Immunoreactions for P53 isoforms are associated with ultrastructural proliferative profiles in benign thyroid nodules

Maria Concetta Trovato (Lead / Corresponding author), Rosaria Maddalena Ruggeri (Lead / Corresponding author), Marco Scardigno, Giacomo Sturniolo, Roberto Vita, Enrica Vitarelli, Grazia Arena, Orazio Gambadoro, Giovanni Sturniolo, Francesco Trimarchi, Salvatore Benvenga, Jean-Christophe Bourdon, Vittorio Cavallari

    Research output: Contribution to journalArticlepeer-review

    2 Citations (Scopus)


    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 micro-follicular 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.

    Original languageEnglish
    Article number11736
    Pages (from-to)1079-1087
    Number of pages9
    JournalHistology and Histopathology
    Issue number10
    Publication statusPublished - Oct 2016


    • p53 isoforms
    • p53
    • Immunohistochemistry
    • Transmission electron microscopy
    • Ultrastructure
    • Apoptotic subcellular phenotypes
    • Proliferating subcellular profiles


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