{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Briest F"],"funding":["Deutsche Forschungsgemeinschaft"],"pagination":["80-98"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7701025"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["Background
Well-differentiated gastroenteropancreatic neuroendocrine neoplasms are rare tumors with a slow proliferation. They are virtually resistant to many DNA-damaging therapeutic approaches, such as chemo- and external beam therapy, which might be overcome by DNA damage inhibition induced by proteasome inhibitors such as bortezomib.Methods and results
In this study, we assessed several combined treatment modalities in vitro and in vivo. By cell-based functional analyses, in a 3D in ovo and an orthotopic mouse model, we demonstrated sensitizing effects of bortezomib combined with cisplatin, radiation and peptide receptor radionuclide therapy (PRRT). By gene expression profiling and western blot, we explored the underlying mechanisms, which resulted in an impaired DNA da"],"journal":["Neoplasia (New York, N.Y.)"],"pubmed_title":["Does the proteasome inhibitor bortezomib sensitize to DNA-damaging therapy in gastroenteropancreatic neuroendocrine neoplasms? - A preclinical assessment in vitro and in vivo."],"pmcid":["PMC7701025"],"funding_grant_id":["335/454-1FUGG"],"pubmed_authors":["Sedding D","Baum RP","Grabowski P","Schmidt F","Bernsen MR","Hartung T","Exner S","Brenner W","Grotzinger C","Fischer C","Albrecht J","Briest F","Kuhl AA","Haeck J","Welzel M","Koziolek EJ"],"additional_accession":[]},"is_claimable":false,"name":"Does the proteasome inhibitor bortezomib sensitize to DNA-damaging therapy in gastroenteropancreatic neuroendocrine neoplasms? - A preclinical assessment in vitro and in vivo.","description":"Background
Well-differentiated gastroenteropancreatic neuroendocrine neoplasms are rare tumors with a slow proliferation. They are virtually resistant to many DNA-damaging therapeutic approaches, such as chemo- and external beam therapy, which might be overcome by DNA damage inhibition induced by proteasome inhibitors such as bortezomib.Methods and results
In this study, we assessed several combined treatment modalities in vitro and in vivo. By cell-based functional analyses, in a 3D in ovo and an orthotopic mouse model, we demonstrated sensitizing effects of bortezomib combined with cisplatin, radiation and peptide receptor radionuclide therapy (PRRT). By gene expression profiling and western blot, we explored the underlying mechanisms, which resulted in an impaired DNA da","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jan","modification":"2026-05-04T03:44:24.873Z","creation":"2021-02-20T09:58:56Z"},"accession":"S-EPMC7701025","cross_references":{"pubmed":["33246310"],"doi":["10.1016/j.neo.2020.11.004"]}}