MUC1 from the Mucin Family as Potential Tools in Breast Cancer Immunotherapy / 한국유방암학회지
Journal of Breast Cancer
;
: 125-133, 2009.
Article
in English
| WPRIM
| ID: wpr-180073
ABSTRACT
Many breast cancer patients develop minimal residual disease that becomes resistance to treatments, and finally are faced with relapse and progression of disease. Currently, immunotherapy has become a potential therapy in treating minimal residual disease and preventing cancer occurrence. Cancer vaccines provide a unique therapeutic modality in that they initiate a dynamic process of activating the host's own immune system. A lot of tumor specific antigens as a target of immune system were identified and some have been applied for cancer vaccine. Mucin 1 (MUC1) oncoprotein, which is overexpressed in breast cancer in contrast with normal mammary tissue, is one of the first tumor antigens shown to be a target for human tumor-specific T cells and thus a valid target for immunotherapy. MUC1 is a high-molecular-weight glycoprotein rich in serine and threonine residues that are O-glycosylated. MUC1 is expressed on glandular epithelia and on epithelial tumors. But, tumor MUC1 differs from normal MUC1 by modified glycan side chains. Over-expression and aberrant glycosylation of MUC1 antigen by epithelial tumors results in endogenous antibody responses in cancer patients to MUC1 antigen. This finding has led to the identification of MUC1 derived peptide epitopes that induce T-cell responses. MUC1 based clinical trials have used peptides, protein, DNA, pulsed dendritic cells, or glycopeptide. This review will summarize the potential utility of breast cancer immunotherapy of MUC1, as well as the structure and function.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Peptides
/
Recurrence
/
Serine
/
Threonine
/
Dendritic Cells
/
Glycosylation
/
Breast
/
Breast Neoplasms
/
DNA
/
Glycoproteins
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Journal of Breast Cancer
Year:
2009
Type:
Article
Similar
MEDLINE
...
LILACS
LIS