Twenty-three family members were screened for the tumor with carcinoembryonic antigen (CEA) assay, barium enema, and proctoscopy; one occult colon cancer was diagnosed.
We have tried to develop a new model consisting of rats transplanted with syngeneic colon carcinoma PROb cells transfected with cDNA coding for the carcinoembryonic antigen (CEA), the human tumor marker most commonly used as target for MAbs.
The lack of direct proportionality between mRNA and protein expression suggests that, as observed in human colon carcinoma and adjacent normal tissue, both transcriptional and post-transcriptional control mechanisms regulate CEA gene family member expression in colon carcinoma cells.
These data suggest that NCA may be more useful as a tumor marker for colon carcinoma than CEA at the level of mRNA, and that transcriptions of the CEA and NCA genes might be regulated by some common mechanisms in malignant and nonmalignant tissues of the colon.
We report here the effect of recombinant human gamma-interferon (HuIFN-gamma) on the expression of human CEA and its related transcripts in several human colon carcinoma and normal human fibroblast cell lines.
Well-differentiated colon cancer cell lines (LS174T and SKCO-1) contained the highest CEA activity which was 35 to 60 times greater than that of less well-differentiated cells (SW620, SW480, and HRT18).
The analysis of the carcinoembryonic antigen (CEA) promoter in the colon carcinoma lines HT-29 and SW403, using HeLa as a control, was performed using gel mobility shift assays and in vitro and in vivo footprinting before and after IFN-gamma treatment.
Transforming growth factor beta 1 regulates the expression of extracellular matrix adhesion molecules and the carcinoembryonic antigen gene family of glycoproteins in the Moser colon carcinoma cell line.
The direct effect of rKGF was confirmed by demonstrating markedly increased carcinoembryonic antigen production in a human colon carcinoma cell line, LIM1899.
Maximal induction of CEA by IFN-gamma and tumor necrosis factor alpha (TNF-alpha) in the colon carcinoma cell line HT-29 occurs at 5-6 days with maximal secreted levels at 14 ng/ml for IFN-gamma and 20 ng/ml for TNF-alpha.
In addition, differentiation of Caco-2 cells during the cell culture period (days 1-21 in culture) was studied in parallel using morphological (light and scanning electron microscopy) and biochemical markers of growth (DNA, RNA and protein content, and beta-actin mRNA and glyceraldehyde phosphate dehydrogenase mRNA expression) and differentiation (alkaline phosphatase activity, carcinoembryonic antigen content).
Expression in cytotoxic T lymphocytes of a single-chain anti-carcinoembryonic antigen antibody. Redirected Fas ligand-mediated lysis of colon carcinoma.
The expression of pCEA correlates well with the CEA production by the specific cell line offering a potential tissue-specific targeting strategy for colon cancer gene therapy.
Ligand activation of this receptor in colon cancer cells causes a considerable reduction in linear and clonogenic growth, increased expression of carcinoembryonic antigen and the reversal of many gene expression events specifically associated with colon cancer.
Treatment of two human colon cancer cell lines (HT-29 and WiDr) with 5-FU + gamma-IFN resulted in an increase of CEA expression higher than that obtainable with both agents alone, although no synergistic effects were obtained.
In order to selectively reverse MDR in malignant tissue without disrupting the function of normal colonocytes, a retroviral vector (pCEAMR) containing anti-mdr1 ribozyme coupled to the carcino-embryonic-antigen (CEA) promoter was constructed and introduced into resistant colon-cancer cells (SW1116R) that produce CEA and into control resistant cells (HeLaK) that do not produce CEA.
Staurosporine (ST), a protein kinase C inhibitor, was found to produce antitumor effects against C22.20, a clonal subline derived from colon cancer HT-29 line, selected for low expression of carcinoembryonic antigen (CEA).