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Role of transforming growth factor-α-related peptides in the autocrine/paracrine control of experimental breast cancer growthin vitro by estradiol, prolactin, and progesterone (1990)

Manni, Andrea ; Wright, Carol ; Badger, Betty ; [et al.]

Springer

Breast cancer research and treatment 15 (1990), S. 73-83

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ISSN: 1573-7217

Keywords: transforming growth factor alpha (TGFα) ; NMU rat mammary tumor ; anti-EGF-receptor antibodies ; soft agar clonogenic assay ; estradiol ; prolactin ; progesterone

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary We have recently suggested that estradiol (E2), prolactin (oPrl), and progesterone (Pg) support the growth of the hormone-responsive N-nitrosomethylurea (NMU) rat mammary tumor in soft agar through autocrine/paracrine mechanisms. To gain insight into the nature of these hormonally regulated growth factors, we tested the ability of two monoclonal antibodies (MAb-425 and 528) directed against the epidermal growth factor receptor (EGF-R) to inhibit the colony-stimulating effects of conditioned media (CM) obtained from E2, oPrl, and Pg-treated NMU rat mammary tumors. Since both MAbs are specific for human EGF-R, MCF-7 breast cancer cells grown in soft agar in the absence of serum were used as our indicator system. Both MAb-425 and 528 totally abolished the colony-stimulating effect of genuine EGF, while having no agonistic/antagonistic action when added alone. Both MAb-425 and 528 markedly inhibited the colony-stimulating effect of rat mammary tumor E2-CM in a dose-dependent fashion. MAb-425 was also found to inhibit the growth-promoting action of Pg-CM, although this effect appeared to be somewhat less consistent and pronounced than that observed with E2-CM. In contrast, the colony-stimulating effect of Prl-CM was only rarely and, usually, modestly affected by the addition of either MAb-425 or 528. Our data suggest that in the NMU mammary tumor grown in soft agar, EGF/TGFα-related peptides are produced upon exposure to E2 and possibly Pg but only rarely following Prl administration. The possible role of these growth factors as mediators of hormonal effects in our experimental system remains to be established.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF01810779

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Monoclonal antibody 425 inhibits growth stimulation of carcinoma cells by exogenous EGF and tumor-derived EGF/TGF-α (1990)

Rodeck, Ulrich ; Williams, Noel ; Murthy, U. ; [et al.]

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 44 (1990), S. 69-79

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ISSN: 0730-2312

Keywords: carcinoma ; autocrine stimulation ; EGF-receptor ; transforming growth factor ; autocrine function ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: Carcinoma cells frequently coexpress transforming growth factor (TGF)-α and its receptor, the epidermal growth factor (EGF) receptor, implicating an autocrine function of carinoma-derived TGF-α. Using a monoclonal antibody (425) to the EGF-receptor, we investigated the role of exogenous and tumor cell-derived EGF/TGF-α mitogenic activities in proliferation of cell lines derived from solid tumors. Monoclonal antibody 425 was chosen for these studies because it inhibits binding of EGF/TGF-α to the EGF-receptor and effectively blocks activation of the EGF-receptor by EGF/TGF-α. Seven malignant cell lines originating from carcinomas of colon, pancreas, breast, squamous epithelia, and bladder expressed surface EGF-receptor and secreted EGF/TGF-α-like mitogenic activities into their tissue culture media. All cell lines were maintained in a defined medium free of exogenous EGF/TGF-α. EGF and TGF-α added to the culture medium stimulated proliferation of five cell lines to comparable levels. EGF/TGF-α-dependent proliferation was significantly reduced by addition of MAb 425 to culture media. In addition, monoclonal antibody 425 reduced proliferation of the five EGF/TGF-α responsive cell lines in the absence of exogenous EGF/TGF-α. Antiproliferative effects induced by monoclonal antibody 425 were reversible and could be overcome by addition of EGF to culture media. Our results indicate that tumor-derived EGF-receptor-reactive mitogens can promote proliferation of carcinoma cells in an autocrine fashion.

Additional Material: 3 Ill.