2025
MIF as an oncogenic driver of low‐heterogeneity melanomas
Tran T, Sánchez‐Zuno G, Kulkarni R, Kluger H, Bucala R. MIF as an oncogenic driver of low‐heterogeneity melanomas. Molecular Oncology 2025, 19: 1295-1298. PMID: 40131169, PMCID: PMC12077282, DOI: 10.1002/1878-0261.70031.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorImproving therapeutic outcomesMigration inhibitory factorPotential therapeutic utilityImmune landscapeMelanoma clonesImmune escapeT cellsImmunoregulatory cytokinesTumor heterogeneityTumor progressionOncogenic driversPathway inhibitorTherapeutic outcomesTumor evolutionInhibitory factorCell proliferationMelanomaTumorCellsAntagonistCytokinesT cell exhaustion: early or late in tumour progression?
Galluzzi L. T cell exhaustion: early or late in tumour progression? Nature Reviews Immunology 2025, 1-2. PMID: 40038448, DOI: 10.1038/s41577-025-01158-1.Peer-Reviewed Original ResearchThe Central Vein Sign as a Radiologic Tool to Predict the Diagnosis of Radiation Necrosis in Intracranial Metastatic Cancer Patients
Antonios J, Adenu-Mensah N, Theriault B, Millares-Chavez M, Huttner A, Aboian M, Chiang V. The Central Vein Sign as a Radiologic Tool to Predict the Diagnosis of Radiation Necrosis in Intracranial Metastatic Cancer Patients. Clinical And Translational Neuroscience 2025, 9: 10. DOI: 10.3390/ctn9010010.Peer-Reviewed Original ResearchCentral vein signRadiation necrosisTumor progressionDiagnosis of radiation necrosisDifferentiate RNCerebral radiation necrosisIntracranial metastatic diseaseCancer therapy responseMetastatic cancer patientsNon-invasive markerMetastatic diseaseSurgical biopsyTherapy responsePredictive markerPatient cohortPrimary treatmentRadiological toolsCancer patientsRadiological imagingTreatment decisionsPerivascular spacesPatientsTreatmentNecrosisMarkersOlaparib in treatment‐refractory isocitrate dehydrogenase 1 (IDH1)– and IDH2‐mutant cholangiocarcinoma: Safety and antitumor activity from the phase 2 National Cancer Institute 10129 trial
Cecchini M, Pilat M, Uboha N, Azad N, Cho M, Davis E, Ahnert J, Tinoco G, Shapiro G, Khagi S, Powers B, Spencer K, Groisberg R, Drappatz J, Chen L, Das B, Bao X, Li J, Narayan A, Vu D, Patel A, Niger M, Doroshow D, Durecki D, Boerner S, Bindra R, Ivy P, Shyr D, Shyr Y, LoRusso P. Olaparib in treatment‐refractory isocitrate dehydrogenase 1 (IDH1)– and IDH2‐mutant cholangiocarcinoma: Safety and antitumor activity from the phase 2 National Cancer Institute 10129 trial. Cancer 2025, 131: e35755. PMID: 39917990, DOI: 10.1002/cncr.35755.Peer-Reviewed Original ResearchConceptsProgression-free survivalHomologous recombination deficiencyClinical benefitNational Cancer InstituteIDH inhibitorsMedian progression-free survivalAccumulation of 2-hydroxyglutaratePhase 2 clinical trialIsocitrate dehydrogenase inhibitorsMedian overall survivalSingle-agent activityNovel combination therapiesEnhance patient selectionSubgroup of patientsOverall survivalOpen-labelCombination therapyIDH mutationsPatient selectionRecombination deficiencySolid tumorsTumor progressionClinical trialsOlaparibCholangiocarcinomaDynamic Contrast-enhanced MRI Processing Comparison for Distinguishing True Progression From Pseudoprogression in High-grade Glioma.
Amer A, Ansari S, Krayyem A, Kundu S, Khose S, Pokhylevych H, Calle S, Patel C, Yang Z, Liu H, Johnson J. Dynamic Contrast-enhanced MRI Processing Comparison for Distinguishing True Progression From Pseudoprogression in High-grade Glioma. Journal Of Computer Assisted Tomography 2025 PMID: 39876523, DOI: 10.1097/rct.0000000000001716.Peer-Reviewed Original ResearchHigh-grade gliomasBlood-brain barrierDCE-MRIPeak contrast enhancementQuantify BBB permeabilityTreatment-related changesFollow-up subjectsKtrans mapsTrue progressionTumor progressionClinical dataConventional MRIPseudoprogressionBBB permeabilityCombined pathologyKtransContrast enhancementT1 enhancementStandard processing methodologyStatistically significant resultsClinical data setsPathologyPatientsGliomaSSS techniqueComprehensive Molecular Profiling of Metastatic Pancreatic Adenocarcinomas
Antony V, Sun T, Dolezal D, Cai G. Comprehensive Molecular Profiling of Metastatic Pancreatic Adenocarcinomas. Cancers 2025, 17: 335. PMID: 39941707, PMCID: PMC11815932, DOI: 10.3390/cancers17030335.Peer-Reviewed Original ResearchMetastatic pancreatic ductal adenocarcinomaPancreatic ductal adenocarcinomaPrimary pancreatic ductal adenocarcinomaMolecular profilingGene mutationsGene copy number alterationsAdvanced-stage pancreatic cancerInsufficient tumor cellsOncomine Comprehensive AssayRate of TP53Copy number alterationsMetastatic diseasePDAC casesPIK3CA mutationsPancreatic cancerPoor prognosisTreatment optionsDuctal adenocarcinomaTumor cellsTumor progressionMolecular alterationsStudy cohortMolecular testingComprehensive assayTherapeutic target
2024
G9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1
Exposito F, Redrado M, Serrano D, Calabuig-Fariñas S, Bao-Caamano A, Gallach S, Jantus-Lewintre E, Diaz-Lagares A, Rodriguez-Casanova A, Sandoval J, San Jose-Eneriz E, Garcia J, Redin E, Senent Y, Leon S, Pio R, Lopez R, Oyarzabal J, Pineda-Lucena A, Agirre X, Montuenga L, Prosper F, Calvo A. G9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1. Cell Death & Disease 2024, 15: 787. PMID: 39488528, PMCID: PMC11531574, DOI: 10.1038/s41419-024-07156-w.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerNon-small cell lung cancer patientsCM-272Treatment of non-small cell lung cancerReprogram tumor cellsAssociated with poor prognosisResponse to chemotherapyCell lung cancerCancer drugsMonitor tumor progressionOverexpression of G9aNSCLC cell linesLung cancer growthCancer drug sensitivityNon-small cell lung cancer growthNon-invasive biomarkersTumor volumeAntitumor efficacyTargeted therapyPoor prognosisCancer modelsTumor cellsInduce cell deathTumor progressionLung cancerEpigenetic control of immunoevasion in cancer stem cells
Galassi C, Esteller M, Vitale I, Galluzzi L. Epigenetic control of immunoevasion in cancer stem cells. Trends In Cancer 2024, 10: 1052-1071. PMID: 39244477, DOI: 10.1016/j.trecan.2024.08.004.Peer-Reviewed Original ResearchCancer stem cellsTumor-targeting immune responsesPopulation of malignant cellsStem cellsResistance to therapyStages of cancer progressionHost immune systemDisease relapseMalignant cellsTumor progressionImmune recognitionNeoplastic cellsImmune responseCancer progressionImmune systemEvade recognitionEpigenetic modification of DNATherapeutic targetCancerEpigenetic modificationsCellsEpigenetic controlModification of DNAImmunotherapyMalignancyNuclear PKM2 binds pre-mRNA at folded G-quadruplexes and reveals their gene regulatory role
Anastasakis D, Apostolidi M, Garman K, Polash A, Umar M, Meng Q, Scutenaire J, Jarvis J, Wang X, Haase A, Brownell I, Rinehart J, Hafner M. Nuclear PKM2 binds pre-mRNA at folded G-quadruplexes and reveals their gene regulatory role. Molecular Cell 2024, 84: 3775-3789.e6. PMID: 39153475, PMCID: PMC11455610, DOI: 10.1016/j.molcel.2024.07.025.Peer-Reviewed Original ResearchRNA-binding proteinsPre-mRNANon-canonical RNA-binding proteinsGene regulatory roleCancer cellsRNA G-quadruplexesG-quadruplexInvasion of cancer cellsTriple-negative breast cancer cellsBreast cancer cellsEpithelial-to-mesenchymal transitionCancer typesNuclear localizationPrecursor mRNANuclear accumulationGene expressionXenograft mouse modelNuclear PKM2Regulatory roleRG4sPKM2Reduced migrationMouse modelTumor progressionPatient survivalPrognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma
Valdez C, Sánchez-Zuno G, Osmani L, Ibrahim W, Galan A, Bacchiocchi A, Halaban R, Kulkarni R, Kang I, Bucala R, Tran T. Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma. Oncotarget 2024, 15: 507-520. PMID: 39028303, PMCID: PMC11259151, DOI: 10.18632/oncotarget.28615.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntigens, Differentiation, B-LymphocyteBiomarkers, TumorFemaleHistocompatibility Antigens Class IIHumansImmune Checkpoint InhibitorsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMelanomaMiddle AgedMutationPrognosisRetrospective StudiesSkin NeoplasmsConceptsMacrophage migration inhibitory factorImmune checkpoint inhibitionD-dopachrome tautomeraseExpression of macrophage migration inhibitory factorDrivers of tumor progressionInflammatory cell markersPatient tumor samplesPatient survival outcomesMigration inhibitory factorStatistically significant differenceCheckpoint inhibitionImmune therapyPrognostic valueSurvival outcomesResistant melanomaGene expressionImproved survivalRetrospective studyInflammatory markersTumor progressionCell markersTumor samplesClinical evidenceMelanomaBulk RNA sequencingOverexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment
Martinez-Terroba E, Plasek-Hegde L, Chiotakakos I, Li V, de Miguel F, Robles-Oteiza C, Tyagi A, Politi K, Zamudio J, Dimitrova N. Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment. Science Immunology 2024, 9: eadh5462. PMID: 38875320, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchConceptsTumor microenvironmentLung adenocarcinomaMetastatic diseasePromoting metastatic diseaseGlobal chromatin accessibilityMetastasis-associated lung adenocarcinoma transcript 1Overexpression of MALAT1Lung adenocarcinoma transcript 1Lung adenocarcinoma metastasisCCL2 blockadeInflammatory reprogrammingEnhanced cell mobilityMacrophage depletionMechanism of actionTumor typesTumor progressionMouse modelCell mobilizationTumorLong noncoding RNAsParacrine secretionMetastasisCell linesTranscript 1MicroenvironmentGeneration of transmitochondrial cybrids in cancer cells
Soler-Agesta R, Ripollés-Yuba C, Marco-Brualla J, Moreno-Loshuertos R, Sato A, Beltrán-Visiedo M, Galluzzi L, Anel A. Generation of transmitochondrial cybrids in cancer cells. Methods In Cell Biology 2024, 189: 23-40. PMID: 39393884, DOI: 10.1016/bs.mcb.2024.05.010.Peer-Reviewed Original ResearchTransmitochondrial cybridsCancer cellsApoptotic cell deathSource of ATPCancer cell functionsMitochondrial genomeCircular genomeNuclear genesMitochondrial DNATransfer RNAMitochondrial proteinsRibosomal RNAMitochondrial componentsIntact mitochondriaMitochondrial functionCybridsCell deathMetabolic intermediatesMitochondriaGenomeCell functionRNACellsTumor progressionAbundant sourceSelective inhibition of tumor microvascular permeability by cavtratin blocks tumor progression in mice
Gratton J, Lin M, Yu J, Weiss E, Jiang Z, Fairchild T, Iwakiri Y, Groszmann R, Claffey K, Cheng Y, Sessa W. Selective inhibition of tumor microvascular permeability by cavtratin blocks tumor progression in mice. Cancer Cell 2024, 42: 1127. PMID: 38821059, DOI: 10.1016/j.ccell.2024.05.009.Peer-Reviewed Original ResearchCOX2-dependent suppression of anticancer immunity
Lira M, Galluzzi L, Vanpouille-Box C. COX2-dependent suppression of anticancer immunity. Trends In Cancer 2024, 10: 573-575. PMID: 38821853, PMCID: PMC11236508, DOI: 10.1016/j.trecan.2024.05.006.Peer-Reviewed Original ResearchInterleukin-2Tumor-targeting immune responsesPromote tumor progressionProstaglandin E<sub>2</sub>Inhibition of mitochondrial metabolismDownregulation of interleukin 2Cancer cell proliferationAnticancer immunityT cellsTumor progressionImmune responseCell proliferationMitochondrial metabolismProstaglandinCancerIs Lipid Metabolism of Value in Cancer Research and Treatment? Part II: Role of Specialized Pro-Resolving Mediators in Inflammation, Infections, and Cancer
Babar M, Nassar A, Nie X, Zhang T, He J, Yeung J, Norris P, Ogura H, Muldoon A, Chen L, Libreros S. Is Lipid Metabolism of Value in Cancer Research and Treatment? Part II: Role of Specialized Pro-Resolving Mediators in Inflammation, Infections, and Cancer. Metabolites 2024, 14: 314. PMID: 38921449, PMCID: PMC11205484, DOI: 10.3390/metabo14060314.Peer-Reviewed Original ResearchResolution of inflammationPro-resolving mediatorsTherapeutic effectOral squamous cell carcinomaT cell responsesSquamous cell carcinomaEicosapentaenoic acid derivativeExcessive neutrophil infiltrationDendritic cell migrationEndogenous lipid mediatorsMetastasis of cancer cellsPro-inflammatory cytokinesSpecialized pro-resolving mediatorsCell carcinomaTumor microenvironmentIschemia-related injuryLung inflammationTumor progressionNeutrophil infiltrationCell debris clearanceCystic fibrosisLung cancerAcute inflammationHerpes virusTherapeutic approachesAdditive Value of Magnetic Resonance Simulation Before Chemoradiation in Evaluating Treatment Response and Pseudoprogression in High-Grade Gliomas
Yadav D, Upadhyay R, Kumar V, Chen M, Johnson J, Langshaw H, Curl B, Farhat M, Talpur W, Beckham T, Yeboa D, Swanson T, Ghia A, Li J, Chung C. Additive Value of Magnetic Resonance Simulation Before Chemoradiation in Evaluating Treatment Response and Pseudoprogression in High-Grade Gliomas. Practical Radiation Oncology 2024, 14: e449-e457. PMID: 38685448, DOI: 10.1016/j.prro.2024.04.009.Peer-Reviewed Original ResearchPseudo-progressionResponse assessmentInterobserver agreementImprove response assessmentPost-operative MRIFollow-up MRIFollow-up imagingEvaluate treatment responseHigh-grade gliomasIndependent blinded reviewIdentification of patientsClinical trial enrollmentWeeks of RTPartial response(PRStable disease(SDRT planningSalvage treatmentTumor responseEarly time pointsMedian intervalImprove patient outcomesTrue progressionProspective studyTreatment responseTumor progressionCancer cell metabolism and antitumour immunity
De Martino M, Rathmell J, Galluzzi L, Vanpouille-Box C. Cancer cell metabolism and antitumour immunity. Nature Reviews Immunology 2024, 24: 654-669. PMID: 38649722, PMCID: PMC11365797, DOI: 10.1038/s41577-024-01026-4.Peer-Reviewed Original ResearchCell-extrinsic mechanismsCancer cell-extrinsic mechanismsCancer cell-intrinsicAntitumour immune responseAdverse microenvironmental conditionsIncreased proliferative potentialAccelerated disease progressionAdaptive immune functionMetabolic rewiringAnticancer immunityMalignant cellsAlteration of metabolismTumor progressionCell-intrinsicMicroenvironmental conditionsDisease progressionProliferative potentialImmune responseCancer cellsImmune functionTherapeutic purposesCancerAlterationsCellsTumorA Single-Arm Phase 2 Trial of Trametinib in Patients with Locally Advanced or Metastatic Epithelioid Hemangioendothelioma.
Schuetze S, Ballman K, Heise R, Ganjoo K, Davis E, George S, Burgess M, Choy E, Shepard D, Tinoco G, Hirbe A, Kelly C, Attia S, Deshpande H, Schwartz G, Siontis B, Riedel R, von Mehren M, Kozlowski E, Chen H, Astbury C, Rubin B. A Single-Arm Phase 2 Trial of Trametinib in Patients with Locally Advanced or Metastatic Epithelioid Hemangioendothelioma. Clinical Cancer Research 2024, 30: 4584-4592. PMID: 38446990, PMCID: PMC11377863, DOI: 10.1158/1078-0432.ccr-23-3817.Peer-Reviewed Original ResearchEpithelioid hemangioendotheliomaMetastatic epithelioid hemangioendotheliomaMedian PFSOS ratesEvidence of tumor progressionPhase 2 trialMedian pain intensityEffects of trametinibMAPK pathwayActivation of MAPK pathwayInhibitor of MEKPalliative benefitPain intensityPain scoresPrimary endpointAssociated with reductionsTrametinibTumor progressionTumor samplesOncogenic driversVascular cancerPatientsPatient safetyResponse ratePFSGlioblastom – aktuelle Therapiekonzepte
Rieger D, Renovanz M, Kurz S, Bombach P, Paulsen F, Roder C, Tatagiba M, Niyazi M, Tabatabai G. Glioblastom – aktuelle Therapiekonzepte. Die Onkologie 2024, 30: 145-156. DOI: 10.1007/s00761-024-01473-7.Peer-Reviewed Original ResearchClinical trialsWorld Health Organization classificationCombination of radiotherapyFirst-line therapyDiagnosis of glioblastomaPatterns of disease progressionTherapeutic clinical trialsTumor Treating FieldsCurrent treatment conceptsCentral nervous systemNeuro-oncology careTemozolomide chemotherapyFirst-linePostoperative therapyPrimary neoplasmsOrganization classificationUnfavorable prognosisTumor progressionClinical statusDisease progressionTreatment conceptTreatment recommendationsBiomarker-basedNervous systemGlioblastomaEGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteiza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth. Cancer Discovery 2024, 14: 524-545. PMID: 38241033, PMCID: PMC11258210, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung adenocarcinoma cellsEGFR phosphorylationImmune responseTransformed epitheliumCancer cellsInflammatory functionsEGFR signalingMacrophage metabolismAlveolar macrophagesIncreased cholesterol synthesisMetabolic supportOncogenic signaling
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