{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bartesaghi S"],"funding":["Associazione Italiana per la Ricerca sul Cancro","Brain Tumour Charity","Medical Research Council","The Brain Tumour Charity"],"pagination":["1059-64"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4313844"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["112(4)"],"pubmed_abstract":["Alterations of mitochondrial metabolism and genomic instability have been implicated in tumorigenesis in multiple tissues. High-grade glioma (HGG), one of the most lethal human neoplasms, displays genetic modifications of Krebs cycle components as well as electron transport chain (ETC) alterations. Furthermore, the p53 tumor suppressor, which has emerged as a key regulator of mitochondrial respiration at the expense of glycolysis, is genetically inactivated in a large proportion of HGG cases. Therefore, it is becoming evident that genetic modifications can affect cell metabolism in HGG; however, it is currently unclear whether mitochondrial metabolism alterations could vice versa promote genomic instability as a mechanism for neoplastic transformation. Here, we show that, in neural progeni"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Inhibition of oxidative metabolism leads to p53 genetic inactivation and transformation in neural stem cells."],"pmcid":["PMC4313844"],"funding_grant_id":["8/47","8/197","MC_U132670601","215","MC_U132674518"],"pubmed_authors":["Galavotti S","Martins LM","Henriquez NV","A D","Nicotera P","Capasso M","Graziano V","Brandner S","Karlsson A","Minieri V","Betts J","Bartesaghi S","De Laurenzi V","Saxena J","Salomoni P"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of oxidative metabolism leads to p53 genetic inactivation and transformation in neural stem cells.","description":"Alterations of mitochondrial metabolism and genomic instability have been implicated in tumorigenesis in multiple tissues. High-grade glioma (HGG), one of the most lethal human neoplasms, displays genetic modifications of Krebs cycle components as well as electron transport chain (ETC) alterations. Furthermore, the p53 tumor suppressor, which has emerged as a key regulator of mitochondrial respiration at the expense of glycolysis, is genetically inactivated in a large proportion of HGG cases. Therefore, it is becoming evident that genetic modifications can affect cell metabolism in HGG; however, it is currently unclear whether mitochondrial metabolism alterations could vice versa promote genomic instability as a mechanism for neoplastic transformation. Here, we show that, in neural progeni","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jan","modification":"2026-03-16T15:33:18.36Z","creation":"2019-03-27T01:44:26Z"},"accession":"S-EPMC4313844","cross_references":{"pubmed":["25583481"],"doi":["10.1073/pnas.1413165112"]}}