Tumor-infiltrating dendritic cells in adenocarcinomas of the breast: A study of 143 neoplasms with a correlation to usual prognostic factors and to clinical outcome

Citation
L. Lespagnard et al., Tumor-infiltrating dendritic cells in adenocarcinomas of the breast: A study of 143 neoplasms with a correlation to usual prognostic factors and to clinical outcome, INT J CANC, 84(3), 1999, pp. 309-314
Citations number
21
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF CANCER
ISSN journal
00207136 → ACNP
Volume
84
Issue
3
Year of publication
1999
Pages
309 - 314
Database
ISI
SICI code
0020-7136(19990621)84:3<309:TDCIAO>2.0.ZU;2-D
Abstract
Dendritic cells (DC) are the most potent antigen-presenting cells, and indu ce antigen-specific immune responses. Infiltration of tumors by DC is thoug ht to reflect the interaction between the host immune system and tumor cell s. Tumor-infiltrating DC (TIDC) are believed to evolve into tumor-antigen p ulsed cells and then to migrate to local lymph nodes, where they activate a nti-tumor immune responses. Indirect clinical evidence supporting this theo ry is provided by studies showing that high TIDC densities are associated w ith favorable prognosis in some tumor types. In the present study, we evalu ated 143 primary breast adenocarcinomas for the presence of DC, using immun ohistochemistry with the anti-S100 protein antibody. We analyzed the relati onship between the degree of infiltration by S100(+) TIDC and the usual pro gnostic factors and clinical outcome. The results show that 42% of breast a denocarcinomas contain S100+ TIDC. The number of S100(+) TIDC varies accord ing to the grade of tumors as follows: GRIII > GRII > GRI. A relationship i s also found between S100+ TIDC and tumor size, lymph-node involvement, est rogen/progesterone receptor status and age. However, the presence of S100() TIDC, even at the highest density, was not correlated with metastasis-fre e survival or overall survival. Int. J. Cancer (Pred. Oncol.) 84:309-314, 1 999. (C) 1999 Wiley-Liss, Inc.