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This article is part of the supplement: 23rd Congress of the International Association for Breast Cancer Research

Meeting abstract

The CC chemokine RANTES as a potential contributor to breast cancer progression

E Azenshtein1, G Luboshits1, S Shina1, E Neumark1, N Vigler2, S Chaitchik3, I Keydar1 and A Ben-Baruch1

1Department of Cell Research and Immunology, George S Wise Faculty of Life Sciences, Tel-Aviv University

2Department of Oncology, Tel-Aviv Sourasky Medical Center

3Department of Oncology, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

from 23rd Congress of the International Association for Breast Cancer Research
Düsseldorf, Germany. 13–16 June 2001

Breast Cancer Res 2001, 3(Suppl 1):A5doi:10.1186/bcr377

Received: 10 May 2001
Published: 29 May 2001

© 2001 BioMed Central Ltd

Meeting abstract

In breast carcinoma, high levels of tumor-associated macrophages are correlated with lymph node metastases and clinical aggressiveness. Potential candidates that may support the recruitment of monocytes from the circulation into breast tumors are the members of the CC subfamily of chemokines. In the present study we evaluated the expression of the CC chemokine RANTES in sections of breast cancer patients diagnosed in different stages of disease. Our results indicate that high incidence and intensity of RANTES expression were directly correlated with a more advanced disease, suggesting that the chemokine may be involved in breast cancer progression.

Analyses performed by using the T47D and MCF-7 human breast adenocarcinoma cells indicated that RANTES expression is tightly regulated by cytokines. Furthermore, the results of our study indicate that T47D-derived RANTES partially contributes to monocyte migration, and suggest that in vivo this chemokine may be involved in inducing monocyte infiltration to breast tumor sites. In the present study we further characterized the paracrine and autocrine mechanisms by which RANTES may support breast cancer progression. The results suggest that RANTES may be involved in a complex process, in which a crosstalk between infiltrating monocytes and the tumor cells may affect tumor progression.

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