Browsing by Subject "P53 isoforms"

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    Expression of p53 and isoforms in beningn and malignant lesions of the head and neck
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Trovato, M.C.; Ruggeri, R.M.; Guzzo, E.; Certo, R.; Alibrandi, A.; Scifo, S.; Scardigno, M.; Vitarelli, E.; Arena, G.; Gambadoro, O.; Catalano, N.; Bourdon, J.C.; Galletti, B.; Galletti, F.; Cavallari, V.
    Background. P53, a crucial suppressor of tumor formation, generates multiple isoforms, whose role in disease is still being defined. Methods. By immunohistochemistry, we studied the expression of P53 protein and relative isoforms in benign papillomas (PA, n=9), inverted papilloma (IPA, n=10) and squamous cell carcinomas (SCC, n=21). Results. In all lesions, P53 isoforms were significantly more expressed than P53. Immunoexpression of P53 matched with P53 isoforms in IPA as well as in SCC. Simultaneous immunoexpression of P53 and related isoforms was double in SCC compared to IPA (10% vs 24%), while expression of P53 isoforms was strongly reduced (70% vs 43%). IPA showed the highest percentage of both reactive cases and immunostained cells expressing P53 isoforms. Conclusions. We found the higher expression of P53 isoforms in IPA and SCC compared to PA, suggesting their role in local aggressiveness and malignant proliferation in head-neck lesions.
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    Immunoreactions for P53 isoforms are associated with ultrastructural proliferative profiles in benign thyroid nodules
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Concetta Trovato, Maria; Ruggeri, Rosaria Maddalena; Scardigno, Marco; Sturniolo, Giacomo; Vita, Roberto; Vitarelli, Enrica; Arena, Grazia; Gambadoro, Orazio; Sturniolo, Giovanni; Trimarchi, Francesco; Benvenga, Salvatore; Bourdon, Jean-Christophe; Cavallari, Vittorio
    Background: P53 isoforms originate from the alternative initiation of P53 gene translation through usage of an internal promoter located in intron 4. All P53 isoforms are spliced in intron 9 and may modulate cell proliferation and cell fate outcome in response to DNA damage. Aim: To examine immunoexpression of P53 isoforms in benign proliferative lesions occurring in multinodular thyroids and to assess the ultrastructural phenotype of P53 distribution in the thyrocytes of those lesions by electron microscopy. Materials and Methods: By immunohistochemistry and transmission electron microscopy (TEM), we evaluated 38 multinodular thyroids containing a total of 102 benign lesions: 38 nodular goiters (NG; colloid=20, parenchymatous=18), 52 follicular adenomas (FA) and 12 Hashimoto’s thyroditis (HT). FA were classified into 10 normo-follicular, 9 macro-follicular, 28 microfollicular and 5 solid variants. Results: Immunoreaction for P53 isoforms was observed in approximately 50% of all lesions, except macrofollicular variant FA (33%). At TEM analysis, immunoreactive NG, FA and TH lesions showed signs of proliferation by simultaneous appearance of dispersed chromatin, increased amounts of cytoplasmic organelles and dilation of the rough endoplasmic reticulum. TEM signs of apoptosis and proliferation were also detected in FA, but with different rates compared to NG. Conclusion: The immunohistochemical expression of P53 isoforms in NG, FA and HT suggests their role in the development of these lesions. Ultrastructural findings support the hypothesis that P53 immunoexpression correlates with reactive proliferative changes in thyrocytes.