{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Koomen DC"],"funding":["National Institute of Diabetes and Digestive and Kidney Diseases","NIDDK NIH HHS","Pentecost Personalized Medicine Foundation","Moffitt Cancer Center","National Cancer Institute","NCI NIH HHS"],"pagination":["3134-3149"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11636643"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(6)"],"pubmed_abstract":["Multiple myeloma is an incurable hematological malignancy that impacts tens of thousands of people every year in the United States. Treatment for eligible patients involves induction, consolidation with stem cell rescue, and maintenance. High-dose therapy with a DNA alkylating agent, melphalan, remains the primary drug for consolidation therapy in conjunction with autologous stem-cell transplantation; as such, melphalan resistance remains a relevant clinical challenge. Here, we describe a proteometabolomic approach to examine mechanisms of acquired melphalan resistance in two cell line models. Drug metabolism, steady-state metabolomics, activity-based protein profiling (ABPP, data available at PRIDE: PXD019725), acute-treatment metabolomics, and western blot analyses have allowed us to fur"],"journal":["Journal of proteome research"],"pubmed_title":["Metabolic Changes Are Associated with Melphalan Resistance in Multiple Myeloma."],"pmcid":["PMC11636643"],"funding_grant_id":["U24 DK097209","P30-CA076292","U24-DK097209","P30 CA076292"],"pubmed_authors":["Garrett TJ","Welsh EA","De Avila G","Liu M","Shain KH","Oliveira PS","Fang B","Hampton OA","Meke LE","Magaletti DM","Tungesvik A","Koomen DC","Jiang Z","Guingab-Cagmat JD","Meads MB","Nishihori T","Eschrich SA","Alugubelli RR","Silva AS","Koomen JM"],"additional_accession":[]},"is_claimable":false,"name":"Metabolic Changes Are Associated with Melphalan Resistance in Multiple Myeloma.","description":"Multiple myeloma is an incurable hematological malignancy that impacts tens of thousands of people every year in the United States. Treatment for eligible patients involves induction, consolidation with stem cell rescue, and maintenance. High-dose therapy with a DNA alkylating agent, melphalan, remains the primary drug for consolidation therapy in conjunction with autologous stem-cell transplantation; as such, melphalan resistance remains a relevant clinical challenge. Here, we describe a proteometabolomic approach to examine mechanisms of acquired melphalan resistance in two cell line models. Drug metabolism, steady-state metabolomics, activity-based protein profiling (ABPP, data available at PRIDE: PXD019725), acute-treatment metabolomics, and western blot analyses have allowed us to fur","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-06-01T17:36:50.818Z","creation":"2025-04-06T00:34:23.436Z"},"accession":"S-EPMC11636643","cross_references":{"pubmed":["34014671"],"doi":["10.1021/acs.jproteome.1c00022"]}}