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
Dendritic cells (DC) are the most potent antigen‐presenting cells, and induce antigen‐specific immune responses. Infiltration of tumors by DC is thought to reflect the interaction between the host immune system and tumor cells. Tumor‐infiltrating DC (TIDC) are believed to evolve into tumor‐antigen p...
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Published in: | International journal of cancer Vol. 84; no. 3; pp. 309 - 314 |
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Main Authors: | , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
New York
John Wiley & Sons, Inc
21-06-1999
Wiley-Liss |
Subjects: | |
Online Access: | Get full text |
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Summary: | Dendritic cells (DC) are the most potent antigen‐presenting cells, and induce antigen‐specific immune responses. Infiltration of tumors by DC is thought to reflect the interaction between the host immune system and tumor cells. Tumor‐infiltrating DC (TIDC) are believed to evolve into tumor‐antigen pulsed cells and then to migrate to local lymph nodes, where they activate anti‐tumor immune responses. Indirect clinical evidence supporting this theory is provided by studies showing that high TIDC densities are associated with favorable prognosis in some tumor types. In the present study, we evaluated 143 primary breast adenocarcinomas for the presence of DC, using immunohistochemistry with the anti‐S100 protein antibody. We analyzed the relationship between the degree of infiltration by S100+ TIDC and the usual prognostic factors and clinical outcome. The results show that 42% of breast adenocarcinomas contain S100+ TIDC. The number of S100+ TIDC varies according to the grade of tumors as follows: GRIII > GRII > GRI. A relationship is also found between S100+ TIDC and tumor size, lymph‐node involvement, estrogen/progesterone receptor status and age. However, the presence of S100+ TIDC, even at the highest density, was not correlated with metastasis‐free survival or overall survival. Int. J. Cancer (Pred. Oncol.) 84:309–314, 1999. © 1999 Wiley‐Liss, Inc. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0020-7136 1097-0215 |
DOI: | 10.1002/(SICI)1097-0215(19990621)84:3<309::AID-IJC19>3.0.CO;2-3 |