Linked Life Data

7594611

Source:http://linkedlifedata.com/resource/pubmed/id/7594611

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1995-12-14
pubmed:abstractText
A tumor-specific cytotoxic T lymphocyte (CTL) immune response has been well documented in melanoma, renal cell carcinoma, and ovarian cancer. Conflicting evidence exists regarding the existence of tumor-specific CTL populations in breast cancer. Tumor cells and tumor-associated lymphocytes (TAL) were isolated from the pleural effusions of six consecutive patients with metastatic breast cancer. After solid-phase anti-CD3 stimulation, TAL cultures were expanded with weekly autologous tumor stimulation and low-dose IL-2 for 3 wk. T cell populations were characterized using flow cytometric analysis and ranged from 49 to 91% CD8+, > 98% CD3+, and < 3% CD16+. Functionally, tumor-stimulated TAL showed tumor-specific recognition of autologous tumor cells (241 +/- 142 LU20/10(7)) and no detectable lysis of autologous fibroblasts, Daudi or K562. Cytotoxicity of TAL against HLA-A2+ allogeneic targets was significantly higher when compared with HLA-A2- tumor cell lines (127 +/- 76 vs 6 +/- 18 LU, p = 0.0001). This cytotoxicity against autologous and allogeneic tumor cells was blocked by anti-HLA-A2 mAb and cold HLA-A2+ targets in cold-target inhibition assays. TAL from all HLA-A2+ patients recognized GP2, a known, HER2/neu-derived tumor-associated peptide Ag that is HLA-A2 restricted. We have shown that TAL obtained from metastatic effusions of breast cancer patients contain lymphocytes that can recognize and lyse autologous and allogeneic tumor cells in a tumor-specific, HLA-A2-restricted fashion. In addition, tumor-specific TAL derived from breast cancer patients can selectively lyse HLA-A2+ pancreatic and ovarian tumor cell targets, suggesting a common HLA-A2-restricted tumor-associated Ag between these distinct epithelial cancers. Further elucidation of the cell-mediated immune response to breast cancer and the identification of shared TAA could result in the development of broadly applicable vaccine therapies for many cancers.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
155
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4486-91
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:7594611-Adenocarcinoma, pubmed-meshheading:7594611-Antigens, CD3, pubmed-meshheading:7594611-Antigens, CD8, pubmed-meshheading:7594611-Breast Neoplasms, pubmed-meshheading:7594611-Cell Division, pubmed-meshheading:7594611-Cross Reactions, pubmed-meshheading:7594611-Epitopes, pubmed-meshheading:7594611-Female, pubmed-meshheading:7594611-HLA-A2 Antigen, pubmed-meshheading:7594611-Humans, pubmed-meshheading:7594611-Interleukin-2, pubmed-meshheading:7594611-Lymphatic Metastasis, pubmed-meshheading:7594611-Lymphocytes, Tumor-Infiltrating, pubmed-meshheading:7594611-Ovarian Neoplasms, pubmed-meshheading:7594611-Pancreatic Neoplasms, pubmed-meshheading:7594611-Receptor, erbB-2, pubmed-meshheading:7594611-T-Lymphocytes, Cytotoxic, pubmed-meshheading:7594611-Tumor Markers, Biological
pubmed:year
1995
pubmed:articleTitle
Tumor-specific and HLA-A2-restricted cytolysis by tumor-associated lymphocytes in human metastatic breast cancer.
pubmed:affiliation
Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't