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T Dettori

Publications and source records attributed to T Dettori.

5 recordsLinked to original sources

Comprehensive conventional and molecular cytogenetic characterization of B-CPAP, a human papillary thyroid carcinoma-derived cell line.

Cell lines derived from different thyroid tumor histotypes are useful for the in vitro study of both the phenotypic and genetic features of these cancers. Although karyotypic changes are known to be associated with thyroid lesions, the chromosome patterns of only a few cell lines have been published. Herein, we report an extensive conventional and molecular cytogenetic investigation of the human papillary thyroid carcinoma derived cell line B-CPAP. Morphological studies and expression of tumor markers in this cell line have been reported previously, but no detailed characterization on the origin of the chromosome markers is available. B-CPAP cells have a rather stable hypertriploid karyotype, with chromosome polysomies and structural chromosome abnormalities featuring whole chromosome arm imbalances. Chromosome banding revealed a main clone with nine chromosome markers, and fluorescence in situ hybridization (FISH) with whole chromosome paint (wcp), partial chromosome paint (pcp), and centromeric probes clarified their origin. The use of centromeric probes provided accurate refinement of the rearrangements classified as whole-arm translocations by banding and FISH with wcp probes. Both chromosomal and array-based comparative genomic hybridization experiments confirmed the cytogenetic characterization of this cell line. Moreover, the use of fluorescence immunophenotyping and interphase cytogenetics as a tool for the investigation of neoplasms (FICTION) technique, which simultaneously shows nuclear ploidy and cytoplasmic immunofluorescence, detailed the oncocytic feature of the cells. Intriguingly, despite their origin, they lack most of the features expressed in papillary thyroid tumor cells and have a chromosomal pattern reminiscent of that of a subgroup of oncocytic malignant thyroid tumors.

Carcinoma, Papillary↗

Lack of melatonin effect on hydrogen peroxide induced bronchoconstriction in isolated and perfused rat lung.

The effect of melatonin on hydrogen peroxide- induced broncho-and vasoconstriction was examined in vivo in the model of the isolated, perfused and ventilated lung. The administration of hydrogen peroxide (500 microM) to the perfusate caused a marked decrease in lung compliance, conductance and flow rate. The administration of melatonin (500 microM) to the perfusate 20 min before and during the hydroperoxide exposure did not cause any change in lung function. Exposure of lung microsomes to hydrogen peroxide (1-100 microM) did not induce any significant increase in malonaldehyde (MDA), an index of lipid peroxidation, and it was not affected by treatment with melatonin (500 microM). On the other hand, brain microsomes exposed to hydrogen peroxide (1-100 microM) give rise to increased levels of MDA, which were decreased by pre-treatment with melatonin (500 microM). The results suggest that melatonin may exert an antioxidant effect in conditions were lipid peroxidation is occurring. Its use may not be relevant in conditions where the mechanisms of the reactive oxygen species damage appears to be lipid peroxidation independent, such as the case of hydrogen peroxide induced broncho- and vasoconstriction.

Animals↗

A case of dermatofibrosarcoma protuberans of the vulva with a COL1A1/PDGFB fusion identical to a case of giant cell fibroblastoma.

Dermatofibrosarcoma protuberans (DFSP) is a highly recurrent low-grade soft tissue sarcoma, which is usually located on the trunk. Presentation in the vulva is rare, with only 13 cases being reported to date, none of which have been investigated at the cytogenetic or molecular level. Specific cytogenetic abnormalities, involving chromosomes 17 and 22, are characteristic features of DFSP and giant cell fibroblastoma (GCF), a tumor closely related to DFSP. These chromosomal rearrangements result in the fusion of the COL1A1 and PDGFB genes in both lesions and show wide variation in the position of the fusion point in COL1A1. Here, we describe a case of DFSP of the vulva with a typical monotonous storiform pattern, with no foci of multinucleated giant cells. Cytogenetic analysis showed a 47,XX,+r karyotype in 50% of the cells, and molecular investigation disclosed the presence of a transcript fusing COL1A1 exon 37 to PDGFB exon 2. This is the first case of DFSP showing such a fusion point, which is intriguingly identical to that found in a GCF case, indicating that the COL1A1/PDGFB fusion point position does not seem to affect tumor morphology. This finding further underlines the very close relationship between these two morphologically distinct entities.

Adult↗

Chromosomal changes in dysplastic nevi.

The dysplastic nevus is considered to be a precursor lesion of melanoma, representing one of the first steps in the progressive transformation from normal melanocyte to melanoma. Various risk degrees of developing cutaneous melanoma in patients with dysplastic nevi have been advanced, based on the presence of dysplastic nevi or melanoma or both in members of the patient's family. We report on the cytogenetic study of three nevi in a young patient with a family history of melanoma. Each nevus showed a simple clonal chromosome change. The t(6;15)(q13;q21) translocation found in one of them seems of particular significance in view of the fact that a similar one, with breakpoint at 6q13 was reported both in an acquired nevus from a patient with a family history of melanoma and in a case of cutaneous metastatic melanoma. These observations seem to support the hypothesis of the existence of a biological continuum between normal melanocyte and melanoma. Furthermore, the finding of chromosome changes similar to those associated with melanoma reinforces the need for a careful follow-up of patients with dysplastic nevi.

Adult↗

Involvement of capsaicin-sensitive nerves in paraquat-induced mortality.

Paraquat (PQ), a broad spectrum herbicide, produces severe lung inflammation and necrosis resulting in pulmonary fibrosis and respiratory failure. Tachykinins are peptides released by sensory C fibers and have the ability of influencing respiratory functions and cellular proliferation. To examine whether the damage caused by PQ involves tachykinins, rats were depleted in their content of tachykinins by systemic treatment with capsaicin prior to PQ exposure. The animal subjected to this treatment showed a 3-fold higher viability compared to those treated with PQ alone (75 vs 27%). Depletion of reduced glutathione (GSH) is associated with oxidative stress produced by reactive oxygen intermediates during PQ metabolism. This is considered to be critical in the pathogenesis of lung damage by PQ. PQ treatment induced a significant depletion of GSH during the first days and a similar effect was also observed in the group of capsaicin-pretreated rats. Four weeks after PQ treatment the levels of GSH were similar to controls in rat pretreated or not with capsaicin plus PQ. This may indicate that the reduced levels of GSH may be associated to the toxicity observed in the acute phase, but not of importance in the final PQ-induced mortality. Neutral endopeptidase (NEP) is an enzyme considered to be critical in controlling the levels of tachykinins. Exposure of crude membrane preparations of rat lung to PQ resulted in a dose-dependent inhibition of NEP activity. Since NEP inactivation may occur in lung following a PQ exposure in vivo, the results indicate that during PQ intoxication a more sustained activity of tachykinins may be present, producing effects such as cell proliferation, fluid extravasation and bronchoconstriction. In conclusion, this finding supports the hypothesis that neuropeptides released from capsaicin-sensitive nerves could be involved in the modulation of PQ-induced lung damage.

Animals↗