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      Determination of TGF β1 protein level in human primary breast cancers and its relationship with survival

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          Abstract

          Transforming growth factor-beta (TGF β)1 is thought to be implicated in breast cancer progression. However, data about the influence of TGF β1 on breast cancer development are conflicting. To clarify the clinical relevance of TGF β1, TGF β1 protein level has been measured by enzyme-immoassay in 193 breast tumour samples. We found that 94.3% of patients expressed TGF β1 with a range of 0–684 pg mg −1 protein. In the overall population, an increase of tumoral TGF β1 was observed in premenopausal patients when compared to postmenopausal subgroup ( P=0.0006). When patients were subdivided according to nodal status, TGF β1 was correlated to type-1 plasminogen activator inhibitor in the node-negative subgroup ( P=0.040). Multivariate analysis revealed that, after lymph node status ( P=0.0002) and urokinase-type plasminogen activator ( P=0.004), TGF β1 was an independent prognostic marker for DFS ( P=0.005) in the overall population. In the node-negative population, TGF β1 was the prominent prognostic factor ( P=0.010). In the same population, Kaplan–Meier curves demonstrated that high TGF β1 level was correlated with a shorter disease-free survival ( P=0.020). These data suggest that the measurement of tumoral TGF β1 protein level, especially for node-negative patients, might help to identify a high-risk population early in tumour progression.

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          TGF-beta1 and Ha-Ras collaborate in modulating the phenotypic plasticity and invasiveness of epithelial tumor cells.

          Metastasis of epithelial tumor cells can be associated with the acquisition of fibroblastoid features and the ability to invade stroma and blood vessels. Using matched in vivo and in vitro culture systems employing fully polarized, mammary epithelial cells, we report here that TGF-beta1 brings about these changes in Ras-transformed cells but not in normal cells. When grown in collagen gels in the absence of TGF-beta, both normal and Ras-transformed mammary epithelial cells form organ-like structures in which the cells maintain their epithelial characteristics. Under these conditions, treatment of normal cells with TGF-beta results in growth arrest. The same treatment renders Ras-transformed epithelial cells fibroblastoid, invasive, and resistant to growth inhibition by TGF-beta. After this epithelial-fibroblastoid conversion, the Ras-transformed cells start to secrete TGF-beta themselves, leading to autocrine maintenance of the invasive phenotype and recruitment of additional cells to become fibroblastoid and invasive. More important, this cooperation of activated Ha-Ras with TGF-beta1 is operative during in vivo tumorigenesis and, as in wound healing processes, is dependent on epithelial-stromal interactions.
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            Evidence that transforming growth factor-beta is a hormonally regulated negative growth factor in human breast cancer cells.

            The hormone-dependent human breast cancer cell line MCF-7 secretes transforming growth factor-beta (TGF-beta), which can be detected in the culture medium in a biologically active form. These polypeptides compete with human platelet-derived TGF-beta for binding to its receptor, are biologically active in TGF-beta-specific growth assays, and are recognized and inactivated by TGF-beta-specific antibodies. Secretion of active TGF-beta is induced 8 to 27-fold under treatment of MCF-7 cells with growth inhibitory concentrations of antiestrogens. Antiestrogen-induced TGF-beta from MCF-7 cells inhibits the growth of an estrogen receptor-negative human breast cancer cell line in coculture experiments; growth inhibition is reversed with anti-TGF-beta antibodies. We conclude that in MCF-7 cells, TGF-beta is a hormonally regulated growth inhibitor with possible autocrine and paracrine functions in breast cancer cells.
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              The Transforming Growth Factor-βs

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                Author and article information

                Journal
                Br J Cancer
                British Journal of Cancer
                0007-0920
                1532-1827
                24 January 2006
                30 January 2006
                : 94
                : 2
                : 239-246
                Affiliations
                [1 ]Assistance Publique-Hopitaux de Marseille, Laboratoire de Transfert en Oncologie Biologique, Faculté de Médecine Secteur Nord, 13916 Marseille Cedex 20, France
                [2 ]INSERM EMI 0359, Laboratoire de Cancérologie Expérimentale, IFR Jean-Roche, Faculté de Médecine Secteur Nord, Bd Pierre Dramard, 13916 Marseille Cedex 20, France
                Author notes
                [* ]Author for correspondence: berthois.y@ 123456jean-roche.univ-mrs.fr
                [3]

                CG was supported by fellowship from ‘Association pour la Recherche contre le Cancer' and ‘Ligue Nationale contre le Cancer'.

                Article
                6602920
                10.1038/sj.bjc.6602920
                2361106
                16404434
                dd15d318-286d-4ffc-aa2b-2e3296ba1eb6
                Copyright 2006, Cancer Research UK
                History
                : 26 July 2005
                : 02 November 2005
                : 25 November 2005
                Categories
                Clinical Studies

                Oncology & Radiotherapy
                transforming growth factor-beta1,survival,breast cancer
                Oncology & Radiotherapy
                transforming growth factor-beta1, survival, breast cancer

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