2025
Mitochondrial succinate feeds T cell exhaustion in cancer
Galluzzi L, Guilbaud E, Garg A. Mitochondrial succinate feeds T cell exhaustion in cancer. Cancer Cell 2025, 43: 168-170. PMID: 39933894, DOI: 10.1016/j.ccell.2025.01.005.Peer-Reviewed Original Research
2023
Abstract B009: Isolating human RCC tumor cells details evolutionary relationships between cancer cell subsets and a role of OXPHOS in disease progression
Sobierajska E, Medina C, Gregorova P, Vo B, Greenwald R, Jansen C, Larsen C, Master V, Kissick H. Abstract B009: Isolating human RCC tumor cells details evolutionary relationships between cancer cell subsets and a role of OXPHOS in disease progression. Cancer Research 2023, 83: b009-b009. DOI: 10.1158/1538-7445.kidney23-b009.Peer-Reviewed Original ResearchOxidative phosphorylationEvolutionary relationshipsRNA-seqCancer cellsCancer cell subsetsRCC tumor cellsWhole-genome sequencingMutation detection sensitivityDisease progressionUnique to cancer cellsKidney cancer cellsCell differentiation pathsIncreased oxidative phosphorylationCell subsetsEpithelial to mesenchymal transitionGenome sequenceIncreased proliferative stateTumor cellsTumor tissuesScRNA-seqOxidative metabolismAssociated with disease recurrenceCD8 T cell numbersMitochondrial potentialMitochondrial fitness
2022
OXPHOS promotes apoptotic resistance and cellular persistence in TH17 cells in the periphery and tumor microenvironment
Hong H, Mbah N, Shan M, Loesel K, Lin L, Sajjakulnukit P, Correa L, Andren A, Lin J, Hayashi A, Magnuson B, Chen J, Li Z, Xie Y, Zhang L, Goldstein D, Carty S, Lei Y, Opipari A, Argüello R, Kryczek I, Kamada N, Zou W, Franchi L, Lyssiotis C. OXPHOS promotes apoptotic resistance and cellular persistence in TH17 cells in the periphery and tumor microenvironment. Science Immunology 2022, 7: eabm8182. PMID: 36399539, PMCID: PMC9853437, DOI: 10.1126/sciimmunol.abm8182.Peer-Reviewed Original ResearchConceptsOxidative phosphorylationBcl-xLApoptotic resistanceIncreased mitochondrial fitnessTargeting oxidative phosphorylationMediators of host defenseMitochondrial oxidative phosphorylationTumor microenvironmentOxidative phosphorylation conditionsAdoptive T cell therapyFunction in vivoImmune responseMurine model of melanomaEffector function in vivoGlutamine anaplerosisOPA-1T-cell therapyCell fateCD4 T cellsImpaired effector functionsAdoptive transfer experimentsMitochondrial fitnessCellular persistenceModel of melanomaT cell proliferationMitochondrial fitness and cancer risk
Kossenkov AV, Milcarek A, Notta F, Jang GH, Wilson JM, Gallinger S, Zhou DC, Ding L, Ghosh JC, Perego M, Morotti A, Locatelli M, Robert ME, Vaira V, Altieri DC. Mitochondrial fitness and cancer risk. PLOS ONE 2022, 17: e0273520. PMID: 36223343, PMCID: PMC9555630, DOI: 10.1371/journal.pone.0273520.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaSenescence-associated secretory phenotypeIndependent patient cohortsPoor patient outcomesAggressive disease variantFolfirinox failureLocal inflammationPatient cohortDuctal adenocarcinomaPatient outcomesPatient riskMultiple malignanciesCancer riskMitochondrial fitnessSecretory phenotypeGene signatureHallmarks of cancerMetastatic propensityNormal tissuesHuman tumorsInterferon SignalingTumorsInner membrane mitochondrial proteinMalignancyMolecular signatures
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