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Biomedical subjects

U Bigozzi

Publications and source records attributed to U Bigozzi.

31 records · Page 2Linked to original sources
PubMedDate not supplied

Hormonal studies in a male with a 47,XXX chromosome constitution: comparison with the hormonal pattern of a 46,XX male and patients with Klinefelter's syndrome.

Chromosome analysis in peripheral blood lymphocytes and skin fibroblasts of a 18 year old chromatin-positive man showed a 47,XXX karyotype. The following hormonal studies were performed: 1) FSH and LH response to GnRH; 2) hypothalamic-pituitary responsiveness to short-term testosterone administration; 3) plasma levels of testosterone, dihydrotestosterone, 17-hydroxyprogesterone, estradiol before and after hCG stimulation. Results were compared with similar studies performed in a 46,XX male and in a group of patients with Klinefelter's syndrome. Our data support the hypothesis that this rare cytogenetical disorder can be considered, from the endocrine point of view, as a variant of the Klinefelter's syndrome.

Adolescent↗
PubMedDate not supplied

In vitro bioeffects of the antiestrogen LY117018 on desmoid tumor and colon cancer cells.

BACKGROUND: Clinical and experimental evidence suggest that estrogen has a role in the natural history of desmoid tumor (DT) and colorectal carcinoma. METHODS: The biological effects of LY117018, a nonsteroidal antiestrogen benzothiophene derivative, were assessed on a human adenocarcinoma cell line (HCT8 cells), and on DT cells and colorectal cancer derived fibroblasts in primary culture. RESULTS: LY117018 inhibited cell proliferation and collagen type I synthesis in DT cells. The compound also reduced cell growth in HCT8 cells and colorectal cancer fibroblasts. Binding experiments revealed the presence of estrogen binding sites in DT cells and frozen tissues but LY117018 did not displace [3H]17 beta E2 binding to DT cells. CONCLUSIONS: Present results demonstrate that LY117018 inhibits epithelial and fibroblastic colon cancer cells proliferation and proliferation and differentiation of desmoid cells in vitro. The lack of displacement of [3H]17 beta E2 binding to desmoid cells by LY117018 suggests the existence of distinct LY117018 binding sites.

Adenocarcinoma↗