Characterization and frequency distribution of lymphoreticular infiltrates in axillary lymph node metastases of invasive ductal carcinoma of the breast

Abstract

One hundred and seventy-five axillary lymph nodes containing metastatic deposits from 46 invasive ductal carcinomas of the breast were evaluated histologically and immunohistologically. The study yielded the following results: (1) tumor-infiltrating lymphoreticular cells preferentially accumulated in the stromal bands; the tumor foci generally showed a considerably lower degree of infiltration; (2j in most cases, monocytes/macrophages (Mono 1 +) represented the overwhelming majority of tumoh -infiltrating cells; (3) next in frequency were T-lymphocytes (Leu-1 +), especially CD4+ lymphocytes (Leu3a+), while CD8+ lymphocytes (Leu-Za+) mostly occurred only in moderate numbers; (4) Blymphocytes (TOIS+), plasma cells, natural killer cells (Leu-7+), tissue mast cells, and T-accessory reticulum cells (OKT 6+) were observed mostly in low or very low numbers, while eosinophils were nearly absent and B-accessory reticulum cells (Ki-M4+) were totally absent from the lymphoreticular infiltrates. Definite conclusions regarding the functional properties of the tumor-infiltrating cells cannot be drawn from an immunohistologic analysis in sifu alone, but the preferred localization of most tumor-infiltrating cells in the stroma does not support an intensive interaction between the host defenses and the metastatic tumor.Cancer 60:3001-3007,1987.UCH RESEARCH has been done to clarify the sig-

Infiltration of immune competent cells into primary tumors and their surrounding connective tissues in mice

“…Most of these immunocompetent cells were not, as expected, located in the epithelial tumor tissue itself but were located in the surrounding connective tissues like the adjacent adipose tissue and the tumor capsule. With these results obtained in mice, we corroborate earlier studies using patient material (Horst and Horny, 1988)10. In addition to the well-explored checkpoint axes controlled by tumor cells acting on lymphocytes, there should be other reasons for this rare in ltration rate of immune competent cells into the tumor tissue itself.…”

“…Our syngeneic WAP-T-breast cancer mouse model re ects the clinical situation well. In a previous study using clinical breast cancer samples, 30% of the tumor in ltrating immunocompetent cells in ductal carcinoma of the breast were present in the surrounding connective tissue(Horst and Horny, 1988)10, while 40% of these cells were present in our syngeneic mouse tumors. Similarly 25% of the in ltrates were noted directly in the epithelial tumor tissues in our WAP-T breast cancers, while it was 19% in the clinical invasive ductal carcinoma cases.…”

“…The present study focuses on cells of the innate immune system to ll the existing knowledge gap concerning dendritic cells, monocytes/macrophages, and NK cells in xenograft and syngeneic mouse models. The clinical importance of these cell populations was already shown by Horst and Horny (1988)…”

Modulation of monocyte matrix metalloproteinase-2 by breast adenocarcinoma cells

“…It appears that TAMs are actually required for the tumor to survive [16-19]. Other studies have also reported an overwhelming predominance of TAMs within the TAL population of both primary [12,20,21] and metastatic [22] breast carcinoma. Moreover, positive relationships between the presence of macrophages and lymph node metastasis [23], c-erbB2 [24], and increased expression of urokinase plasminogen activator (uPA) [25] in breast cancer have been reported.…”

Does [meso-1,2-Bis(2,6-dichloro-4-hydroxyphenyl)ethylenediamine]-dichloro-platinum(II) Act as an Immune Response Modifier? Part III: Progressively Growing MXT-M-3,2 Breast Cancer Stimulates the Proliferation of Phagocytes in B6D2F1 Mice

“…Their reduced capacity to produce NO and lyse tumor cells can be partially reversed by INFγ [58,61] . The results of Lopez and ---1) Monocyte-and macrophage-rich mononuclear infiltrates, frequently observed in primary breast cancers and their metastases, presumably have the same causality [37,38] . 2) Concerning the physiology of GM-CSF in host defense see ref.…”