Expression of cell surface antigens on cultured tumor cells

Cikes, Matko; Friberg, Sten

doi:10.1016/b978-0-7204-0623-8.50016-6

Cited by 10 publications

(7 citation statements)

References 200 publications

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“…Thus, production of CEA, occurring primarily in the stationary phase of growth, is similar to the findings of other investigators with respect to the expression of viral-induced tumor-associated and for transplanta tion antigens [5][6][7]36]. …”

Section: Discussionsupporting

confidence: 86%

Observations on the Synthesis of Carcinoembryonic Antigen by an Established Human Colonic Carcinoma Cell Line

Drewinko¹,

Yang²

1980

Oncology

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Some properties and kinetics of synthesis of the carcinoembryonic antigen (CEA-LoVo) produced by an established human colon carcinoma cell line were analyzed. CEA-LoVo was assayed by the method of Chu and Reynoso which was standardized against the activity of the First British Standard for CEA. CEA-LoVo was stable at -20 and 4°C. At 37 °C, CEA-LoVo degraded at the rate of 1.4%/day in cell-free supernatants, and at the rate of 6.6%/day in the supernatants of monolayer cultures. CEA-LoVo was sensitive to enzymatic treatment with trypsin (∼55% loss) and extraction of PCA ( > 70% loss). The elution profile of CEA-LoVo in Concanavalin A-Sepharose B coincided with that of the First British Standard for CEA. No A or B blood group antigenic activity was noted. Studies employing immunofluorescent and horseradish peroxidase-labeled antibody techniques demonstrated heavy membrane and moderate intracytoplasmic localization. The greatest amount of net synthesis occurred for cells in the stationary phase while CEA-LoVo release occurred maximally in the lag phase.

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Section: Discussionsupporting

confidence: 86%

Observations on the Synthesis of Carcinoembryonic Antigen by an Established Human Colonic Carcinoma Cell Line

Drewinko¹,

Yang²

1980

Oncology

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“…Renewal of proteins may occur in either a continuous or a discontinuous process (28). Although many cell surface receptors have been shown to be expressed continuously throughout the growth of a cell, others have been demonstrated to have growth phase-related expression (4). Examples of quantitative changes in expression include membrane-bound immunoglobulin (19), CD4 (23), murine leukemia virus major envelope protein (32), ␤2-integrins (38), the tumor necrosis factor receptor (31), and CD40 (9).…”

Section: Discussionmentioning

confidence: 99%

Attachment of Toxoplasma gondii to Host Cells Involves Major Surface Protein, SAG-1 (P-30)

Mineo

Kasper²

1994

Experimental Parasitology

139

102

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The initial attachment of Toxoplasma tachyzoites to target host cells is an important event in the life cycle of the parasite and hence critical in the pathogenesis of this infection. The efficiency of Toxoplasma attachment to synchronized populations of Chinese hamster ovary cells and bovine kidney cells was investigated by using a glutaraldehyde-fixed host cell assay system. For both cell lines, parasite attachment increased as the synchronized host cells proceeded from the G1 phase to the mid-S phase and then decreased as the cells entered the G2-M boundary. Postulating that these differences in attachment reflect the upregulation of a specific receptor, polyclonal antibodies were generated against whole MDBK antigen at 0 and 4 h into the S phase. Both antisera were shown to inhibit parasite attachment to both synchronous and asynchronous host cell populations. However, the attachment blockade observed with the 4-h antiserum was significantly greater than that with the 0-h antiserum, completely abolishing the cell cycle-dependent increase in attachment found in control samples. These findings suggest that Toxoplasma tachyzoites bind specifically to a host cell receptor which is upregulated in the mid-S phase of the cell cycle.Toxoplasma gondii is an obligate intracellular parasite in which host cell invasion is an essential component of its life cycle. In addition to having an extremely broad host range (6), T. gondii is uniquely promiscuous in vitro, infecting every mammalian cell as well as insect and primary fish cell lines (3, 39). The invasion process is highly ordered, initiated by the binding of the apical end of the tachyzoite to the host cell plasma membrane. As it enters, the parasite is visibly constricted at the site of a tight junction with the host cell plasma membrane. This constriction moves posteriorly along the length of the parasite as it moves into the host cell (1, 25). Short cytoplasmic projections reseal the host membrane (8, 30), leaving the parasite inside a specialized parasitophorous vacuole (36).Attachment to the host cell is thus the first step required for the process of invasion and hence is critical for its continued survival. Although the process of attachment was described more than 30 years ago, the identification of parasite ligands and cell surface receptors remains incomplete (16). Previous work from our laboratories has demonstrated an important role for the major tachyzoite surface protein SAG1 as a parasite ligand (13,14,27). With a fixed host cell system, attachment can be inhibited by using some anti-SAG1 monoclonal antibodies and, in addition, attachment is quantitatively reduced in chemically mutagenized parasite mutants lacking antigenic SAG1 (26).The broad host cell range of T. gondii implies either the presence of a highly conserved host cell receptor or that the parasite can utilize a variety of different receptors. Specificity is suggested in that attachment is saturable in competition assays (26) and can be inhibited with the neoglycoprotein bovine serum albu...

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“…In cell culture studies the expression of the membrane bound antigens including blood group antigens has been related to different stages in the cell cycle (FRANKS & DAWSON 1966, CiKES 1970, 1971a, b, KARB & GOLDSTEIN 1971, KUHNS & PANN 1973.The proportion of cells demonstrating mem.brane bound antigens was decreased when the cells exhibited the highest growth rate.…”

Section: Lood Group Antigens In Cystsmentioning

confidence: 99%

Blood group antigens A and B in ameloblastomas, odontogenic keratocysts and non‐keratinizing cysts

Vedtofte

Dabelsteen

1975

European J Oral Sciences

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The expression of blood group antigens A and B has been studied in 8 ameloblastomas, 16 odontogenic keratocysts from patients with basal cell nevus syndrome, 11 odontogenic keratocysts from patients without the syndrome, and 12 non-keratinizing odontogenic cysts, using a double layer immunofluorescence staining technique. The amount of antigen in the lesions was compared with the content of antigen in normal buccal mucosa from e^ch patient. All ameloblastomas reacted negatively, three cysts from the patients with the basal cell nevus syndrome reacted negatively, and the odontogenic keratocysts from patients without the syndrome as well as the non-keratinizing odontogenic cysts all gave a positive reaction.' _ . .• •. . •• •

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Expression of cell surface antigens on cultured tumor cells

Cited by 10 publications

References 200 publications

Observations on the Synthesis of Carcinoembryonic Antigen by an Established Human Colonic Carcinoma Cell Line

Observations on the Synthesis of Carcinoembryonic Antigen by an Established Human Colonic Carcinoma Cell Line

Attachment of Toxoplasma gondii to Host Cells Involves Major Surface Protein, SAG-1 (P-30)

Blood group antigens A and B in ameloblastomas, odontogenic keratocysts and non‐keratinizing cysts

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