Expression of Colorectal Carcinoma-Associated Antigens in Colonic Polyps

Rr, Salem; Bc, Wolf; Hf, Sears; Pt, Lavin; Ts, Ravikumar; DeCoste, Deborah; Jc, D'Emilia; Herlyn, Meenhard; Schlom, J.; Ls, Gottlieb

doi:10.1006/jsre.1993.1136

Cited by 19 publications

(13 citation statements)

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“…11,12 Ep-CAM is present in high amounts in normal colorectal tissue, but its expression increases in polyps 13 and carcinomas. 14 In tumor cells, increased Ep-CAM expression promotes cellcell adhesion.…”

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confidence: 99%

Loss of membranous Ep-CAM in budding colorectal carcinoma cells

et al. 2007

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Tumor budding is a histological feature that reflects loss of adhesion of tumor cells and is associated with locoregional metastasis of colorectal carcinoma. Although nuclear localization of b-catenin is associated with tumor budding, the molecular mechanism remains largely elusive. In this study, we hypothesize that the epithelial cell adhesion molecule (Ep-CAM) is involved in tumor budding. In order to address this question, we performed immunohistochemistry on Ep-CAM using three different antibodies (monoclonal antibodies Ber-ep4 and 311-1K1 and a polyclonal antibody) and a double staining on b-catenin and Ep-CAM. In addition, Ep-CAM mRNA was monitored with mRNA in situ hybridization. Subsequently, we determined the effect of Ep-CAM staining patterns on tumor spread in rectal cancer. In contrast to the tumor mass, budding cells of colorectal carcinoma displayed lack of membranous but highly increased cytoplasmic Ep-CAM staining and nuclear translocation of b-catenin. mRNA in situ hybridization suggested no differences in Ep-CAM expression between the invasive front and the tumor mass. Importantly, reduced Ep-CAM staining at the invasive margin of rectal tumor specimens (n ¼ 133) correlated significantly with tumor budding, tumor grade and an increased risk of local recurrence (P ¼ 0.001, P ¼ 0.04 and P ¼ 0.03, respectively). These data demonstrate abnormal processing of Ep-CAM at the invasive margin of colorectal carcinomas. Our observations indicate that loss of membranous Ep-CAM is associated with nuclear b-catenin localization and suggest that this contributes to reduced cell-cell adhesions, increased migratory potential and tumor budding.

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Loss of membranous Ep-CAM in budding colorectal carcinoma cells

et al. 2007

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“…However, it is also true for other types of epithelium, such as transitional epithelium (urothelium), where the level of Ep-CAM expression correlates to the tumor grade (52), or simple epithelia, such as mammary gland, where enhanced levels of Ep-CAM in carcinomas are associated with a bad prognosis (46). In colon, where the normal level of Ep-CAM is relatively high, a further increase in Ep-CAM expression is observed in relation to polyp development (38). An interesting example of the relationship between Ep-CAM expression and proliferation in normal tissue is the hair follicle, where Ep-CAM is expressed only in the highly proliferative zone (47).…”

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Cytoplasmic Tail Regulates the Intercellular Adhesion Function of the Epithelial Cell Adhesion Molecule

Balzar

Bakker

Briaire-de-Bruijn

et al. 1998

Molecular and Cellular Biology

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“…First described in 1965 (Gold and Freedman, 1965), it is now routinely used as a serum marker in the management of gastrointestinal cancers (National Institutes of Health, 1981;Guadagni et al, 1993), as well as other carcinomas (Thomas et al, 1990). CEA has also been extensively studied, in particular, by immunohistochemical techniques for its expression in malignant and benign lesions, and in normal tissues (Goldenberg et al, 1976;Salem et al, 1993). The gene for CEA has been cloned and has been found to belong to the immunoglobulin supergene family (Paxton et al, 1987).…”

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“…The majority of the studies evaluating CEA expression in tumors and normal tissues have employed semi-quantitative immunohistochemical techniques (Goldenberg et al, 1976;and Salem et al, 1993). One study demonstrated the ability to quantitate CEA by radioimmunoassay on formalin-fixed tissue samples (Goldenberg et al, 1976).…”

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Quantitative analysis of CEA expression in colorectal adenocarcinoma and serum: Lack of correlation

Guadagni¹,

Roselli

Cosimelli³

et al. 1997

Int. J. Cancer

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Tissues and sera from 110 patients diagnosed with colorectal primary carcinoma, 20 patients with benign colorectal diseases and 31 healthy donors were subjected to quantitative CEA analysis. Multiple samples from tumor lesions and autologous histologically normal mucosa (10 cm from the tumor) were obtained at the time of surgery (cancer patients) or endoscopy (benign patients and healthy volunteers). CEA content was measured in protein extracts obtained from these tissues using a quantitative RIA method. A limit of normality for CEA content was established as 300 ng/mg of protein. When this was taken as cut‐off, 104 of 110 (94.5%) tumor lesions and 51 of 110 (46.4%) autologous histologically normal colonic mucosa from cancer patients had elevated CEA levels. No correlation with stage of disease was found, while a correlation was observed with degree of tumor differentiation. A statistically significant difference between CEA content in tumor lesions and in histologically normal mucosa from cancer patients was observed (p = −0.001). Moreover, CEA content was statistically higher in the normal mucosa from cancer patients than in that from healthy donors (p = 0.005). CEA content in tissue specimens from benign lesions differed significantly from that in tissue from healthy donors (p = 0.005) and in carcinoma lesions (p < 0.001). The highest CEA content was observed in benign lesions with severe dysplasia. No statistical correlation between CEA content in carcinoma tissues and serum CEA levels (r = 0.195, p = .13) was found. Therefore, in considering diagnosis or therapy with anti‐CEA MAbs for colorectal‐carcinoma patients, or potential therapies with anti‐CEA recombinant vaccines, serum CEA levels should not be taken as indicating CEA expression in tumor lesions. Int. J. Cancer 72:949–954, 1997. © 1997 Wiley‐Liss, Inc.

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Expression of Colorectal Carcinoma-Associated Antigens in Colonic Polyps

Cited by 19 publications

References 0 publications

Loss of membranous Ep-CAM in budding colorectal carcinoma cells

Loss of membranous Ep-CAM in budding colorectal carcinoma cells

Cytoplasmic Tail Regulates the Intercellular Adhesion Function of the Epithelial Cell Adhesion Molecule

Quantitative analysis of CEA expression in colorectal adenocarcinoma and serum: Lack of correlation

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