Selected Articles from This Issue

Abstract

Highlights| April 01 2023 Selected Articles from This Issue Author & Article Information Online ISSN: 1557-3125 Print ISSN: 1541-7786 ©2023 American Association for Cancer Research2023American Association for Cancer Research Mol Cancer Res (2023) 21 (4): 291. https://doi.org/10.1158/1541-7786.MCR-21-4-HI Related Content A commentary has been published: Multi-substrate Metabolic Tracing Reveals Marked Heterogeneity and Dependency on Fatty Acid Metabolism in Human Prostate Cancer A commentary has been published: Targeting ULK1 Decreases IFNγ-Mediated Resistance to Immune Checkpoint Inhibitors A commentary has been published: Evolutionary Characteristics and Immunologic Divergence of Lung and Brain Metastasis Lesions in NSCLC View more A commentary has been published: Scaffolding Protein Connector Enhancer of Kinase Suppressor of Ras 1 (CNKSR1) Regulates MAPK Inhibition Responsiveness in Pancreas Cancer via Crosstalk with AKT Signaling View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record April 1 2023 Citation Selected Articles from This Issue. Mol Cancer Res 1 April 2023; 21 (4): 291. https://doi.org/10.1158/1541-7786.MCR-21-4-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search While metabolic reprogramming is an established hallmark of cancer, specific metabolic pathways that are altered in human prostate tumors — as well as the degree of heterogeneity to which they are altered among tumors — remain largely unsolved. In their study, Fidelito and colleagues performed radiometric and stable isotope tracing using serially transplantable patient-derived xenografts (PDXs) to define the metabolic landscape of human prostate tumors. The authors found that the PDXs oxidize diverse substrates including glucose, glutamine, lactate, and fatty acids, and to a greater degree than do benign prostate tissues. Isotope tracing revealed that prostate tumor cells tend to use glucose for acetyl-CoA production, and process glutamine via the tricarboxylic acid cycle. Notably, substrate utilization exhibited marked heterogeneity among samples, and, correspondingly, responses to pharmacologic inhibitors targeting diverse metabolic pathways varied among samples. However, adenocarcinoma, neuroendocrine, primary, and metastatic PDX-derived organoids all displayed dependencies on fatty acid uptake and... You do not currently have access to this content.