Matches in SemOpenAlex for { <https://semopenalex.org/work/W3025630022> ?p ?o ?g. }
- W3025630022 abstract "Abstract Polyploidization frequently precedes tumorigenesis but also occurs during normal development in several tissues. Hepatocyte ploidy is controlled by the PIDDosome during development and regeneration. The PIDDosome multi-protein complex is activated by supernumerary centrosomes to induce p53 and restrict proliferation of polyploid cells, otherwise prone for chromosomal instability. PIDDosome-deficiency in the liver results in drastically increased polyploidy. To investigate PIDDosome-induced p53-activation in the pathogenesis of liver cancer, we chemically induced hepatocellular carcinoma (HCC) in mice. Strikingly, PIDDosome-deficiency reduced tumor number and burden, despite the inability to activate p53 in polyploid cells. Liver tumors arise primarily from cells with low ploidy, indicating an intrinsic pro-tumorigenic effect of PIDDosome-mediated ploidy restriction. These data suggest that hyperpolyploidization caused by PIDDosome-deficiency protects from HCC. Moreover, high tumor cell density, as a surrogate marker of low ploidy, predicts of survival of HCC patients receiving liver transplantation. Together, we show that the PIDDosome is a potential therapeutic target to manipulate hepatocyte polyploidization for HCC prevention and tumor cell density serves as a novel prognostic marker for recurrence free survival in HCC patients." @default.
- W3025630022 created "2020-05-21" @default.
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- W3025630022 date "2020-05-14" @default.
- W3025630022 modified "2023-09-25" @default.
- W3025630022 title "PIDDosome-induced p53-activation for ploidy restriction facilitates hepatocarcinogenesis" @default.
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- W3025630022 doi "https://doi.org/10.1101/2020.05.13.092486" @default.
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