ArticleThe Journal of clinical investigation2020
Disrupting a converging metabolic target turns up the immunologic-heat in pancreatic tumors.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- Integrating multi-modal transcriptomics identifies cellular subtypes with distinct roles in PDAC progression.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Tumor microenvironment-responsive engineered hybrid nanomedicine for photodynamic-immunotherapy via multi-pronged amplification of reactive oxygen species.Nature communications · 2025Article
- The interaction between UBR7 and PRMT5 drives PDAC resistance to gemcitabine by regulating glycolysis and immune microenvironment.Cell death & disease · 2024Article
- HMGA1 induces FGF19 to drive pancreatic carcinogenesis and stroma formation.The Journal of clinical investigation · 2023Article
- Glucose metabolism and tumour microenvironment in pancreatic cancer: A key link in cancer progression.Frontiers in immunology · 2022Review
- Hypoxia-Driven Oncometabolite L-2HG Maintains Stemness-Differentiation Balance and Facilitates Immune Evasion in Pancreatic Cancer.Cancer research · 2021Article
- Bioinformatic Analysis of Correlation between Immune Infiltration and COVID-19 in Cancer Patients.International journal of biological sciences · 2020Article
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Abstract
Pancreatic ductal adenocarcinomas (PDACs) are classically immunologically cold tumors that have failed to demonstrate a significant response to immunotherapeutic strategies. This feature is attributed to both the immunosuppressive tumor microenvironment (TME) and limited immune cell access due to the surrounding stromal barrier, a histological hallmark of PDACs. In this issue of the JCI, Sharma et al. employ a broad glutamine antagonist, 6-diazo-5-oxo-l-norleucine (DON), to target a metabolic program that underlies both PDAC growth and hyaluronan production. Their findings describe an approach to converting the PDAC TME into a hot TME, thereby empowering immunotherapeutic strategies such as anti-PD1 therapy.
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