{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Boufaied N"],"funding":["Dana-Farber Cancer Institute","Canadian Institutes of Health Research (CIHR)","AIRC Foundation for Cancer Research","World Cancer Research Fund International","U.S. Department of Defense (DOD)","U.S. Department of Defense","Dana-Farber Cancer Institute (DFCI)","World Cancer Research Fund International (WCRF)","Canadian Institutes of Health Research"],"pagination":["1834-1855"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11148549"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["84(11)"],"pubmed_abstract":["Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation of metabolites that reprogram the tumor microenvironment (TME) and drive cancer could facilitate development of precision nutrition approaches. Using the Hi-MYC prostate cancer mouse model, we demonstrated that an obesogenic high-fat diet (HFD) rich in saturated fats accelerates the development of c-MYC-driven invasive prostate cancer through metabolic rewiring. Although c-MYC modulated key metabolic pathways, interaction with an obesogenic HFD was necessary to induce glycolysis and lactate accumulation in tumors. These metabolic changes were associated with augmented infiltration of CD206+ and PD-"],"journal":["Cancer research"],"pubmed_title":["Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer."],"pmcid":["PMC11148549"],"funding_grant_id":["PJT-180368","PC150263","IIG_FULL_2022_020","IG-21966","PJT-162246","Claudia Adams Barr Award in Innovative Basic Cancer Research"],"pubmed_authors":["Hallal T","Cacciatore S","Sabbioneda S","Boufaied N","Zhao X","Liu Y","Homsy K","Labbe DP","Luthold C","Maga G","Lalli D","Imada EL","Spratt DE","Michelotti G","Bordeleau F","Nguyen QD","Davicioni E","Butler LM","Giunchi F","Ellis L","Storaci AM","de Polo A","Photopoulos C","Di Matteo A","Mucci LA","Ghigna C","Syamala S","Huang Y","Loda M","Chetta P","Sheridan PA","Marchionni L","Vaira V","Zadra G"],"additional_accession":[]},"is_claimable":false,"name":"Obesogenic High-Fat Diet and MYC Cooperate to Promote Lactate Accumulation and Tumor Microenvironment Remodeling in Prostate Cancer.","description":"Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation of metabolites that reprogram the tumor microenvironment (TME) and drive cancer could facilitate development of precision nutrition approaches. Using the Hi-MYC prostate cancer mouse model, we demonstrated that an obesogenic high-fat diet (HFD) rich in saturated fats accelerates the development of c-MYC-driven invasive prostate cancer through metabolic rewiring. Although c-MYC modulated key metabolic pathways, interaction with an obesogenic HFD was necessary to induce glycolysis and lactate accumulation in tumors. These metabolic changes were associated with augmented infiltration of CD206+ and PD-","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-06-02T09:01:34.681Z","creation":"2026-04-16T03:13:13.241Z"},"accession":"S-EPMC11148549","cross_references":{"pubmed":["38831751"],"doi":["10.1158/0008-5472.CAN-23-0519"]}}