2024
Novel non‐invasive molecular signatures for oral cavity cancer, by whole transcriptome and small non‐coding RNA sequencing analyses: Predicted association with PI3K/AKT/mTOR pathway
Vageli D, Doukas P, Townsend J, Pickering C, Judson B. Novel non‐invasive molecular signatures for oral cavity cancer, by whole transcriptome and small non‐coding RNA sequencing analyses: Predicted association with PI3K/AKT/mTOR pathway. Cancer Medicine 2024, 13: e7309. PMID: 38819439, PMCID: PMC11141334, DOI: 10.1002/cam4.7309.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiomarkers, TumorCarcinoma, Squamous CellCase-Control StudiesFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMiddle AgedMouth NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerRNA, Small UntranslatedSalivaSequence Analysis, RNASignal TransductionTOR Serine-Threonine KinasesTranscriptomeConceptsOral squamous cell carcinomaPost-treatment monitoringHealthy controlsOral cavity cancer patientsOral cavity cancerIdentification of molecular biomarkersSquamous cell carcinomaPatients relative to HCSamples of salivaMonitoring of patientsCell carcinomaPost-treatment monitoring of patientsSmoking historySerum miRNAsCancer patientsEfficient clinical toolEffective preventive careTherapeutic approachesMRNA signatureRNA sequencing analysisClinical testingSerumPatientsMolecular biomarkersClinical toolIntegrated mutational landscape analysis of poorly differentiated high-grade neuroendocrine carcinoma of the uterine cervix
Bellone S, Jeong K, Halle M, Krakstad C, McNamara B, Greenman M, Mutlu L, Demirkiran C, Hartwich T, Yang-Hartwich Y, Zipponi M, Buza N, Hui P, Raspagliesi F, Lopez S, Paolini B, Milione M, Perrone E, Scambia G, Altwerger G, Ravaggi A, Bignotti E, Huang G, Andikyan V, Clark M, Ratner E, Azodi M, Schwartz P, Quick C, Angioli R, Terranova C, Zaidi S, Nandi S, Alexandrov L, Siegel E, Choi J, Schlessinger J, Santin A. Integrated mutational landscape analysis of poorly differentiated high-grade neuroendocrine carcinoma of the uterine cervix. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2321898121. PMID: 38625939, PMCID: PMC11046577, DOI: 10.1073/pnas.2321898121.Peer-Reviewed Original ResearchConceptsWhole-exome sequencingPatient-derived-xenograftsBase excision repairCopy number lossMultiregion whole-exome sequencingCopy number gainHigh-grade neuroendocrine carcinomaCNV analysisPhylogenetic analysisEvolutionary historyNeuroendocrine cervical cancerHuman papillomavirus DNAMutator phenotypeSensitivity to afatinibGenetic landscapeRecurrent mutationsRNA sequencingGene fusionsMutational landscape analysisExcision repairGenesMutationsPan-HERConsistent with deficiencyNeuroendocrine carcinomaNCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells
Sánchez J, Alemán A, Henao J, Olaya J, Ehrlich B. NCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells. Journal Of Physiology And Biochemistry 2024, 80: 451-463. PMID: 38564162, PMCID: PMC11074019, DOI: 10.1007/s13105-024-01016-z.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCalciumCalcium SignalingCell Line, TumorFemaleHumansNeuronal Calcium-Sensor ProteinsNeuronsNeuropeptidesPhosphatidylinositol 3-KinasesSignal TransductionTRPA1 Cation ChannelConceptsTransient receptor potential channel ankyrin 1Breast cancerPI3K pathwayNCS-1Chemotherapy-induced peripheral neuropathyCa2+ channelsK pathwayCa2+ influxNCS-1 expressionBreast cancer cellsCa2+ sensorCa2+ homeostasisCa2+ dynamicsNeuronal calcium sensor-1MDA-MB-231Fura-2Open probabilityPain sensationAnkyrin 1Peripheral neuropathyTRPA1 channelsCo-immunoprecipitationChannel functionRegulatory componentsCellular pathwaysAntioxidant Efficacy of Hwangryunhaedok-tang through Nrf2 and AMPK Signaling Pathway against Neurological Disorders In Vivo and In Vitro
Bae S, Lee W, Bak S, Lee S, Hwang S, Kim G, Koo B, Park S, Yoo H, Kim C, Kang H, Oh T, Kim Y. Antioxidant Efficacy of Hwangryunhaedok-tang through Nrf2 and AMPK Signaling Pathway against Neurological Disorders In Vivo and In Vitro. International Journal Of Molecular Sciences 2024, 25: 2313. PMID: 38396988, PMCID: PMC10889506, DOI: 10.3390/ijms25042313.Peer-Reviewed Original ResearchConceptsFormation of neurofibrillary tanglesNeurofibrillary tanglesAlzheimer's diseaseImpaired clearance of amyloid betaSignaling pathwayClearance of amyloid betaAMPK signaling pathwayActivate signaling pathwaysAlzheimer's disease in vivoInhibition of cell apoptosisCause of dementiaAmyloid-betaHT-22 cellsNeuritic plaquesIn vitroMitochondrial dysfunctionOxidative stressCell apoptosisDisease in vivoROS generationHT-22Prevent ADAMPKDisorders in vivoProtein levels
2023
PI3Kδ Pathway Dysregulation and Unique Features of Its Inhibition by Leniolisib in Activated PI3Kδ Syndrome and Beyond
Cant A, Chandra A, Munro E, Rao V, Lucas C. PI3Kδ Pathway Dysregulation and Unique Features of Its Inhibition by Leniolisib in Activated PI3Kδ Syndrome and Beyond. The Journal Of Allergy And Clinical Immunology In Practice 2023, 12: 69-78. PMID: 37777067, PMCID: PMC10872751, DOI: 10.1016/j.jaip.2023.09.016.Peer-Reviewed Original ResearchMeSH KeywordsClass I Phosphatidylinositol 3-KinasesHumansPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPyrimidinesConceptsPI3Kδ inhibitorsActivated PI3Kδ SyndromeImmune cell developmentPI3Kδ syndromeSpecific inhibitory propertiesAdverse eventsTreatment optionsPI3Kδ activityHematological malignanciesPathway dysregulationInborn errorsDrug mechanismsGenetic hyperactivationLeniolisibSyndromeΔ isoformsCell developmentInhibitorsInhibitory propertiesΓ isoformsColitisNeutropeniaTolerabilityMalignancyHepatotoxicitySMAD4 maintains the fluid shear stress set point to protect against arterial-venous malformations
Banerjee K, Lin Y, Gahn J, Cordero J, Gupta P, Mohamed I, Graupera M, Dobreva G, Schwartz M, Ola R. SMAD4 maintains the fluid shear stress set point to protect against arterial-venous malformations. Journal Of Clinical Investigation 2023, 133: e168352. PMID: 37490341, PMCID: PMC10503796, DOI: 10.1172/jci168352.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArteriovenous MalformationsBone Morphogenetic ProteinsEndothelial CellsMiceMice, KnockoutPhosphatidylinositol 3-KinasesTelangiectasia, Hereditary HemorrhagicConceptsActivin-like kinase 1Fluid shear stressSMAD family member 4Arterial identityCyclin-dependent kinase inhibitors Cdkn2aVascular network formsEndothelial cellsVascular stabilitySensitivity of ECsBMP signalsPI3K/AktFamily member 4Downstream effectorsProtein 9Kinase 1Vascular developmentBone morphogenic protein 9Mechanism of synergyMorphological responsesSMAD4 deletionEC proliferationMember 4Multi-omic analysis reveals metabolic pathways that characterize right-sided colon cancer liver metastasis
Morris M, Jain A, Sun B, Kurbatov V, Muca E, Zeng Z, Jin Y, Roper J, Lu J, Paty P, Johnson C, Khan S. Multi-omic analysis reveals metabolic pathways that characterize right-sided colon cancer liver metastasis. Cancer Letters 2023, 574: 216384. PMID: 37716465, PMCID: PMC10620771, DOI: 10.1016/j.canlet.2023.216384.Peer-Reviewed Original ResearchMeSH KeywordsCarcinoma, Renal CellColonic NeoplasmsHumansKidney NeoplasmsLiver NeoplasmsMetabolic Networks and PathwaysMultiomicsPhosphatidylinositol 3-KinasesConceptsLiver metastasesColon cancer liver metastasisCancer liver metastasesSided colon cancerSubset of patientsGrowth factor betaMulti-omics analysisFatty acid oxidationMetastatic diseaseInferior survivalClinical differencesClinical behaviorUntargeted metabolomics analysisTumor behaviorColon cancerBile acidsTumor cell metabolismFactor betaPatientsMetastasisPI3K-AktReactive oxygen speciesMEK-ERKLiquid chromatography-mass spectrometryRCCToward Precision Oncology in Glioblastoma with a Personalized Cancer Genome Reporting Tool and Genetic Changes Identified by Whole Exome Sequencing
Erdogan O, Özkaya Ş, Erzik C, Bilguvar K, Arga K, Bayraklı F. Toward Precision Oncology in Glioblastoma with a Personalized Cancer Genome Reporting Tool and Genetic Changes Identified by Whole Exome Sequencing. OMICS A Journal Of Integrative Biology 2023, 27: 426-433. PMID: 37669106, DOI: 10.1089/omi.2023.0117.Peer-Reviewed Original ResearchMeSH KeywordsDNA Copy Number VariationsExome SequencingGlioblastomaHumansPhosphatidylinositol 3-KinasesPrecision MedicineConceptsTreatment optionsWhole-exome sequencingPrecision/personalized medicineExome sequencingLimited treatment optionsGenetic alterationsPersonalized medicinePotential therapeutic targetAggressive brain tumorTumor tissue samplesPoor prognosisGBM patientsTargetable pathwaysBrain tumorsTherapeutic targetLarger studyMolecular findingsNeurosurgical oncologyGenomic profilingPatientsPersonalized therapyMolecular profilingAkt/GlioblastomaPrecision oncologyChylomicrons Regulate Lacteal Permeability and Intestinal Lipid Absorption
Zarkada G, Chen X, Zhou X, Lange M, Zeng L, Lv W, Zhang X, Li Y, Zhou W, Liu K, Chen D, Ricard N, Liao J, Kim Y, Benedito R, Claesson-Welsh L, Alitalo K, Simons M, Ju R, Li X, Eichmann A, Zhang F. Chylomicrons Regulate Lacteal Permeability and Intestinal Lipid Absorption. Circulation Research 2023, 133: 333-349. PMID: 37462027, PMCID: PMC10530007, DOI: 10.1161/circresaha.123.322607.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCapillary PermeabilityChylomicronsEndothelial CellsLymphatic VesselsMiceMonomeric GTP-Binding ProteinsPhosphatidylinositol 3-KinasesVascular Endothelial Growth Factor AConceptsLymphatic endothelial cellsCell-cell junctionsCytoskeleton contractionMolecular biology approachesSmall GTPase Rac1Cytoskeletal contractilityBiology approachGTPase Rac1Stress fibersA SignalingPI3KLipid uptakePermeability regulationLymphatic permeabilityIntestinal lipid absorptionLEC junctionJunction openingEndothelial cellsLymphatic capillariesVEGFR-2Fundamental mechanismsLymphatic barrierLymphatic vesselsVascular endothelial growthLymphatic junctionsPTEN Loss Confers Resistance to Anti-PD-1 Therapy in Non-Small Cell Lung Cancer by Increasing Tumor Infiltration of Regulatory T Cells.
Exposito F, Redrado M, Houry M, Hastings K, Molero-Abraham M, Lozano T, Solorzano J, Sanz-Ortega J, Adradas V, Amat R, Redin E, Leon S, Legarra N, Garcia J, Serrano D, Valencia K, Robles-Oteiza C, Foggetti G, Otegui N, Felip E, Lasarte J, Paz-Ares L, Zugazagoitia J, Politi K, Montuenga L, Calvo A. PTEN Loss Confers Resistance to Anti-PD-1 Therapy in Non-Small Cell Lung Cancer by Increasing Tumor Infiltration of Regulatory T Cells. Cancer Research 2023, 83: 2513-2526. PMID: 37311042, DOI: 10.1158/0008-5472.can-22-3023.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerLung squamous carcinomaAnti-PD-1 therapyRegulatory T cellsCell lung cancerImmunosuppressive microenvironmentLung cancerImmunotherapy resistanceT cellsWorse progression-free survivalCell death protein 1PTEN lossAnti-TGFβ antibodyConversion of CD4PI3K/AKT/mTOR pathwayProgression-free survivalDeath protein 1Treatment of miceImmunosuppressive tumor microenvironmentPTEN/PI3K/AKT/mTOR pathwayAKT/mTOR pathwayPD-L1TLR agonistsTumor rejectionSquamous carcinomaMultiple PIK3CA mutation clonality correlates with outcomes in taselisib + fulvestrant-treated ER+/HER2–, PIK3CA-mutated breast cancers
Hutchinson K, Chen J, Savage H, Stout T, Schimmoller F, Cortés J, Dent S, Harbeck N, Jacot W, Krop I, Trabucco S, Sivakumar S, Sokol E, Wilson T. Multiple PIK3CA mutation clonality correlates with outcomes in taselisib + fulvestrant-treated ER+/HER2–, PIK3CA-mutated breast cancers. Genome Medicine 2023, 15: 28. PMID: 37101291, PMCID: PMC10131374, DOI: 10.1186/s13073-023-01181-8.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsClass I Phosphatidylinositol 3-KinasesFemaleFulvestrantHumansMutationPhosphatidylinositol 3-KinasesReceptor, ErbB-2ConceptsPI3K pathwayBreast cancerK pathwayP110α inhibitionLonger progression-free survivalReceptor tyrosine kinasesProgression-free survivalMetastatic breast cancerComprehensive genomic profilingPI3K pathway genesFurther clinical investigationP110α inhibitorsHigh response rateSolid tumor typesBreast cancer tumorsP110α catalytic subunitClinical trialsClinical investigationIndependent cohortImportant molecular determinantResponse rateTumor typesPIK3CA geneConclusionsOur studyTumor DNACo-mutations and KRAS G12C inhibitor efficacy in advanced NSCLC
Negrao M, Araujo H, Lamberti G, Cooper A, Akhave N, Zhou T, Delasos L, Hicks J, Aldea M, Minuti G, Hines J, Aredo J, Dennis M, Chakrabarti T, Scott S, Bironzo P, Scheffler M, Christopoulos P, Stenzinger A, Riess J, Kim S, Goldberg S, Li M, Wang Q, Qing Y, Ni Y, Truong M, Lee R, Ricciuti B, Alessi J, Wang J, Resuli B, Landi L, Tseng S, Nishino M, Digumarthy S, Rinsurongkawong W, Rinsurongkawong V, Vaporciyan A, Blumenschein G, Zhang J, Owen D, Blakely C, Mountzios G, Shu C, Bestvina C, Garassino M, Marrone K, Gray J, Patel S, Cummings A, Wakelee H, Wolf J, Scagliotti G, Cappuzzo F, Barlesi F, Patil P, Drusbosky L, Gibbons D, Meric-Bernstam F, Lee J, Heymach J, Hong D, Heist R, Awad M, Skoulidis F. Co-mutations and KRAS G12C inhibitor efficacy in advanced NSCLC. Cancer Discovery 2023, 13: 1556-1571. PMID: 37068173, PMCID: PMC11024958, DOI: 10.1158/2159-8290.cd-22-1420.Peer-Reviewed Original ResearchMeSH KeywordsCarcinoma, Non-Small-Cell LungDNA HelicasesHumansKelch-Like ECH-Associated Protein 1Lung NeoplasmsMutationNF-E2-Related Factor 2Nuclear ProteinsPhosphatidylinositol 3-KinasesTranscription FactorsConceptsNon-small cell lung cancerAdvanced non-small cell lung cancerClinical outcomesPatient stratificationRas gene alterationsInferior clinical outcomesCell lung cancerEarly disease progressionPoor clinical outcomesTumor suppressor genePrognostic subgroupsCombination therapyInferior outcomesIndividual tumorsGene alterationsCo-mutationsClinical outcome predictionDNA damage response/repairLung cancerGenomic alterationsSuppressor geneDisease progressionInhibitor efficacyTreatment personalizationPatientsER+, HER2− advanced breast cancer treated with taselisib and fulvestrant: genomic landscape and associated clinical outcomes
Chen J, Jacot W, Cortés J, Krop I, Dent S, Harbeck N, De Laurentiis M, Diéras V, Im Y, Stout T, Schimmoller F, Savage H, Hutchinson K, Wilson T. ER+, HER2− advanced breast cancer treated with taselisib and fulvestrant: genomic landscape and associated clinical outcomes. Molecular Oncology 2023, 17: 2000-2016. PMID: 36892268, PMCID: PMC10552898, DOI: 10.1002/1878-0261.13416.Peer-Reviewed Original ResearchConceptsProgression-free survivalBreast cancerShorter progression-free survivalNeurofibromin 1Advanced breast cancerBreast cancer patientsP53 pathway genesPI3K inhibitorsPI3K inhibitionBaseline ctDNAEndocrine therapyClinical outcomesCancer patientsEstrogen receptorCatalytic subunit alphaTumor DNATaselisibK inhibitorsK inhibitionPI3KOutcomesCancerAlterationsGenomic landscapeProtein p53Rare-variant association analysis reveals known and new age-related hearing loss genes
Cornejo-Sanchez D, Li G, Fabiha T, Wang R, Acharya A, Everard J, Kadlubowska M, Huang Y, Schrauwen I, Wang G, DeWan A, Leal S. Rare-variant association analysis reveals known and new age-related hearing loss genes. European Journal Of Human Genetics 2023, 31: 638-647. PMID: 36788145, PMCID: PMC10250305, DOI: 10.1038/s41431-023-01302-2.Peer-Reviewed Original ResearchAgedApoptosis Regulatory ProteinsCalcium-Binding ProteinsHumansPhosphatidylinositol 3-KinasesPresbycusisTrans-ActivatorsPI3K Pathway Alterations in Peritoneal Metastases are Associated with Earlier Recurrence in Patients with Colorectal Cancer Undergoing Optimal Cytoreductive Surgery
Peerenboom R, Dhiman A, Witmer H, Spurr L, Polite B, Eng O, Shergill A, Turaga K. PI3K Pathway Alterations in Peritoneal Metastases are Associated with Earlier Recurrence in Patients with Colorectal Cancer Undergoing Optimal Cytoreductive Surgery. Annals Of Surgical Oncology 2023, 30: 3114-3122. PMID: 36637640, DOI: 10.1245/s10434-022-12784-7.Peer-Reviewed Original ResearchConceptsOptimal cytoreductive surgeryPI3K pathway alterationsRecurrence-free survivalAssociated with early recurrenceCytoreductive surgeryCRC-PMPeritoneal metastasisRTK-RASEarly recurrenceImpact of tumor biologyReduced risk of recurrenceCRC-PM patientsMonths to recurrenceBiologically heterogeneous diseaseRisk of recurrenceCox proportional hazards modelsRTK-RAS pathwayClinically meaningful impactPI3KFrequency of alterationsSignaling pathwayProportional hazards modelCytoreduced patientsOptimal cytoreductionConclusionsIn patientsIdentification of a neutrophil-specific PIK3R1 mutation facilitates targeted treatment in a patient with Sweet syndrome
Bhattacharya S, Basu S, Sheng E, Murphy C, Wei J, Kersh A, Nelson C, Bryer J, Ashchyan H, Steele K, Forrestel A, Seykora J, Micheletti R, James W, Rosenbach M, Leung T. Identification of a neutrophil-specific PIK3R1 mutation facilitates targeted treatment in a patient with Sweet syndrome. Journal Of Clinical Investigation 2023, 133: e162137. PMID: 36355435, PMCID: PMC9797331, DOI: 10.1172/jci162137.Peer-Reviewed Original ResearchMeSH KeywordsAdrenal Cortex HormonesClass Ia Phosphatidylinositol 3-KinaseFemaleHumansMiddle AgedMutationNeutrophilsPhosphatidylinositol 3-KinasesSweet SyndromeConceptsSteroid-sparing agentSweet's syndromeInflammatory diseasesCorticosteroid-related side effectsElevated IL-1Febrile neutrophilic dermatosisDramatic therapeutic responseReceptor 1 antagonistNeutrophil respiratory burstMultiorgan inflammatory diseasePersonalized medicine approachPI3K/AktSuccessful clinical interventionNeutrophilic dermatosisFrontline therapyRefractory casesNeutrophilic infiltrateBlood countIL-1βNeutrophil functionNeutrophil migrationTherapeutic responseLiver enzymesClinical challengeIL-1
2022
Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization
Bersell K, Yang T, Mosley J, Glazer A, Hale A, Kryshtal D, Kim K, Steimle J, Brown J, Salem J, Campbell C, Hong C, Wells Q, Johnson A, Short L, Blair M, Behr E, Petropoulou E, Jamshidi Y, Benson M, Keyes M, Ngo D, Vasan R, Yang Q, Gerszten R, Shaffer C, Parikh S, Sheng Q, Kannankeril P, Moskowitz I, York J, Wang T, Knollmann B, Roden D. Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization. Circulation 2022, 147: 824-840. PMID: 36524479, PMCID: PMC9992308, DOI: 10.1161/circulationaha.122.062193.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArrhythmias, CardiacBrugada SyndromeHumansMiceMyocytes, CardiacNAV1.5 Voltage-Gated Sodium ChannelPhenotypePhosphatidylinositol 3-KinasesReceptors, Platelet-Derived Growth FactorSodiumConceptsPlatelet-derived growth factorInduced pluripotent stem cellsBrugada syndromeArrhythmia syndromesSerum platelet-derived growth factorSodium currentGeneral transcriptional mechanismFramingham Heart Study cohortPI3KPDGF receptor expressionLate sodium currentCardiac sodium currentCardiac transcription factorsSmall molecule perturbationsCurrent-clamp experimentsCardiac sodium channel geneSodium channel geneFramingham Heart StudyMurine model systemPluripotent stem cellsMonogenic arrhythmia syndromesReceptor blockadeElectrophysiologic abnormalitiesQTc intervalStudy cohortDistinct subcellular localisation of intramyocellular lipids and reduced PKCε/PKCθ activity preserve muscle insulin sensitivity in exercise-trained mice
Gaspar R, Lyu K, Hubbard B, Leitner B, Luukkonen P, Hirabara S, Sakuma I, Nasiri A, Zhang D, Kahn M, Cline G, Pauli J, Perry R, Petersen K, Shulman G. Distinct subcellular localisation of intramyocellular lipids and reduced PKCε/PKCθ activity preserve muscle insulin sensitivity in exercise-trained mice. Diabetologia 2022, 66: 567-578. PMID: 36456864, PMCID: PMC11194860, DOI: 10.1007/s00125-022-05838-8.Peer-Reviewed Original ResearchConceptsProtein kinase CsSubcellular compartmentsDistinct subcellular localisationMuscle insulin sensitivityMultiple subcellular compartmentsInsulin receptor kinaseNovel protein kinase CsActivation of PKCεSubcellular localisationPKCθ translocationReceptor kinasePlasma membraneSubcellular distributionTriacylglycerol contentCrucial pathwaysIntramuscular triacylglycerol contentRC miceDiacylglycerolConclusions/interpretationThese resultsPKCεPM compartmentPhosphorylationMuscle triacylglycerol contentSkeletal muscleRecent findingsKeeping RelApse in Chk: molecular mechanisms of Chk1 inhibitor resistance in lymphoma
Black E, Joo Y, Kabeche L. Keeping RelApse in Chk: molecular mechanisms of Chk1 inhibitor resistance in lymphoma. Biochemical Journal 2022, 479: 2345-2349. PMID: 36416754, PMCID: PMC9704517, DOI: 10.1042/bcj20220461.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCheckpoint Kinase 1FemaleLymphomaMiceNeoplasm Recurrence, LocalPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProtein KinasesConceptsReplication stressChk1 activityDNA damage response pathwayChk1 inhibitorsDNA replication stressInhibitor resistanceDamage response pathwayGenome instabilityPI3K/AktResponse pathwaysMolecular mechanismsNovel roleChk1Cancer therapyCancer developmentFemale fertilityDevelopment of resistancePathwayLethal levelsMultiple mechanismsAlternative pathwayNF-κBDrug resistanceIntriguing targetDisease statesSignaling network model of cardiomyocyte morphological changes in familial cardiomyopathy
Khalilimeybodi A, Riaz M, Campbell S, Omens J, McCulloch A, Qyang Y, Saucerman J. Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy. Journal Of Molecular And Cellular Cardiology 2022, 174: 1-14. PMID: 36370475, PMCID: PMC10230857, DOI: 10.1016/j.yjmcc.2022.10.006.Peer-Reviewed Original Research
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