{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9(9)"],"submitter":["Petroni M"],"pubmed_abstract":["MRE11 is a component of the MRE11/RAD50/NBS1 (MRN) complex, whose activity is essential to control faithful DNA replication and to prevent accumulation of deleterious DNA double-strand breaks. In humans, hypomorphic mutations in these genes lead to DNA damage response (DDR)-defective and cancer-prone syndromes. Moreover, MRN complex dysfunction dramatically affects the nervous system, where MRE11 is required to restrain MYCN-dependent replication stress, during the rapid expansion of progenitor cells. MYCN activation, often due to genetic amplification, represents the driving oncogenic event for a number of human tumors, conferring bad prognosis and predicting very poor responses even to the most aggressive therapeutic protocols. This is prototypically exemplified by neuroblastoma, where M"],"journal":["Cell death & disease"],"pagination":["895"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6117286"],"repository":["biostudies-literature"],"pubmed_title":["MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumors."],"pmcid":["PMC6117286"],"pubmed_authors":["Petroni M","Cardinali B","Bartolazzi A","Infante P","Petricci E","Sardina F","Locatelli E","Sahun Roncero M","Di Marcotullio L","Soddu S","Giannini G","Di Giulio S","Capalbo C","Belardinilli F","Comes Franchini M","Fabretti F","Coppa A","Tessitore A","Colicchia V","Gulino A"],"additional_accession":[]},"is_claimable":false,"name":"MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumors.","description":"MRE11 is a component of the MRE11/RAD50/NBS1 (MRN) complex, whose activity is essential to control faithful DNA replication and to prevent accumulation of deleterious DNA double-strand breaks. In humans, hypomorphic mutations in these genes lead to DNA damage response (DDR)-defective and cancer-prone syndromes. Moreover, MRN complex dysfunction dramatically affects the nervous system, where MRE11 is required to restrain MYCN-dependent replication stress, during the rapid expansion of progenitor cells. MYCN activation, often due to genetic amplification, represents the driving oncogenic event for a number of human tumors, conferring bad prognosis and predicting very poor responses even to the most aggressive therapeutic protocols. This is prototypically exemplified by neuroblastoma, where M","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Aug","modification":"2025-04-04T23:34:51.11Z","creation":"2019-03-26T23:54:10Z"},"accession":"S-EPMC6117286","cross_references":{"pubmed":["30166519"],"doi":["10.1038/s41419-018-0924-z"]}}