{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fiascarelli A"],"funding":["Regione Lazio","NCI NIH HHS"],"pagination":["13-23"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10147754"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["199(1)"],"pubmed_abstract":["<h4>Purpose</h4>Dysregulation of the PI3K pathway is one of the most common events in breast cancer. Here we investigate the activity of the PI3K inhibitor MEN1611 at both molecular and phenotypic levels by dissecting and comparing its profile and efficacy in HER2 + breast cancer models with other PI3K inhibitors.<h4>Methods</h4>Models with different genetic backgrounds were used to investigate the pharmacological profile of MEN1611 against other PI3K inhibitors. In vitro studies evaluated cell viability, PI3K signaling, and cell death upon treatment with MEN1611. In vivo efficacy of the compound was investigated in cell line- and patient-derived xenografts models.<h4>Results</h4>Consistent with its biochemical selectivity, MEN1611 demonstrated lower cytotoxic activity in a p110δ-driven ce"],"journal":["Breast cancer research and treatment"],"pubmed_title":["Antitumor activity of the PI3K δ-sparing inhibitor MEN1611 in PIK3CA mutated, trastuzumab-resistant HER2 + breast cancer."],"pmcid":["PMC10147754"],"funding_grant_id":["P30 CA008748"],"pubmed_authors":["Scaltriti M","Irrissuto C","Carrisi C","Merlino G","Fiascarelli A","Binaschi M","Bellarosa D","de Stanchina E","Salerno M","Bigioni M","Bisignano D","Tunici P","Talucci S","Capano S","Arribas J","Paoli A","Bressan A"],"additional_accession":[]},"is_claimable":false,"name":"Antitumor activity of the PI3K δ-sparing inhibitor MEN1611 in PIK3CA mutated, trastuzumab-resistant HER2 + breast cancer.","description":"<h4>Purpose</h4>Dysregulation of the PI3K pathway is one of the most common events in breast cancer. Here we investigate the activity of the PI3K inhibitor MEN1611 at both molecular and phenotypic levels by dissecting and comparing its profile and efficacy in HER2 + breast cancer models with other PI3K inhibitors.<h4>Methods</h4>Models with different genetic backgrounds were used to investigate the pharmacological profile of MEN1611 against other PI3K inhibitors. In vitro studies evaluated cell viability, PI3K signaling, and cell death upon treatment with MEN1611. In vivo efficacy of the compound was investigated in cell line- and patient-derived xenografts models.<h4>Results</h4>Consistent with its biochemical selectivity, MEN1611 demonstrated lower cytotoxic activity in a p110δ-driven ce","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2026-05-28T16:49:59.368Z","creation":"2025-02-19T02:56:24.368Z"},"accession":"S-EPMC10147754","cross_references":{"pubmed":["36913051"],"doi":["10.1007/s10549-023-06895-2"]}}