Featured Publications
A clonal expression biomarker associates with lung cancer mortality
Biswas D, Birkbak N, Rosenthal R, Hiley C, Lim E, Papp K, Boeing S, Krzystanek M, Djureinovic D, La Fleur L, Greco M, Döme B, Fillinger J, Brunnström H, Wu Y, Moore D, Skrzypski M, Abbosh C, Litchfield K, Al Bakir M, Watkins T, Veeriah S, Wilson G, Jamal-Hanjani M, Moldvay J, Botling J, Chinnaiyan A, Micke P, Hackshaw A, Bartek J, Csabai I, Szallasi Z, Herrero J, McGranahan N, Swanton C. A clonal expression biomarker associates with lung cancer mortality. Nature Medicine 2019, 25: 1540-1548. PMID: 31591602, PMCID: PMC6984959, DOI: 10.1038/s41591-019-0595-z.Peer-Reviewed Original ResearchMeSH KeywordsAgedBiomarkers, TumorClonal EvolutionDisease-Free SurvivalDNA Copy Number VariationsExomeExome SequencingFemaleGene Expression Regulation, NeoplasticGenetic HeterogeneityHumansLung NeoplasmsMalePrognosisRisk FactorsTranscriptomeConceptsNon-small cell lung cancerClinicopathological risk factorsCell lung cancerLung cancer mortalityPrognostic gene expression signaturesCancer cell proliferationGene expression signaturesCancer mortalityLung cancerRisk factorsExpression-based biomarkersCopy number gainsDisease subtypesClinical descriptorsTranscriptomic biomarkersIndividual tumorsCancer typesDiagnostic precisionMolecular biomarkersExpression signaturesCell proliferationDNA copy number gainsBiomarkersPatientsIntratumor heterogeneityProspective validation of ORACLE, a clonal expression biomarker associated with survival of patients with lung adenocarcinoma
Biswas D, Liu Y, Herrero J, Wu Y, Moore D, Karasaki T, Grigoriadis K, Lu W, Veeriah S, Naceur-Lombardelli C, Magno N, Ward S, Frankell A, Hill M, Colliver E, de Carné Trécesson S, East P, Malhi A, Snell D, O’Neill O, Leonce D, Mattsson J, Lindberg A, Micke P, Moldvay J, Megyesfalvi Z, Dome B, Fillinger J, Nicod J, Downward J, Szallasi Z, Hackshaw A, Jamal-Hanjani M, Kanu N, Birkbak N, Swanton C. Prospective validation of ORACLE, a clonal expression biomarker associated with survival of patients with lung adenocarcinoma. Nature Cancer 2025, 6: 86-101. PMID: 39789179, PMCID: PMC11779643, DOI: 10.1038/s43018-024-00883-1.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAgedBiomarkers, TumorExome SequencingFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiddle AgedPrognosisProspective StudiesTranscriptomeConceptsLung adenocarcinomaStage I diseaseClinicopathological risk factorsSurvival of patientsResponse to treatmentRNA sequencing dataI diseaseSequence dataMetastatic clonesNeedle biopsyIndividual tumorsLung expressionTranscription signalsPrognostic informationWhole exomeExpressed genesChemotherapy sensitivityProspective validationSurvival associationsTranscriptomic heterogeneityHuman tumorsEvolutionary measuresChromosomal instabilityRisk factorsNatural history
2024
TRACERx analysis identifies a role for FAT1 in regulating chromosomal instability and whole-genome doubling via Hippo signalling
Lu W, Zalmas L, Bailey C, Black J, Martinez-Ruiz C, Pich O, Gimeno-Valiente F, Usaite I, Magness A, Thol K, Webber T, Jiang M, Saunders R, Liu Y, Biswas D, Ige E, Aerne B, Grönroos E, Venkatesan S, Stavrou G, Karasaki T, Al Bakir M, Renshaw M, Xu H, Schneider-Luftman D, Sharma N, Tovini L, Jamal-Hanjani M, McClelland S, Litchfield K, Birkbak N, Howell M, Tapon N, Fugger K, McGranahan N, Bartek J, Kanu N, Swanton C. TRACERx analysis identifies a role for FAT1 in regulating chromosomal instability and whole-genome doubling via Hippo signalling. Nature Cell Biology 2024, 27: 154-168. PMID: 39738653, PMCID: PMC11735399, DOI: 10.1038/s41556-024-01558-w.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCadherinsCarcinoma, Non-Small-Cell LungCell Line, TumorChromosomal InstabilityGene Expression Regulation, NeoplasticHippo Signaling PathwayHumansLung NeoplasmsMiceMitosisProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsYAP-Signaling ProteinsConceptsWhole-genome doublingStructural chromosome instabilityChromosomal instabilityHomologous recombinationNumerical chromosome instabilityNon-small-cell lung cancerHR deficiencyPersistent replication stressGenome doublingRadial chromosomesHippo signalingReplication stressChromosomal translocationsEvolutionary adaptationDriver eventsGenetic alterationsFAT1Increased tumor heterogeneityChromosomeCO depletionYAP1Downstream mechanismsRepair deficiencyIntratumour heterogeneityExperimental approach
2019
Pulmonary venous circulating tumor cell dissemination before tumor resection and disease relapse
Chemi F, Rothwell D, McGranahan N, Gulati S, Abbosh C, Pearce S, Zhou C, Wilson G, Jamal-Hanjani M, Birkbak N, Pierce J, Kim C, Ferdous S, Burt D, Slane-Tan D, Gomes F, Moore D, Shah R, Al Bakir M, Hiley C, Veeriah S, Summers Y, Crosbie P, Ward S, Mesquita B, Dynowski M, Biswas D, Tugwood J, Blackhall F, Miller C, Hackshaw A, Brady G, Swanton C, Dive C. Pulmonary venous circulating tumor cell dissemination before tumor resection and disease relapse. Nature Medicine 2019, 25: 1534-1539. PMID: 31591595, PMCID: PMC6986897, DOI: 10.1038/s41591-019-0593-1.Peer-Reviewed Original ResearchConceptsNon-small-cell lung cancerEarly-stage non-small-cell lung cancerDisease relapseGenomic profilingHigh risk of recurrenceDetection of circulating tumor cellsRisk of recurrenceTumor cell disseminationTime of surgeryPredictors of relapsePotential clinical utilityCurative intentPrimary tumorSurgical resectionTumor resectionTumor stagePredicting relapseCell disseminationTumor cellsLung cancerMutational overlapRelapseMultivariate analysisSurgeryHigh risk
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