{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Quesnel-Vallieres M"],"funding":["BLRD VA","National Cancer Institute","NCI NIH HHS","National Institute of General Medical Sciences","U.S. Department of Veterans Affairs","NIGMS NIH HHS"],"pagination":["489-499"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11456044"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(3)"],"pubmed_abstract":["Background and objective
Acute myelogenous leukemia (AML) is a common blood cancer marked by heterogeneity in disease and diverse genetic abnormalities. Additional therapies are needed as the 5-year survival remains below 30%. Trametinib is a mitogen-activated extracellular signal-regulated kinase (MEK) inhibitor that is widely used in solid tumors and also in tumors with activating RAS mutations. A subset of patients with AML carry activating RAS mutations; however, a small-scale clinical trial with trametinib showed little efficacy. Here, we sought to identify transcriptomic determinants of trametinib sensitivity in AML.Methods
We tested the activity of trametinib against a panel of tumor cells from patients with AML ex vivo and compared this with RNA sequencing (RNA-Seq)"],"journal":["Drugs in R&D"],"pubmed_title":["Trametinib Sensitivity is Defined by a Myeloid Differentiation Profile in Acute Myeloid Leukemia."],"pmcid":["PMC11456044"],"funding_grant_id":["I01BX004662","I01 BX004662","R35 GM118048","U01 CA232563"],"pubmed_authors":["Cherry S","Quesnel-Vallieres M","Moore J","Barash Y","Schultz DC","Lynch KW","Carroll M","Orlenko A","Lo Y","Roth D","Ritchie M"],"additional_accession":[]},"is_claimable":false,"name":"Trametinib Sensitivity is Defined by a Myeloid Differentiation Profile in Acute Myeloid Leukemia.","description":"Background and objective
Acute myelogenous leukemia (AML) is a common blood cancer marked by heterogeneity in disease and diverse genetic abnormalities. Additional therapies are needed as the 5-year survival remains below 30%. Trametinib is a mitogen-activated extracellular signal-regulated kinase (MEK) inhibitor that is widely used in solid tumors and also in tumors with activating RAS mutations. A subset of patients with AML carry activating RAS mutations; however, a small-scale clinical trial with trametinib showed little efficacy. Here, we sought to identify transcriptomic determinants of trametinib sensitivity in AML.Methods
We tested the activity of trametinib against a panel of tumor cells from patients with AML ex vivo and compared this with RNA sequencing (RNA-Seq)","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-06-01T07:03:55.557Z","creation":"2025-04-04T01:53:33.876Z"},"accession":"S-EPMC11456044","cross_references":{"pubmed":["39316279"],"doi":["10.1007/s40268-024-00491-5"]}}