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MetabolomicsIFN-γ-driven iNOS induction in macrophages mediates CAR T cell resistance in B cell lymphoma
Chimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but subsets of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. To uncover tumor microenvironment (TME)-induced resistance mechanisms, we e...
2026-05-31 | MTBLS14634 | MetaboLights
MetabolomicsIFN-γ-driven iNOS induction in macrophages mediates CAR T cell resistance in B cell lymphoma (Glucose Tracer)
Chimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but subsets of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. To uncover tumor microenvironment (TME)-induced resistance mechanisms, we e...
2026-05-31 | MTBLS14641 | MetaboLights
MetabolomicsGREM1 Deficiency induced Bone Marrow Adipose Niche promotes B-cell Acute Lymphoblastic Leukemia Disease Progression
Relapse and disease progression are the primary causes of treatment failure and subsequent mortality in children B-cell acute lymphocytic leukemia (B-ALL). At diagnosis and during treatment, the bone marrow adipose microenvironment is commonly observed in pediatric leukemia. However, the relationshi...
2024-09-23 | MTBLS10103 | MetaboLights
MetabolomicsIFN-γ-driven iNOS induction in macrophages mediates CAR T cell resistance in B cell lymphoma (CAR-T Metabolites)
Chimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but subsets of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. To uncover tumor microenvironment (TME)-induced resistance mechanisms, we e...
2026-05-31 | MTBLS14640 | MetaboLights
MetabolomicsLimited nutrient availability in the tumor microenvironment renders pancreatic tumors sensitive to allosteric IDH1 inhibitors

Nutrient-deprived conditions in the tumor microenvironment (TME) restrain cancer cell viability due to increased free radicals and reduced energy production. In pancreatic cancer cells, a cytosolic metabolic enzyme, wild-type isocitrate dehydrogenase 1 (wtIDH1), enables the adaptation to these co...

2022-04-29 | MTBLS4722 | MetaboLights
MetabolomicsMulti-omic Molecular Characterization and Diagnostic Biomarkers for Occult Hepatitis B Infection and HBsAg-Positive Hepatitis B Infection

BACKGROUND: The pathological and physiological characteristics between HBsAg-positive HBV infection and occult hepatitis B infection (OBI) are currently unclear. This study aimed to explore the immune microenvironment in the peripheral circulation of OBI patients through integration of proteomic ...

2024-11-05 | MTBLS11406 | MetaboLights
MetabolomicsGDF15 hijacks B cells to fuel the lifeblood of tumor salvage pyrimidine synthesis
B cell-tumor crosstalk has emerged as a critical determinant of tumor progression; however, its role in metabolic reprogramming and therapeutic resistance remains poorly understood. Here, we uncover a metabolic feedback loop that drives resistance to dihydroorotate dehydrogenase (DHODH) inhibitors. ...
2026-09-27 | MTBLS15820 | MetaboLights
MetabolomicsObesogenic high-fat diet and MYC cooperate to promote lactate accumulation and tumor microenvironment remodeling in prostate cancer (Murine prostate assays)

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 and drive cancer could facilitate development...

2024-04-10 | MTBLS3317 | MetaboLights
MetabolomicsObesogenic high-fat diet and MYC cooperate to promote lactate accumulation and tumor microenvironment remodeling in prostate cancer (Murine serum assays)

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 and drive cancer could facilitate development...

2024-04-10 | MTBLS3316 | MetaboLights
MetabolomicsHif1α-Dependent Uncoupling Of Glycolysis Suppresses Tumor Cell Proliferation
Hypoxia-inducible factor-1α (HIF1α) attenuates mitochondrial activity while promoting glycolysis. Paradoxically, it remains unknown why lower glycolysis is compromised in human clear cell renal cell carcinomas (ccRCC), in which HIF1α acts a tumor suppressor by inhibiting cell autonomous proliferatio...
2024-03-15 | MTBLS8901 | MetaboLights
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