eosinophils was found in the inflammatory, mainly peritumoral infiltrate, at the level of 14.5 (11.00; 18.00) in the CSFV. Invasive tumor growth with penetration into the muscle layer was accompanied by a decrease in inflammatory infiltration. The number of cells in the CSFV was 49.70 (43.50; 54.80). When the tumor invaded the entire thickness of the intestinal wall at the border with adipose tissue, the number of cells in the CSFV was 28.50 (21.45; 33.75). Mucin-producing carcinoma was characterized by a lower intensity of inflammatory infiltrate. The number of cells in the CSFV in the mucosal lamina propria in mucin-producing carcinoma was 42.40 (35.65; 48.55). At the border with the muscular layer and in case of invasion into the intestinal wall thickness, the number of inflammatory infiltrate cells decreased and amounted to 26.50 (18.90; 32.40) and 18.75 (14.00; 22.30), respectively. In areas of severe sclerotic changes, inflammatory infiltration was not detected. Tumor invasion into adipose tissue was accompanied by a mild diffuse inflammatory infiltrate in the surrounding tissues, at the level of 12.50 (7.40; 16.45) cells in the CSFV.

Conclusions. The inflammatory infiltration in the intestinal mucosa in colorectal carcinoma is represented by lymphocytes, macrophages, plasma cells and cells of myeloid lineage and is maximally expressed in the intestinal mucosa. Invasion of the adenocarcinoma into the muscle layer and invasion of the entire intestinal wall is accompanied by a decrease in peritumor inflammatory infiltration. Mucin-producing carcinoma is characterized by a lower intensity of inflammatory infiltrate compared to tubular adenocarcinoma.