{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["de Sauvage MA"],"funding":["Terry and Jean de Gunzburg MGH Research Scholar Award","Breast Cancer Research Foundation","NCI NIH HHS","National Institutes of Health","NIH HHS","Demetra Fund of the Hellenic Women’s Association"],"pagination":["889-901"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11066918"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(5)"],"pubmed_abstract":["Background
Immune checkpoint inhibitors (ICI) have revolutionized cancer treatment; however, only a subset of patients with brain metastasis (BM) respond to ICI. Activating mutations in the mitogen-activated protein kinase signaling pathway are frequent in BM. The objective of this study was to evaluate whether therapeutic inhibition of extracellular signal-regulated kinase (ERK) can improve the efficacy of ICI for BM.Methods
We used immunotypical mouse models of BM bearing dual extracranial/intracranial tumors to evaluate the efficacy of single-agent and dual-agent treatment with selective ERK inhibitor LY3214996 (LY321) and anti-programmed death receptor 1 (PD-1) antibody. We verified target inhibition and drug delivery, then investigated treatment effects on T-cell respo"],"journal":["Neuro-oncology"],"pubmed_title":["The ERK inhibitor LY3214996 augments anti-PD-1 immunotherapy in preclinical mouse models of BRAFV600E melanoma brain metastasis."],"pmcid":["PMC11066918"],"funding_grant_id":["5R01CA227156-02","R01 CA227156","ELFF-17"],"pubmed_authors":["Batchelor E","de Sauvage MA","Yamazawa E","Torrini C","Sullivan E","Wakimoto H","Zhang BS","Nieblas-Bedolla E","Summers EJ","Marion B","Markson SC","Brastianos PK","Nayyar N"],"additional_accession":[]},"is_claimable":false,"name":"The ERK inhibitor LY3214996 augments anti-PD-1 immunotherapy in preclinical mouse models of BRAFV600E melanoma brain metastasis.","description":"Background
Immune checkpoint inhibitors (ICI) have revolutionized cancer treatment; however, only a subset of patients with brain metastasis (BM) respond to ICI. Activating mutations in the mitogen-activated protein kinase signaling pathway are frequent in BM. The objective of this study was to evaluate whether therapeutic inhibition of extracellular signal-regulated kinase (ERK) can improve the efficacy of ICI for BM.Methods
We used immunotypical mouse models of BM bearing dual extracranial/intracranial tumors to evaluate the efficacy of single-agent and dual-agent treatment with selective ERK inhibitor LY3214996 (LY321) and anti-programmed death receptor 1 (PD-1) antibody. We verified target inhibition and drug delivery, then investigated treatment effects on T-cell respo","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2025-04-04T01:46:07.073Z","creation":"2025-04-04T01:46:07.073Z"},"accession":"S-EPMC11066918","cross_references":{"pubmed":["38134951"],"doi":["10.1093/neuonc/noad248"]}}