2025
Imetelstat in myeloid malignancies: current data and future directions
Bidikian A, Bewersdorf J, Kewan T, Podoltsev N, Stahl M, Zeidan A. Imetelstat in myeloid malignancies: current data and future directions. Expert Review Of Anticancer Therapy 2025, ahead-of-print: 1-12. PMID: 40116730, DOI: 10.1080/14737140.2025.2482721.Peer-Reviewed Original ResearchMyelodysplastic syndromeLR-MDSClinical trialsPotential disease-modifying propertiesLow-risk myelodysplastic syndromesElevated liver enzymesLR-MDS patientsTreat myelodysplastic syndromeSearch of PubMedTransfusion independenceEssential thrombocythemiaInfusion reactionsMyeloid malignanciesDisease-modifying propertiesCombination therapySurvival benefitEffective telomerase inhibitorImetelstatTelomerase reactivationPatient populationLiver enzymesMyelofibrosisCancer cellsMalignancyConference abstractsHMBOX1 reverses autophagy mediated 5-fluorouracil resistance through promoting HACE1-induced ubiquitination and degradation of ATG5 in colorectal cancer
Gao Y, Fu S, Peng Y, Zhou Y, Zhu J, Zhang X, Cai C, Han Y, Shen H, Zeng S. HMBOX1 reverses autophagy mediated 5-fluorouracil resistance through promoting HACE1-induced ubiquitination and degradation of ATG5 in colorectal cancer. Autophagy 2025, ahead-of-print: 1-22. PMID: 40126194, DOI: 10.1080/15548627.2025.2477443.Peer-Reviewed Original ResearchColorectal cancer cellsColorectal cancerCancer cellsColorectal cancer tissuesColorectal cancer tissues of patientsLiquid chromatography-tandem mass spectrometryChromatography-tandem mass spectrometryFetal human colonProgression-free survivalClinical colorectal cancer tissuesFirst-line treatmentCell Counting Kit-8Cancer tissues of patientsPostoperative colorectal cancerCaspase 3Transmission electron microscopyCounting Kit-8Tissues of patientsMass spectrometryCleaved caspase 3Stable diseaseComplete responsePartial responseOverall survivalRegulation of chemoresistanceMitochondrial 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 ResearchGPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis
Ristić D, Bärnthaler T, Gruden E, Kienzl M, Danner L, Herceg K, Sarsembayeva A, Kargl J, Schicho R. GPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis. Frontiers In Immunology 2025, 15: 1513547. PMID: 39885986, PMCID: PMC11779727, DOI: 10.3389/fimmu.2024.1513547.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaModel of pancreatic ductal adenocarcinomaImmune tumor microenvironmentTumor microenvironmentT cellsKO miceEndocannabinoid systemWT miceTumor growthCD8<sup>+</sup> T cellsG protein-coupled receptor 55Suppress T cell functionCancer cellsMurine pancreatic ductal adenocarcinomaCD3<sup>+</sup> T cellsExpression of PDL1T cell influxImmune cell compositionT cell functionTumor microenvironment cellsMigration of T cellsReduced tumor weightImmune cell populationsT cell activationCell linesHarnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition
Glaviano A, Lau H, Carter L, Lee E, Lam H, Okina E, Tan D, Tan W, Ang H, Carbone D, Yee M, Shanmugam M, Huang X, Sethi G, Tan T, Lim L, Huang R, Ungefroren H, Giovannetti E, Tang D, Bruno T, Luo P, Andersen M, Qian B, Ishihara J, Radisky D, Elias S, Yadav S, Kim M, Robert C, Diana P, Schalper K, Shi T, Merghoub T, Krebs S, Kusumbe A, Davids M, Brown J, Kumar A. Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition. Journal Of Hematology & Oncology 2025, 18: 6. PMID: 39806516, PMCID: PMC11733683, DOI: 10.1186/s13045-024-01634-6.Peer-Reviewed Original ResearchConceptsEpithelial-mesenchymal transitionTumor microenvironmentCancer progressionTherapeutic resistanceCancer therapyTumor microenvironment componentsTumor microenvironment modulationModulation of epithelial-mesenchymal transitionPromote tumor growthImprove treatment efficacyTumor microenvironment signalsTargeted cancer therapyTarget various componentsTherapeutic challengeTreatment responseTumor growthPromote metastasisTherapeutic strategiesTreatment efficacyEpithelial cellsMesenchymal traitsCancer cellsExtracellular matrix componentsCancerResistance mechanisms
2024
Development of a small molecule-based two-photon photosensitizer for targeting cancer cells
Lee D, Cao Y, Juvekar V, Sauraj, Noh C, Shin S, Liu Z, Kim H. Development of a small molecule-based two-photon photosensitizer for targeting cancer cells. Journal Of Materials Chemistry B 2024, 12: 12232-12238. PMID: 39469993, DOI: 10.1039/d4tb01706d.Peer-Reviewed Original ResearchConceptsTarget cancer cellsReactive oxygen speciesPhotodynamic therapyCancer cellsDiverse cell linesInduced ROS productionColon cancer tissuesTwo-photon (TPCell deathLow dark toxicityCancer modelsTwo-photon photosensitizerROS productionCancer selectivityInduce cell damageThree-dimensional spheroidsCell linesTP excitationImaging-guided photodynamic therapyCancer tissuesOxygen speciesTP-PDTColibactin Exerts Androgen-dependent and -independent Effects on Prostate Cancer
Agrawal R, Al-Hiyari S, Hugh-White R, Hromas R, Patel Y, Williamson E, Mootor M, Gonzalez A, Fu J, Haas R, Jordan M, Wickes B, Mohammed G, Tian M, Doris M, Jobin C, Wernke K, Pan Y, Yamaguchi T, Herzon S, Boutros P, Liss M. Colibactin Exerts Androgen-dependent and -independent Effects on Prostate Cancer. European Urology Oncology 2024 PMID: 39547899, DOI: 10.1016/j.euo.2024.10.015.Peer-Reviewed Original ResearchProstate cancerInduction of genomic instabilityPC diagnosisPC etiologyColibactin-producing Escherichia coliEtiology of prostate cancerProstate cancer cellsProstate cancer diagnosisSomatic point mutationsCombination in vitroGenomic instabilityAndrogen-dependentColon cancerPatient populationProstateClinical cohortInitial cancerSomatic mutationsCancer cellsDihydrotestosteroneGenetic dysfunctionSingle cell lineCancerCell linesDiagnosisMetastasis of colon cancer requires Dickkopf-2 to generate cancer cells with Paneth cell properties.
Shin J, Park J, Lim J, Jeong J, Dinesh R, Maher S, Kim J, Park S, Hong J, Wysolmerski J, Choi J, Bothwell A. Metastasis of colon cancer requires Dickkopf-2 to generate cancer cells with Paneth cell properties. ELife 2024, 13 PMID: 39535280, PMCID: PMC11560131, DOI: 10.7554/elife.97279.Peer-Reviewed Original ResearchConceptsCancer cellsDickkopf-2Analysis of transcriptomeGeneration of cancer cellsPositive cancer cellsStem cell niche factorsColon cancer cellsPaneth cell differentiationHepatocyte nuclear factor 4 alphaLysozyme positive cellsChromatin accessibilityHNF4A proteinSingle-cell RNA sequencing analysisCell propertiesPaneth cell markersSequence analysisChromatin immunoprecipitationPromoter regionTranscription factorsTranscriptome analysisColon cancerColon cancer metastasisReduction of liver metastasisDownstream targetsCell differentiationMetastasis of colon cancer requires Dickkopf-2 to generate cancer cells with Paneth cell properties
Shin J, Park J, Lim J, Jeong J, Dinesh R, Maher S, Kim J, Park S, Hong J, Wysolmerski J, Choi J, Bothwell A. Metastasis of colon cancer requires Dickkopf-2 to generate cancer cells with Paneth cell properties. ELife 2024, 13 DOI: 10.7554/elife.97279.3.Peer-Reviewed Original ResearchCancer cellsDickkopf-2Promoter region of Sox9Analysis of transcriptomeGeneration of cancer cellsPositive cancer cellsStem cell niche factorsColon cancer cellsPaneth cell differentiationHepatocyte nuclear factor 4 alphaLysozyme positive cellsChromatin accessibilityHNF4A proteinSingle-cell RNA sequencing analysisCell propertiesPaneth cell markersSequence analysisChromatin immunoprecipitationPromoter regionTranscription factorsTranscriptome analysisColon cancerColon cancer metastasisReduction of liver metastasisDownstream targetsA TRilogy of ATR’s Non-Canonical Roles Throughout the Cell Cycle and Its Relation to Cancer
Joo Y, Ramirez C, Kabeche L. A TRilogy of ATR’s Non-Canonical Roles Throughout the Cell Cycle and Its Relation to Cancer. Cancers 2024, 16: 3536. PMID: 39456630, PMCID: PMC11506335, DOI: 10.3390/cancers16203536.Peer-Reviewed Original ResearchDNA damage responseNon-canonical rolesCell cyclePromote faithful chromosome segregationDetect mechanical forcesDNA damage response pathwayFaithful chromosome segregationDNA damage checkpointRad3-related proteinNuclear membrane integrityCancer therapy targetATR inhibitorsChromosome segregationDamage checkpointDamage responseApical kinaseDamaged DNAMembrane integrityAtaxia telangiectasiaNon-canonicalCancer cellsDNAClinical trialsCancer therapyClinical relevanceTranscriptional repression by HDAC3 mediates T cell exclusion from Kras mutant lung tumors
McGuire C, Meehan A, Couser E, Bull L, Minor A, Kuhlmann-Hogan A, Kaech S, Shaw R, Eichner L. Transcriptional repression by HDAC3 mediates T cell exclusion from Kras mutant lung tumors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317694121. PMID: 39388266, PMCID: PMC11494357, DOI: 10.1073/pnas.2317694121.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzamidesCell Line, TumorChemokine CXCL10Gene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistone DeacetylasesHumansLung NeoplasmsMiceMutationProto-Oncogene Proteins p21(ras)PyridinesPyridonesPyrimidinonesT-LymphocytesTranscription, GeneticTumor MicroenvironmentConceptsT cell recruitmentLung tumorsHistone deacetylase 3Enhanced T cell recruitmentCombined treatmentLung tumors in vivoGenetically engineered mouse modelsT cell exclusionInhibition of histone deacetylase 3Tumor immune microenvironmentTumor growth controlKRAS mutant lung tumorsTumors in vivoLung cancer cellsImmune microenvironmentT cellsTissue-specific fashionMouse modelPathway inhibitorTumorPharmacological inhibitionCancer cellsFunction in vivoTranscriptional regulationTranscriptional repressionThe hallmarks of cancer immune evasion
Galassi C, Chan T, Vitale I, Galluzzi L. The hallmarks of cancer immune evasion. Cancer Cell 2024, 42: 1825-1863. PMID: 39393356, DOI: 10.1016/j.ccell.2024.09.010.Peer-Reviewed Original ResearchCancer immune evasionHost immune systemImmune evasionNeoplastic cellsImmune systemImmune effector cellsConventional therapeutic strategiesModern immunotherapyAnticancer immunosurveillanceEffector cellsImmune escapeImmunoevasion mechanismsMalignant cellsMicroscopic neoplasmsCancer outgrowthImmune cytotoxicityImmune recognitionTherapeutic strategiesEpigenetic alterationsCancer cellsCell precursorsCancerCellsHallmarksImmunotherapyCarrier-free multifunctional nanomedicine for enhanced hyperthermic intraperitoneal chemotherapy against abdominal pelvic tumors
Fang H, Zhang L, Wu Y, Chen L, Deng Z, Zheng Z, Wang Y, Yang Y, Chen Q. Carrier-free multifunctional nanomedicine for enhanced hyperthermic intraperitoneal chemotherapy against abdominal pelvic tumors. Chemical Engineering Journal 2024, 498: 155781. DOI: 10.1016/j.cej.2024.155781.Peer-Reviewed Original ResearchHyperthermic intraperitoneal chemotherapyImmunogenic cell deathDamage-associated molecular patternsPelvic tumorsIntraperitoneal chemotherapyGambogic acidAnti-tumor immune response in vivoInfiltration of cytotoxic T lymphocytesTriggering immunogenic cell deathRelease of damage-associated molecular patternsCancer cellsImmune responses in vivoCytotoxic T lymphocytesInduce apoptosis of cancer cellsApoptosis of cancer cellsResponses in vivoInhibitor of heat shock proteinCell deathHyperthermia-induced cell deathPenetration of nanoparticlesTumor extracellular matrixHeat shock proteinsOvarian cancerTumor microenvironmentT lymphocytesClass Effect Unveiled: PPARγ Agonists and MEK Inhibitors in Cancer Cell Differentiation
Ben-Yishay R, Globus O, Balint-Lahat N, Arbili-Yarhi S, Bar-Hai N, Bar V, Aharon S, Kosenko A, Zundelevich A, Berger R, Ishay-Ronen D. Class Effect Unveiled: PPARγ Agonists and MEK Inhibitors in Cancer Cell Differentiation. Cells 2024, 13: 1506. PMID: 39273076, PMCID: PMC11394433, DOI: 10.3390/cells13171506.Peer-Reviewed Original ResearchConceptsMEK inhibitorsBreast cancer cellsEpithelial-to-mesenchymal transitionCancer cellsPPARg agonistsDrug resistanceTherapeutic approachesTriple-negative breast cancerMurine breast cancer cellsAggressive breast cancer subtypeDevelopment of drug resistanceCancer cell plasticityBreast cancer subtypesCombination of pioglitazoneOvercome drug resistanceDedifferentiated cancer cellsBreast cancer progressionCancer cell differentiationCytoskeleton rearrangementLipid droplet accumulationCell trans-differentiationBreast cancerCancer subtypesCell plasticityTherapeutic strategiesCell-specific models reveal conformation-specific RAF inhibitor combinations that synergistically inhibit ERK signaling in pancreatic cancer cells
Sevrin T, Imoto H, Robertson S, Rauch N, Dyn'ko U, Koubova K, Wynne K, Kolch W, Rukhlenko O, Kholodenko B. Cell-specific models reveal conformation-specific RAF inhibitor combinations that synergistically inhibit ERK signaling in pancreatic cancer cells. Cell Reports 2024, 43: 114710. PMID: 39240715, PMCID: PMC11474227, DOI: 10.1016/j.celrep.2024.114710.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaResistance to RAFResistant PDAC cellsPancreatic cancer cellsPancreatic ductal adenocarcinoma cell linesProtein expression profilesTumor-specific variationsIsogenic pairsCell-specific modelsConformational specificityERK signalingInhibitor combinationsERK pathwayKRAS mutationsTargeted therapyExpression profilesMEK inhibitorsDuctal adenocarcinomaCancer cellsKRAS mutantPhospho-ERKCell linesPDAC cellsCell viabilityDifferential sensitivityDNA nanoswitches pack an anti-cancer punch
Zhou K, Lin C. DNA nanoswitches pack an anti-cancer punch. Nature Nanotechnology 2024, 19: 1765-1766. PMID: 39209995, DOI: 10.1038/s41565-024-01749-4.Commentaries, Editorials and LettersMetabolic regulation of the mitochondrial immune checkpoint
Montrose D, Saha S, Galluzzi L. Metabolic regulation of the mitochondrial immune checkpoint. OncoImmunology 2024, 13: 2394247. PMID: 39206097, PMCID: PMC11352702, DOI: 10.1080/2162402x.2024.2394247.Peer-Reviewed Original ResearchConceptsTumor-targeting immune responsesColorectal cancer cellsAnticancer immunityImmune checkpointsActivation of cGASMalignant cellsImmune responseCancer cellsDisrupt mitochondrial functionAccumulation of mitochondrial DNACytosolic accumulationMitochondrial dysfunctionMetabolic regulationMitochondrial DNAMitochondrial functionSerine resultsCellsDysfunctionNuclear 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 survivalExploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells
Park B, Kim S, Yu S, Kim K, Jeon H, Ahn S. Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells. Biomolecules 2024, 14: 997. PMID: 39199385, PMCID: PMC11352368, DOI: 10.3390/biom14080997.Peer-Reviewed Original ResearchPC-3 cellsProstate cancer PC-3 cellsGK deficiencyCell deathProstate cancerAnti-cancer agentsKinase 1Apoptotic cell deathDNA microarray analysisHuman prostate cancer PC-3 cellsCancer cell deathModulating tumor microenvironmentProstate cancer cellsBiomarkers of cell deathX chromosomeReduced cell viabilityEpigenetic regulationExpression vectorInvestigated genesSynthesis of triglyceridesMicroarray analysisGenetic alterationsTumor microenvironmentNovel roleCancer cellsThe Potential Therapeutic Effects of Botulinum Neurotoxins on Neoplastic Cells: A Comprehensive Review of In Vitro and In Vivo Studies
Safarpour D, Tavassoli F, Jabbari B. The Potential Therapeutic Effects of Botulinum Neurotoxins on Neoplastic Cells: A Comprehensive Review of In Vitro and In Vivo Studies. Toxins 2024, 16: 355. PMID: 39195765, PMCID: PMC11358967, DOI: 10.3390/toxins16080355.Peer-Reviewed Original ResearchIn vivo studiesNeoplastic cellsReview of in vitroBotulinum neurotoxinBotulinum toxinMode of deliveryAnti-neoplastic treatmentProgression of cancer cellsIn vivo deliveryAnti-neoplastic potentialIn vitro effectsPotential therapeutic effectsNon-neuronal cellsNeoplastic cell linesHigh dosesTherapeutic effectCancer cellsClostridium difficileControlled studiesApoptotic effectsCell linesDisruption of cell membranesPrimary neuronsSystematic reviewCell cytoplasm
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