{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang W"],"funding":["National Institute of Allergy and Infectious Diseases","NIAID NIH HHS","U.S. Department of Defense","NCI NIH HHS"],"pagination":["754083"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8546266"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12"],"pubmed_abstract":["Myeloid-derived suppressor cells (MDSCs) are a hetero geneous group of cells, which can suppress the immune response, promote tumor progression and impair the efficacy of immunotherapies. Consequently, the pharmacological targeting of MDSC is emerging as a new immunotherapeutic strategy to stimulate the natural anti-tumor immune response and potentiate the efficacy of immunotherapies. Herein, we leveraged genetically modified models and a small molecule inhibitor to validate Calcium-Calmodulin Kinase Kinase 2 (CaMKK2) as a druggable target to control MDSC accumulation in tumor-bearing mice. The results indicated that deletion of CaMKK2 in the host attenuated the growth of engrafted tumor cells, and this phenomenon was associated with increased antitumor T cell response and decreased accumu"],"journal":["Frontiers in immunology"],"pubmed_title":["Calcium/Calmodulin Dependent Protein Kinase Kinase 2 Regulates the Expansion of Tumor-Induced Myeloid-Derived Suppressor Cells."],"pmcid":["PMC8546266"],"funding_grant_id":["R01 CA218442","U19 AI067798","CA140307"],"pubmed_authors":["Swann E","Racioppi L","Sundaramoorthy P","Berrong M","Kang Y","Lento W","Liu Y","Zou Y","Huang W","Jauhari S","Luz A","Chao N","Meyer JN"],"additional_accession":[]},"is_claimable":false,"name":"Calcium/Calmodulin Dependent Protein Kinase Kinase 2 Regulates the Expansion of Tumor-Induced Myeloid-Derived Suppressor Cells.","description":"Myeloid-derived suppressor cells (MDSCs) are a hetero geneous group of cells, which can suppress the immune response, promote tumor progression and impair the efficacy of immunotherapies. Consequently, the pharmacological targeting of MDSC is emerging as a new immunotherapeutic strategy to stimulate the natural anti-tumor immune response and potentiate the efficacy of immunotherapies. Herein, we leveraged genetically modified models and a small molecule inhibitor to validate Calcium-Calmodulin Kinase Kinase 2 (CaMKK2) as a druggable target to control MDSC accumulation in tumor-bearing mice. The results indicated that deletion of CaMKK2 in the host attenuated the growth of engrafted tumor cells, and this phenomenon was associated with increased antitumor T cell response and decreased accumu","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2025-05-18T12:08:33.931Z","creation":"2025-05-18T12:08:33.931Z"},"accession":"S-EPMC8546266","cross_references":{"pubmed":["34712241"],"doi":["10.3389/fimmu.2021.754083"]}}