Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P283

ECE2007 Poster Presentations (1) (659 abstracts)

In vitro effects of 17 βE2 and raloxifene on desmoid tumour derived cells

Lucia Picariello 1 , Silvia Carbonell Sala 2 , Valentina Martineti 2 , Alessia Gozzini 2 , Maria Luisa Brandi 2 & Francesco Tonelli 1

1Department of Clinical Physiopathology - University of Florence, Florence, Italy; 2Department of Internal Medicine - University of Florence, Florence, Italy.

Desmoid tumours (DT) are a benign manifestation of familial adenomatous polyposis. The prevalent development in young fertile women, the regression during menopause or with tamoxifen treatment, underlie the potential role of estrogens and Estrogen Receptors (ERs) in the pathogenesis of these tumors. To investigate this hypothesis, the expression of ERs α and β in desmoid tumors derived cell cultures, the effects of 17βE2 and of raloxifene on DT cell proliferation has been evaluated ‘in vitro’.

Primary cultures from DT tissues obtained from seven patients were developed. RT-PCR and Western blotting analysis revealed that all the cultures expressed ERs α and β. In addition, also the RT-PCR and immunohystochemical analysis on the correspondent tissue samples confirmed the presence of ERs in these tumours. Treatment with 17βE2 (10−12 to 10−6 M) induced a dose-dependent cell growth, 10−9 M significantly increasing (120% to 250%) cell proliferation of the cell cultures. Raloxifene (10−7 to 5×10−6 M) reduced cell growth in a dose-dependent manner, with 5×10−6 M dose always significantly reducing both cell number (20% to 90%), without affecting apoptosis, as shown by DNA ladder assay. When 17βE2 and raloxifene effects were evaluated either alone or in combination, raloxifene was capable to significantly reduce (from 40% to 80%) the proliferative effects of 17βE2.

Although the study was made on a few samples these preliminary results showed that the different effects of 17βE2 and raloxifene on cell proliferation were probably linked to a different expression of ERα or Erβ in these cells.

These findings support on estrogenic role in the control of DT proliferation providing evidence for raloxifene effect on ‘in vitro’ DT cell growth and viability. All together the ‘in vitro’ and the previous ‘in vivo’ studies encourage future investigation into a possible role of this SERM in the prevention and/or treatment of DT.

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