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Suri, C.* ; Pande, B.* ; Sahithi, L.S.* ; Swarnkar, S.* ; Khelkar, T.* ; Verma, H.K.

Metabolic crossroads: Unravelling immune cell dynamics in gastrointestinal cancer drug resistance.

Cancer Drug Resist. 8:27 (2025)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Metabolic reprogramming within the tumor microenvironment (TME) plays a critical role in driving drug resistance in gastrointestinal cancers (GI), particularly through the pathways of fatty acid oxidation and glycolysis. Cancer cells often rewire their metabolism to sustain growth and reshape the TME, creating conditions such as nutrient depletion, hypoxia, and acidity that impair antitumor immune responses. Immune cells within the TME also undergo metabolic alterations, frequently adopting immunosuppressive phenotypes that promote tumor progression and reduce the efficacy of therapies. The competition for essential nutrients, particularly glucose, between cancer and immune cells compromises the antitumor functions of effector immune cells, such as T cells. Additionally, metabolic by-products like lactate and kynurenine further suppress immune activity and promote immunosuppressive populations, including regulatory T cells and M2 macrophages. Targeting metabolic pathways such as fatty acid oxidation and glycolysis presents new opportunities to overcome drug resistance and improve therapeutic outcomes in GI cancers. Modulating these key pathways has the potential to reinvigorate exhausted immune cells, shift immunosuppressive cells toward antitumor phenotypes, and enhance the effectiveness of immunotherapies and other treatments. Future strategies will require continued research into TME metabolism, the development of novel metabolic inhibitors, and clinical trials evaluating combination therapies. Identifying and validating metabolic biomarkers will also be crucial for patient stratification and treatment monitoring. Insights into metabolic reprogramming in GI cancers may have broader implications across multiple cancer types, offering new avenues for improving cancer treatment.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Gastrointestinal cancers; immune cells; tumor microenvironment; metabolic pathways; drug resistance; Tumor Microenvironment; Suppressor-cells; Glutamine-metabolism; Gastric-cancer; Mechanisms; 5-fluorouracil; Chemotherapy; Strategies; Inhibitor; Efficacy
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 2578-532X
e-ISSN 2578-532X
Zeitschrift Cancer Drug Resistance
Quellenangaben Band: 8, Heft: , Seiten: , Artikelnummer: 27 Supplement: ,
Verlag OAE Publishing Inc.
Verlagsort 245 E Main St, St122, Alhambra, Ca 91801 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Health and Immunity (LHI)
POF Topic(s) 80000 - German Center for Lung Research
Forschungsfeld(er) Lung Research
PSP-Element(e) G-501810-007
DOI 10.20517/cdr.2024.164
WOS ID 001421103800001
Scopus ID 105013570327
Scopus ID 105004398658
PubMed ID 40051496
Erfassungsdatum 2025-04-28
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