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    Transforming growth factor beta 1 (TGF-beta 1) expression in proliferating thyroid disease

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    In order to clarify some of the molecular mechanisms involved in the pathogenesis of thyroid proliferating diseases we have investigated the role of TGF-beta in thyroid carcinoma, adenoma and multinodular goiter. TGF-beta 1 expression studies were carried out in surgically removed thyroid tissue isolated from 15 patients affected by multinodular goiter, 4 patients affected by papillary carcinoma and 4 patients affected by follicular adenoma. TGF-beta 1 gene expression, evaluated by Northern analysis, dramatically increased in malignant proliferating thyroid disease and decreased drasticly in multinodular goiter patients with respect to normal thyroid. Immunocytochemical analysis demonstrated that TGF-beta 1 is produced by an autocrine mechanism in the carcinoma and in the benign thyroid disease (multinodular goiter), whereas TGF-beta seems to be produced in adenoma tissues in both an autocrine and a paracrine fashion. This feature further supports the hypothesis that TGF-beta may contribute to regulation of thyrocyte growth and differentiation

    Transforming growth factor-beta1 and insulin growth factor-1 expression in ovarian endometriotic cysts: a preliminary study

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    Increased concentrations of TGF-beta1 in endometriotic tissue are considered important in the pathophysiology of endometrial diseases since TGF-beta1 may inhibit natural killer activity and induce angiogenesis and proliferation of endometrial stromal cells. In the present study we report on TGF-beta1, IGF-I and their receptor localization, as detected by Northern hybridization and immunohistochemistry, in ovarian endometriotic tissues removed during surgical procedures. We detected comparable expression of IGF-1 and IGF-1 receptor in the stromal and epithelial compartments, thus confirming disregulated expression of the IGF system in ovarian endometriosis. On the contrary, strongly increased TGF-beta1 steady state level mRNA expression was detected in all endometriotic samples. In addition, we demonstrated weak TGF-beta1 immunohistochemical expression in the epithelial lining and intense expression in the cellular stroma of ovarian endometriomas, thus suggesting that TGF-beta1 could have an important role in the maintenance and propagation of the disease. On the basis of these preliminary results we can assume that TGF-beta1, IGF-1 and their receptors may play an important role in the pathogenesis of endometriosis

    TGF-beta1 and IGF-1 expression are differently regulated by serum in metastatic and non-metastatic human breast cancer cells.

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    Transforming growth factor-beta (TGF-beta) exerts an inhibitory effect on epithelial cell proliferation while insulin-like growth factor-1 (IGF-1) is a positive regulator of proliferation and together they may participate in driving neoplastic progression. The regulation of TGF-beta1 and IGF-1 gene expression was analyzed in an in vitro model of an estrogen receptor positive (ER+), non-metastatic (MCF-7) and an (ER-), metastatic (MDA-MB-435) breast cancer cell line, respectively. Our results indicate a loss of the regulation of TGF-beta1 and the gain of the expression and upregulation of IGF-1 pathways during malignant progression. These data demonstrate that two factors, convergent on cell growth, can have divergent roles in the regulation of the expression of TGF-beta1

    Transforming growth factor-beta(1) in hemangioma of the ovary

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    Hemangioma of the ovary is extremely rare. We report the case of a 32-year-old woman who complained of pelvic pain due to a large right adnexal mass. On surgical exploration a 10 x 8 cm hemangioma of the ovary was resected. Expression of transforming growth factor-beta(1) was studied, and the possible role of this molecule in the development of the tumor is discussed
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