2023
Epigenetic markers and therapeutic targets for metastasis
Kravitz C, Yan Q, Nguyen D. Epigenetic markers and therapeutic targets for metastasis. Cancer And Metastasis Reviews 2023, 42: 427-443. PMID: 37286865, PMCID: PMC10595046, DOI: 10.1007/s10555-023-10109-y.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsEpigenomic alterationsLineage integrityTherapeutic targetEpigenetic markersCancer cellsGenetic aberrationsCurrent knowledgeHuman tumorsMalignant cell cloneTumor progressionDNANumber of discoveriesCell clonesDisseminated diseaseCertain organsPrimary tumorTherapeutic responseMetastatic cancerEpigenomeChromatinHistonesLiquid biopsyAlterationsClonesTargetThe correlation of ESR1 genetic aberrations with estrogen receptor and progesterone receptor status in metastatic and primary estrogen receptor-positive breast carcinomas
Moreira-Dinzey J, Zhan H, Rozenblit M, Krishnamurti U, Harigopal M, Zhong M, Liang Y. The correlation of ESR1 genetic aberrations with estrogen receptor and progesterone receptor status in metastatic and primary estrogen receptor-positive breast carcinomas. Human Pathology 2023, 137: 56-62. PMID: 37127079, DOI: 10.1016/j.humpath.2023.04.017.Peer-Reviewed Original ResearchConceptsMetastatic tumorsBreast carcinomaGenetic aberrationsPR statusPrimary tumorBreast cancerControl groupER/PR statusEstrogen receptor-positive breast carcinomasER-positive breast cancerER positivity rateMetastatic breast cancerProgesterone receptor statusMetastatic breast carcinomaMore liver metastasesPrimary breast carcinomaWild-type groupEstrogen receptor 1 geneReceptor 1 geneWild-type controlsLiver metastasesReceptor statusClinicopathological featuresER expressionControl tumorsTumoral Intraductal Neoplasms of the Bile Ducts Comprise Morphologically and Genetically Distinct Entities.
Wang T, Askan G, Ozcan K, Rana S, Zehir A, Bhanot U, Yantiss R, Rao D, Wahl S, Bagci P, Balci S, Balachandran V, Jarnagin W, Adsay N, Klimstra D, Basturk O. Tumoral Intraductal Neoplasms of the Bile Ducts Comprise Morphologically and Genetically Distinct Entities. Archives Of Pathology & Laboratory Medicine 2023, 147: 1390-1401. PMID: 36821179, DOI: 10.5858/arpa.2022-0343-oa.Peer-Reviewed Original ResearchConceptsIntraductal oncocytic papillary neoplasmIntraductal papillary neoplasmIntraductal tubulopapillary neoplasmIntraductal neoplasmsPapillary neoplasmBile ductTargeted next-generation sequencingMale to female ratioHigh-grade dysplasiaRecurrent genetic aberrationsCopy number variantsTumor suppressor geneFollow-up informationDisease-related deathNext-generation sequencingWnt signaling pathwayGenetically distinct entitiesCK20 expressionGenetic aberrationsFemale ratioFollow-upTubulopapillary neoplasmNeoplasmsSuppressor geneFrequent alterations
2021
A review of FLT3 inhibitors in acute myeloid leukemia
Zhao JC, Agarwal S, Ahmad H, Amin K, Bewersdorf JP, Zeidan AM. A review of FLT3 inhibitors in acute myeloid leukemia. Blood Reviews 2021, 52: 100905. PMID: 34774343, PMCID: PMC9846716, DOI: 10.1016/j.blre.2021.100905.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsAcute myeloid leukemiaFLT3 mutationsMyeloid leukemiaTreatment of AMLInhibitor maintenance therapyDrug resistance mechanismsCommon genetic aberrationsConsolidation chemotherapyRefractory FLT3Maintenance therapyPoor prognosisPrognostic implicationsStromal protectionFLT3 inhibitorsStandard inductionADMIRAL studyFLT3Genetic aberrationsLeukemiaResistance mechanismsMutationsMonotherapyChemotherapyPrognosisGilteritinib
2018
Clinical outcomes of adolescents and young adults with advanced solid tumours participating in phase I trials
Sundar R, McVeigh T, Dolling D, Petruckevitch A, Diamantis N, Ang J, Chenard-Poiriér M, Collins D, Lim J, Ameratunga M, Khan K, Kaye S, Banerji U, Lopez J, George A, de Bono J, van der Graaf W. Clinical outcomes of adolescents and young adults with advanced solid tumours participating in phase I trials. European Journal Of Cancer 2018, 101: 55-61. PMID: 30025230, DOI: 10.1016/j.ejca.2018.06.003.Peer-Reviewed Original ResearchConceptsPhase I trialPhase I clinical trialAdvanced solid tumorsI trialOverall survivalAYA patientsSolid tumorsCancer syndromesCohort of AYA patientsMolecular characterisation of tumoursOutcomes of AYA patientsClinical benefit rateMedian overall survivalOutcomes of AYAsSomatic genetic aberrationsSignificant family historyRoyal Marsden HospitalHereditary cancer syndromesCharacterisation of tumoursTherapeutic treatment optionsClinical outcomes of adolescentsClinical trial dataDrug Development UnitYoung adultsGenetic aberrationsTime to Move to Earlier Intervention for Thoracic Aortic Aneurysm?
Gryaznov A, Ziganshin B, Elefteriades J. Time to Move to Earlier Intervention for Thoracic Aortic Aneurysm? Structural Heart 2018, 2: 10-22. DOI: 10.1080/24748706.2017.1404664.Peer-Reviewed Original ResearchThoracic aortic aneurysmBody surface areaAortic aneurysmMost life-threatening complicationsAortic growth rateEarly prophylactic interventionAcute aortic dissectionLife-threatening complicationsPatient/yearProphylactic surgical interventionSpecific genetic aberrationsAortic dissectionAortic sizeAortic diseaseCurrent gold standardSurgical interventionPatient heightProphylactic interventionsThoracic aortaAneurysm diseaseCommon causeFamily historyEarly diagnosisEarly interventionGenetic aberrations
2017
Clinical outcomes of adolescents and young adults (AYA) with advanced solid tumors participating in phase I trials.
Sundar R, McVeigh T, Petruckevitch A, Diamantis N, Ang J, Chenard-Poirier M, Collins D, Lim J, Ameratunga M, Khan K, Kaye S, Banerji U, Lopez J, De Bono J, Van Der Graaf W. Clinical outcomes of adolescents and young adults (AYA) with advanced solid tumors participating in phase I trials. Journal Of Clinical Oncology 2017, 35: 10536-10536. DOI: 10.1200/jco.2017.35.15_suppl.10536.Peer-Reviewed Original ResearchPhase I trialAdvanced solid tumorsPhase I studyAYA patientsI trialFamily historySolid tumorsDrug Development UnitClinical outcomesOutcomes of AYA patientsMedian progression free survivalMolecular characterization of tumorsClinical benefit rateProgression free survivalSomatic genetic aberrationsRoyal Marsden HospitalHereditary cancer syndromesClinical outcomes of adolescentsCharacterization of tumorsMedian OSSystemic chemotherapyFree survivalGenetic aberrationsPredictive biomarkersBenefit rateR634W KIT Mutation in an Adult With Systemic Mastocytosis
Astle JM, Rose MG, Racke FK, Tormey CA, Siddon AJ. R634W KIT Mutation in an Adult With Systemic Mastocytosis. Lab Medicine 2017, 48: 253-257. PMID: 28520972, DOI: 10.1093/labmed/lmx026.Peer-Reviewed Original Research
2016
Epigenetics in Cancer: A Hematological Perspective
Stahl M, Kohrman N, Gore SD, Kim TK, Zeidan AM, Prebet T. Epigenetics in Cancer: A Hematological Perspective. PLOS Genetics 2016, 12: e1006193. PMID: 27723796, PMCID: PMC5065123, DOI: 10.1371/journal.pgen.1006193.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsEpigenetic mechanismsEpigenetic regulationNext-generation sequencingEpigenetic therapyCell agingAdvanced phase patientsEpigeneticsGeneration sequencingCancer cellsGenetic aberrationsPhase patientsClinical responseImmune responseHematological perspectiveProduction of drugsMyeloid malignanciesBody of dataCancerOncogenesisSequencingMechanismRegulationFatePhosphoinositide 3-kinase inhibitors induce DNA damage through nucleoside depletion
Juvekar A, Hu H, Yadegarynia S, Lyssiotis C, Ullas S, Lien E, Bellinger G, Son J, Hok R, Seth P, Daly M, Kim B, Scully R, Asara J, Cantley L, Wulf G. Phosphoinositide 3-kinase inhibitors induce DNA damage through nucleoside depletion. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: e4338-e4347. PMID: 27402769, PMCID: PMC4968752, DOI: 10.1073/pnas.1522223113.Peer-Reviewed Original ResearchMeSH KeywordsAminopyridinesAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell ProliferationDNA DamageDNA, NeoplasmFemaleHumansMice, Inbred C57BLMice, Inbred NODMice, KnockoutMice, SCIDMorpholinesNucleosidesPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsPoly(ADP-ribose) Polymerase InhibitorsTriple Negative Breast NeoplasmsConceptsDNA damagePI3KDNA synthesisNonoxidative pentose phosphate pathwayProtein kinase AktPentose phosphate pathwayKinase AktPI3K inhibitor BKM120DNA repairPI3K inhibitorsPI3K inhibitionPhosphate pathwayCarbon flux studiesCell deathNucleotide synthesisNucleotide triphosphatesMutational backgroundK inhibitionK inhibitorsGenetic aberrationsMouse modelPARP inhibitionInhibitorsBRCA1Triple-negative breast cancerDeciphering and Targeting Oncogenic Mutations and Pathways in Breast Cancer
Santarpia L, Bottai G, Kelly CM, Győrffy B, Székely B, Pusztai L. Deciphering and Targeting Oncogenic Mutations and Pathways in Breast Cancer. The Oncologist 2016, 21: 1063-1078. PMID: 27384237, PMCID: PMC5016060, DOI: 10.1634/theoncologist.2015-0369.Peer-Reviewed Original ResearchConceptsBreast cancerCancer-causing genesCopy number variationsRNA speciesRNA editingGenomic variationNext-generation sequencingRNA sequencingGenomic complexityGenomic portraitGreater genomic complexityOncogenic mutationsOncogenic eventsTarget profilingRare mutationsMutationsRecurrent mutationsSomatic variantsGenetic aberrationsFormal clinical trialsPotential therapeutic implicationsDriver mutationsSequencingGermline variantsMolecular abnormalitiesComprehensive molecular profiling and analysis of mutual exclusivity of genetic aberrations (MEGA) of intra- and extrahepatic cholangiocarcinomas (IHC and EHC) evaluation of prognostic features and potential targets for intervention.
Lowery M, Ptashkin R, Jordan E, Berger M, Zehir A, Kemeny N, O'Reilly E, Jarnagin W, Harding J, DeMatteo R, D'Angelica M, Cercek A, LY M, Salehi E, Hechtman J, Schultz N, Hyman D, Klimstra D, Saltz L, Abou-Alfa G. Comprehensive molecular profiling and analysis of mutual exclusivity of genetic aberrations (MEGA) of intra- and extrahepatic cholangiocarcinomas (IHC and EHC) evaluation of prognostic features and potential targets for intervention. Journal Of Clinical Oncology 2016, 34: 4088-4088. DOI: 10.1200/jco.2016.34.15_suppl.4088.Peer-Reviewed Original Research
2014
Genetic/familial high-risk assessment: breast and ovarian, version 1.2014.
Daly M, Pilarski R, Axilbund J, Buys S, Crawford B, Friedman S, Garber J, Horton C, Kaklamani V, Klein C, Kohlmann W, Kurian A, Litton J, Madlensky L, Marcom P, Merajver S, Offit K, Pal T, Pasche B, Reiser G, Shannon K, Swisher E, Voian N, Weitzel J, Whelan A, Wiesner G, Dwyer M, Kumar R. Genetic/familial high-risk assessment: breast and ovarian, version 1.2014. Journal Of The National Comprehensive Cancer Network 2014, 12: 1326-38. PMID: 25190698, DOI: 10.6004/jnccn.2014.0127.Peer-Reviewed Original ResearchConceptsNCCN GuidelinesAssessment of genetic mutationsGenetic/Familial High-Risk AssessmentDevelopment of breastManagement of patientsHamartoma tumor syndromeOvarian cancerGenetic aberrationsGenetic testing/counselingTumor syndromeIncreased riskGenetic mutationsHigh-risk assessmentDiagnostic criteriaBreastNCCNMutationsBRCA1/BRCA2Genetic/FamilialTP53PatientsSyndromeCancerCowdenGuidelines
2013
The PI3K/Akt/mTOR axis in head and neck cancer: functions, aberrations, cross‐talk, and therapies
Vander Broek R, Mohan S, Eytan D, Chen Z, Van Waes C. The PI3K/Akt/mTOR axis in head and neck cancer: functions, aberrations, cross‐talk, and therapies. Oral Diseases 2013, 21: 815-825. PMID: 24219320, DOI: 10.1111/odi.12206.Peer-Reviewed Original ResearchConceptsAkt/mTOR axisPI3K/Akt/mTOR axisDNA copy number variationsMTOR axisCopy number variationsPI3K/Akt/mTORDysregulation of mRNAsNeck squamous cell carcinomaPI3K/AKT/mTOR pathwayAKT/mTOR pathwayAkt/mTORSquamous cell carcinomaPathway leadCell survivalNumber variationsPI3KMalignant phenotypeMTOR pathwayNormal physiologyCell carcinomaHNSCC casesNeck cancerClinical studiesProtein expressionGenetic aberrationsMantle cell lymphoma in cyclin D1 transgenic mice with Bim-deficient B cells
Katz SG, LaBelle JL, Meng H, Valeriano RP, Fisher JK, Sun H, Rodig SJ, Kleinstein SH, Walensky LD. Mantle cell lymphoma in cyclin D1 transgenic mice with Bim-deficient B cells. Blood 2013, 123: 884-893. PMID: 24352880, PMCID: PMC3916879, DOI: 10.1182/blood-2013-04-499079.Peer-Reviewed Original ResearchConceptsMantle cell lymphomaCyclin D1 transgenic miceCyclin D1 overexpressionB cellsCell lymphomaAggressive B-cell lymphomasSubset of miceTransgenic mouse modelB-cell lymphomaDeletion of BimPathogenesis of MCLHuman mantle cell lymphomaDevelopment of MCLStimulation regimensConventional chemotherapyMouse modelLymphoid maturationTransgenic miceLymphomaBIM deletionSelective expansionMiceProapoptotic BimPathogenesisGenetic aberrations
2012
Arg/Abl2 promotes invasion and attenuates proliferation of breast cancer in vivo
Gil-Henn H, Patsialou A, Wang Y, Warren MS, Condeelis JS, Koleske AJ. Arg/Abl2 promotes invasion and attenuates proliferation of breast cancer in vivo. Oncogene 2012, 32: 2622-2630. PMID: 22777352, PMCID: PMC3473103, DOI: 10.1038/onc.2012.284.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationErbB ReceptorsFemaleGene Knockdown TechniquesHumansLung NeoplasmsMAP Kinase Signaling SystemMiceMice, SCIDNeoplasm InvasivenessNeoplasm MetastasisNeoplasm TransplantationProto-Oncogene Proteins c-ablsrc-Family KinasesTransplantation, HeterologousConceptsTumor cell invasionBreast cancer cellsTyrosine kinaseCancer cellsCell invasionNon-receptor tyrosine kinaseRas-MAPK signalingRas-MAPK pathwayGene expression patternsSrc tyrosine kinaseInvasion-associated genesUncontrolled cell divisionProliferation-associated genesMetastatic cancer cellsCell divisionExpression patternsEGF receptorTumor cell proliferationPromotes InvasionMouse xenograft modelCell proliferationMultistep processGenetic aberrationsKinaseGenes
2010
A Stapled BIM BH3 Helix Restores Apoptosis In Bim-Null Mantle Cell Lymphoma
Katz S, Labelle J, Godes M, Fisher J, Bird G, Walensky L. A Stapled BIM BH3 Helix Restores Apoptosis In Bim-Null Mantle Cell Lymphoma. Blood 2010, 116: 437. DOI: 10.1182/blood.v116.21.437.437.Peer-Reviewed Original ResearchMantle cell lymphomaCell lymphomaAggressive B-cell lymphomasDevelopment of splenomegalyRAG2-deficient miceB-cell lymphomaLymphoproliferative diseaseOrgan infiltrationMCL cell linesConventional chemotherapyHematologic cancersAnti-apoptotic proteinsBone marrowNormal parenchymaVivo modelPro-apoptotic proteinsCell-permeable peptideLymphomaPro-apoptotic activityGenetic aberrationsMiceBcl-2TUNEL positivityPro-apoptotic Bcl-2 family protein BimCaspase-3/7PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor–positive breast cancer
Loi S, Haibe-Kains B, Majjaj S, Lallemand F, Durbecq V, Larsimont D, Gonzalez-Angulo AM, Pusztai L, Symmans WF, Bardelli A, Ellis P, Tutt AN, Gillett CE, Hennessy BT, Mills GB, Phillips WA, Piccart MJ, Speed TP, McArthur GA, Sotiriou C. PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor–positive breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 10208-10213. PMID: 20479250, PMCID: PMC2890442, DOI: 10.1073/pnas.0907011107.Peer-Reviewed Original ResearchMeSH KeywordsAntibiotics, AntineoplasticAntineoplastic Agents, HormonalBase SequenceBreast NeoplasmsCell Line, TumorClass I Phosphatidylinositol 3-KinasesDNA PrimersFemaleGene Expression ProfilingHumansMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesMutationNeoplasms, Hormone-DependentOligonucleotide Array Sequence AnalysisPhosphatidylinositol 3-KinasesPrognosisProteinsProto-Oncogene Proteins c-aktReceptor, ErbB-2Receptors, EstrogenSignal TransductionSirolimusTamoxifenTOR Serine-Threonine KinasesTranscription FactorsConceptsBreast cancerPIK3CA mutationsClinical outcomesEstrogen receptor-positive breast cancerReceptor-positive breast cancerGene signaturePIK3CA mutation statusPI3K/mTOR inhibitorBetter clinical outcomesPI3K/mTOR inhibitionHuman breast cancerBC cell linesPIK3CA mutant breast cancersCommon genetic aberrationsTamoxifen monotherapyBetter prognosisMTOR inhibitorsBetter outcomesMutation statusMTOR inhibitionPathway activationExperimental modelGenetic aberrationsPrognosisCell lines
2006
SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells
Sprangers M, Feldhahn N, Liedtke S, Jumaa H, Siebert R, Müschen M. SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells. Oncogene 2006, 25: 5180-5186. PMID: 16636677, DOI: 10.1038/sj.onc.1209520.Peer-Reviewed Original ResearchConceptsLymphoblastic leukemiaRecombinase activityRAG1/2 expressionB-cell lineage leukemiaDouble-strand break eventsLymphoma cellsSecondary genetic aberrationsB-cell lymphomaB-cell lymphoma cellsB-lymphoid malignanciesB-cell malignanciesB cell receptorVH gene rearrangementsMalignant progressionLeukemiaFrequent featureGenetic aberrationsGene rearrangementsCells resultsRearrangement activityLineage leukemiaMalignancyVH replacementDeficiencyExpression
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