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Massimo Santoro

Researcher at University of Turin

Publications -  185
Citations -  15848

Massimo Santoro is an academic researcher from University of Turin. The author has contributed to research in topics: Thyroid carcinoma & Thyroid. The author has an hindex of 66, co-authored 173 publications receiving 14778 citations. Previous affiliations of Massimo Santoro include Flanders Institute for Biotechnology & University of Eastern Piedmont.

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Autocrine stimulation by osteopontin plays a pivotal role in the expression of the mitogenic and invasive phenotype of RET/PTC-transformed thyroid cells

TL;DR: It is shown that osteopontin (OPN), a secreted glycoprotein, is a major RET/PTC-induced transcriptional target in PC Cl 3 thyroid follicular cells and triggers an autocrine loop involving OPN and CD44 that sustains proliferation and invasion of transfomedPC Cl 3 thyrocytes.
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The receptor-type protein tyrosine phosphatase J antagonizes the biochemical and biological effects of RET-derived oncoproteins.

TL;DR: RET is identified as a novel substrate of PTPRJ andPTPRJ expression levels may affect tumor phenotype associated with RET/PTC1 and RET(C634R) mutants, and resistance to PTPRj may be part of the mechanism of RET oncogenic conversion secondary to the M918T mutation.
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Zebrafish as a model to explore cell metabolism

TL;DR: The most recent methods and studies on cell metabolism are summarized, which support the overall value for the zebrafish model system not only to study metabolism but also metabolic disease states.
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Mitogenic Effects of the Up-Regulation of Minichromosome Maintenance Proteins in Anaplastic Thyroid Carcinoma

TL;DR: MCM proteins are overexpressed in ATC and sustain the high proliferative capacity of ATC cells, suggesting that p53 knock-out contributes to MCM7 up-regulation in A TC.
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RET/PTC1 oncogene signaling in PC Cl 3 thyroid cells requires the small GTP-binding protein Rho.

TL;DR: It is concluded that Rho is implicated in the actin reorganization and cell survival mediated by the chimeric RET/PTC1 oncogene in thyroid epithelial cells, both phenotypes being cell type- andOncogene type-specific.