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1.
Int J Oncol ; 24(6): 1413-8, 2004 Jun.
Article in English | MEDLINE | ID: mdl-15138582

ABSTRACT

Breast cancer metastasizes from the primary site to the axillary lymph nodes (LN). It is unknown whether tumor metastasis abolishes or enhances the ability of LN cells to develop a specific response to the Ag expressed by the tumor, and whether an immune response to the same Ag is present in the tumor-free LN. We stimulated lymphocytes from a metastasis negative (Met-) and a metastasis positive (Met+) LN, invaded by a HER-2+ tumor, from the same patient, with HER-2 peptides E75 (369-377) and G89 (776-778). E75 define a CTL epitope presented by HLA-A2, while G89 define a CD4+ cell recognized epitope. Met- LN responded to E75+G89 with higher expansion of E75 TCR+ CD45RO+ CCR7- (CCR7-) and E75-TCR+ CD45RO+ CCR7+ (CCR7+) cells than Met+ LN. Stimulation with E75+G89 induced a significant increase in CCR7+ cells in Met- LN compared with Met+ LN. The levels of IFN-alpha and IL-15 were higher in Met- LN cultures stimulated with E75+G89 than in Met+ LN cultures. This increase did not correlate with the levels of induction of IFN-gamma, IL-4, and IL-10. The finding of higher expansion of Ag specific CCR7+ cells and of differentiation to CCR7- cells, which define the TCM and TEM subsets respectively, in Met- LN, by G89 is novel for tumor systems. This may have implications for preventative vaccination strategies for breast and ovarian cancer.


Subject(s)
Breast Neoplasms/immunology , CD8-Positive T-Lymphocytes/immunology , Immunologic Memory , Lymph Nodes/cytology , Lymphatic Metastasis/pathology , Receptor, ErbB-2/immunology , T-Lymphocytes, Cytotoxic/immunology , Breast Neoplasms/metabolism , Breast Neoplasms/pathology , CD8-Positive T-Lymphocytes/cytology , Carcinoma, Ductal/immunology , Carcinoma, Ductal/metabolism , Carcinoma, Ductal/secondary , Epitopes, T-Lymphocyte/immunology , Female , HLA-A2 Antigen/metabolism , Humans , Interferon-alpha/metabolism , Interferon-gamma/metabolism , Interleukin-10/metabolism , Interleukin-15/metabolism , Interleukin-4/metabolism , Leukocyte Common Antigens/metabolism , Lymph Nodes/immunology , Lymphocyte Activation , Neoplasm Invasiveness/pathology , Peptide Fragments/immunology , Peptide Fragments/metabolism , Receptor, ErbB-2/metabolism , Receptors, Antigen, T-Cell/immunology , Receptors, Antigen, T-Cell/metabolism , Receptors, CCR7 , Receptors, Chemokine/metabolism , T-Lymphocytes, Cytotoxic/cytology , Tumor Cells, Cultured
2.
Clin Cancer Res ; 9(9): 3222-34, 2003 Aug 15.
Article in English | MEDLINE | ID: mdl-12960107

ABSTRACT

Many clinical studies have been undertaken to assess the therapeutic potential of vaccination and have included a large variety of cancer immunogens. Most of these studies involved patients with metastatic cancer, which is characterized by the most aggressive malignant cells, the longest-lasting disease, and the failure of all standard cytotoxic treatments. The presence of tumor over long periods and the toxicity of previous treatments tend to negatively affect immune responsiveness to tumor antigens presented by the vaccine. In this review, we analyze the ability of past and current vaccine therapies to induce clinical responses in breast cancer. To date, clinical responses have been observed by using vaccines targeting HER-2/neu protein, human telomerase reverse transcriptase, carcinoembryonic antigen, and carbohydrate antigen given after stem cell rescue. The review concludes with a discussion of possible future directions for vaccine development and applications.


Subject(s)
Breast Neoplasms/drug therapy , Cancer Vaccines , Animals , Antigens, Neoplasm/chemistry , Carbohydrates/chemistry , Carcinoembryonic Antigen/biosynthesis , DNA-Binding Proteins , Humans , Models, Chemical , Neoplasm Metastasis , Receptor, ErbB-2/metabolism , Telomerase/metabolism , Time Factors
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