PMID- 10606205
OWN - NLM
STAT- MEDLINE
DCOM- 20000120
LR  - 20191103
IS  - 0946-2716 (Print)
IS  - 0946-2716 (Linking)
VI  - 77
IP  - 10
DP  - 1999 Oct
TI  - The biology of the 17-1A antigen (Ep-CAM).
PG  - 699-712
AB  - The glycoprotein recognized by the monoclonal antibody (mAb) 17-1A is present on 
      most carcinomas, which makes it an attractive target for immunotherapy. Indeed,
      adjuvant treatment with mAb 17-1A did successfully reduce the 5 years mortality
      among colorectal cancer patients with minimal residual disease. Currently the
      antibody is approved for clinical use in Germany, and is on its way to approval
      in a number of other countries. New immunotherapeutic strategies targeting the
      17-1A antigen are in development or even in early-phase clinical trials.
      Therefore, a better understanding of the biology of the 17-1A antigen may result 
      in improved strategies for the treatment and diagnosis of human carcinomas. In
      this review the properties of the 17-1A antigen are discussed concerning tumor
      biology and the function of the molecule. This 40-kDa glycoprotein functions as
      an Epithelial Cell Adhesion Molecule, therefore the name Ep-CAM was suggested.
      Ep-CAM mediates Ca2+-independent homotypic cell-cell adhesions. Formation of
      Ep-CAM-mediated adhesions has a negative regulatory effect on adhesions mediated 
      by classic cadherins, which may have strong effects on the differentiation and
      growth of epithelial cells. Indeed, in vivo expression of Ep-CAM is related to
      increased epithelial proliferation and negatively correlates with cell
      differentiation. A regulatory function of Ep-CAM in the morphogenesis of
      epithelial tissue has been demonstrated for a number of tissues, in particular
      pancreas and mammary gland. The function of Ep-CAM should be taken into
      consideration when developing new therapeutic approaches targeting this molecule.
FAU - Balzar, M
AU  - Balzar M
AD  - Department of Pathology, Leiden University Medical Center, The Netherlands.
FAU - Winter, M J
AU  - Winter MJ
FAU - de Boer, C J
AU  - de Boer CJ
FAU - Litvinov, S V
AU  - Litvinov SV
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Germany
TA  - J Mol Med (Berl)
JT  - Journal of molecular medicine (Berlin, Germany)
JID - 9504370
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Cadherins)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Epithelial Cell Adhesion Molecule)
RN  - 0 (Fetal Proteins)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Antibodies, Monoclonal/therapeutic use
MH  - Antigens, Neoplasm/analysis/genetics/immunology/*physiology
MH  - Biomarkers, Tumor/analysis
MH  - Breast/chemistry/embryology
MH  - Cadherins/physiology
MH  - Carcinoma/chemistry/diagnosis/*immunology/therapy
MH  - Cell Adhesion/physiology
MH  - Cell Adhesion Molecules/analysis/genetics/immunology/*physiology
MH  - Cell Differentiation
MH  - Cell Transformation, Neoplastic
MH  - Chromosomes, Human, Pair 4/genetics
MH  - Epithelial Cell Adhesion Molecule
MH  - Epithelial Cells/cytology/metabolism
MH  - Evolution, Molecular
MH  - Female
MH  - Fetal Proteins/physiology
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes
MH  - Humans
MH  - Immunohistochemistry
MH  - Immunotherapy
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Morphogenesis
MH  - Multigene Family
MH  - Organ Specificity
MH  - Pancreas/chemistry/embryology
MH  - Protein Conformation
MH  - Protein Structure, Tertiary
RF  - 84
EDAT- 1999/12/22 00:00
MHDA- 1999/12/22 00:01
CRDT- 1999/12/22 00:00
PHST- 1999/12/22 00:00 [pubmed]
PHST- 1999/12/22 00:01 [medline]
PHST- 1999/12/22 00:00 [entrez]
AID - 10.1007/s001099900038 [doi]
PST - ppublish
SO  - J Mol Med (Berl). 1999 Oct;77(10):699-712. doi: 10.1007/s001099900038.