scholarly journals Modulation of MUC1 mucin as an escape mechanism of breast cancer cells from autologous cytotoxic T-lymphocytes

2001 ◽  
Vol 84 (9) ◽  
pp. 1258-1264 ◽  
Author(s):  
K Kontani ◽  
O Taguchi ◽  
T Narita ◽  
M Izawa ◽  
N Hiraiwa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
T Lymphocytes ◽  
Cancer Cells ◽  
Cytotoxic T Lymphocytes ◽  
Breast Cancer Cells ◽  
Escape Mechanism ◽  
Muc1 Mucin

Generation of CD8+ Cytotoxic T Lymphocytes Against Breast Cancer Cells by Stimulation with Mammaglobin-A-Pulsed Dendritic Cells

2003 ◽  
Vol 79 (1) ◽  
pp. 133-136 ◽  
Author(s):  
Partha P. Manna ◽  
Andrés Jaramillo ◽  
Kanchana Majumder ◽  
Lacey G. Campbell ◽  
Timothy P. Fleming ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dendritic Cells ◽  
T Lymphocytes ◽  
Cancer Cells ◽  
Cytotoxic T Lymphocytes ◽  
Breast Cancer Cells

scholarly journals Dendritic cells loaded with killed breast cancer cells induce differentiation of tumor-specific cytotoxic T lymphocytes

2004 ◽  
Vol 6 (4) ◽  
Author(s):  
Eve-Marie Neidhardt-Berard ◽  
Frederic Berard ◽  
Jacques Banchereau ◽  
A Karolina Palucka
Keyword(s):  
Breast Cancer ◽  
Dendritic Cells ◽  
T Lymphocytes ◽  
Cancer Cells ◽  
Cytotoxic T Lymphocytes ◽  
Breast Cancer Cells

scholarly journals BSCI-25. THE ROLE OF THE IFNγ PATHWAY IN BREAST CANCER BRAIN METASTASIS FORMATION

2019 ◽  
Vol 1 (Supplement_1) ◽  
pp. i5-i5
Author(s):  
Route Pedrosa ◽  
Benjamin Schrijver ◽  
Rute B Marques ◽  
Pieter J M Leenen ◽  
Wim A Dik ◽  
...  
Keyword(s):  
Breast Cancer ◽  
T Lymphocytes ◽  
Brain Metastasis ◽  
Brain Metastases ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
T Cell Response ◽  
Activated T Cells ◽  
Breast Cancer Brain Metastasis

Abstract In previous work, we showed the prominence of the T cell response in the formation of brain metastases of primary ER-negative breast cancers. We also showed that prior co-cultured breast cancer cells with stimulated T lymphocytes bear an overexpression of Guanylate-binding protein 1 (GBP1) and possess an increased trespassing ability through an in vitro blood-brain barrier (BBB) model. In addition, we demonstrated a predilection for metastasizing to the brain of breast cancer cells that were co-cultured with activated T cells in a mouse model. In the present work, we show that activated CD8+ cytotoxic T lymphocytes, rather than CD4+ lymphocytes, are the main cause of increasing the ability of breast cancer cells to cross the BBB. While synthetic IFNγ does not change the ability of breast cancer cells to cross the BBB, this study shows that the T lymphocyte-secreted IFNγ activates the STAT1-dependent IFNγ pathway in breast cancer cells, enabling them to cross the in vitro BBB. Direct inhibition of soluble IFNγ or blocking of the IFNγ-specific receptor in breast cancer cells significantly decreases their ability to cross the BBB. The results illustrate that IFNγ signaling pathway is one of the crucial pathways in the formation of brain metastasis of ER- breast cancer. The interference with the IFNγ pathway will develop preventive strategies against the formation of brain metastases of breast cancer.

Effects of paclitaxel on cytokine synthesis by unprimed human monocytes, T lymphocytes, and breast cancer cells

1998 ◽  
Vol 46 (2) ◽  
pp. 104-112 ◽  
Author(s):  
Charise M. White ◽  
Brian K. Martin ◽  
Li-Fen Lee ◽  
J. Stephen Haskill ◽  
Jenny P.-Y. Ting
Keyword(s):  
Breast Cancer ◽  
T Lymphocytes ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Human Monocytes ◽  
Cytokine Synthesis
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