2025
FAK inhibition combined with the RAF-MEK clamp avutometinib overcomes resistance to targeted and immune therapies in BRAF V600E melanoma
Lubrano S, Cervantes-Villagrana R, Faraji F, Ramirez S, Sato K, Adame-Garcia S, Officer A, Arang N, Rigiracciolo D, Anguiano Quiroz P, Martini C, Wang Y, Ferguson F, Bacchiocchi A, Halaban R, Coma S, Holmen S, Pachter J, Aplin A, Gutkind J. FAK inhibition combined with the RAF-MEK clamp avutometinib overcomes resistance to targeted and immune therapies in BRAF V600E melanoma. Cancer Cell 2025, 43: 428-445.e6. PMID: 40020669, PMCID: PMC11903146, DOI: 10.1016/j.ccell.2025.02.001.Peer-Reviewed Original ResearchConceptsBRAF V600E melanomaFocal adhesion kinaseV600E melanomaFAK inhibitorActivated focal adhesion kinaseFocal adhesion kinase inhibitionRaf-MEKActivation of focal adhesion signalingFocal adhesion kinase inhibitorResistance to BRAFiSyngeneic mouse modelMAPK pathway inhibitionFocal adhesion signalingPro-apoptotic activityMelanoma patientsAdhesion signalingImmune therapyBRAF mutationsBRAFiTranscriptome analysisMelanomaMouse modelPathway inhibitionBRAFMelanoma cellsHeme promotes venetoclax resistance in multiple myeloma through MEK-ERK signaling and purine biosynthesis
Nair R, Vu A, Freer A, Bhatia K, Wang D, Savani M, Matulis S, Lonial S, Jaye D, Boise L, Seo S, Corson T, Nooka A, Bhatt S, McBrayer S, Gupta V, Hu X, Barwick B, Reddi A, Shanmugam M. Heme promotes venetoclax resistance in multiple myeloma through MEK-ERK signaling and purine biosynthesis. Blood 2025, 145: 732-747. PMID: 39693611, DOI: 10.1182/blood.2024025690.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCell Line, TumorDrug Resistance, NeoplasmHemeHumansMAP Kinase Signaling SystemMultiple MyelomaPurinesSulfonamidesConceptsElectron transport chainBcl-2Heme biosynthesisBCL-2 antagonismElectron transport chain activityIron-containing prosthetic groupMultiple myelomaB-cell lymphoma 2MEK-ERK signalingGene signatureActivation of prosurvivalApoptotic thresholdPurine biosynthesisPenultimate enzymePyrimidine biosynthesisMetabolic rewiringTransport chainProtein kinaseMultiple Myeloma Research Foundation CoMMpass studyBiosynthesisPurine synthesisGenetic profilePrimary MM cellsProsthetic groupProgression-free survivalExploring Glypican-3 targeted CAR-NK treatment and potential therapy resistance in hepatocellular carcinoma
Yang L, Pham K, Xi Y, Wu Q, Liu D, Robertson K, Liu C. Exploring Glypican-3 targeted CAR-NK treatment and potential therapy resistance in hepatocellular carcinoma. PLOS ONE 2025, 20: e0317401. PMID: 39841705, PMCID: PMC11753693, DOI: 10.1371/journal.pone.0317401.Peer-Reviewed Original ResearchConceptsGlypican-3Hepatocellular carcinomaCAR-NKNatural killerCell linesCAR-NK therapyCAR-NK cellsTreatment of hepatocellular carcinomaNK cell lineAnti-tumor effectsCancer-related mortalitySuppressed tumor growthPrimary liver cancerInfluence therapeutic outcomesCells in vitroHepatocellular carcinoma treatmentHepG2 cells in vitroNK92MI cellsImmunotherapy strategiesNSG miceImmunotherapy targetOncofetal glycoproteinTherapy resistanceImprove patient outcomesPoor prognosisHarnessing 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 ResearchMeSH KeywordsAnimalsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansMolecular Targeted TherapyNeoplasmsSignal TransductionTumor MicroenvironmentConceptsEpithelial-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 mechanismsLethal clinical outcome and chemotherapy and immunotherapy resistance in patients with urothelial carcinoma with MDM2 amplification or overexpression
Jin K, Ding Y, Xu J, Liu Z, Zeng H, Su X, Zhang L, Sun J, Wu Y, Liu H, Chang Y, Zhu Y, Wang Z, Xu L, Zhang W, Xu J. Lethal clinical outcome and chemotherapy and immunotherapy resistance in patients with urothelial carcinoma with MDM2 amplification or overexpression. Journal For ImmunoTherapy Of Cancer 2025, 13: e010964. PMID: 39762080, PMCID: PMC11749520, DOI: 10.1136/jitc-2024-010964.Peer-Reviewed Original ResearchMeSH KeywordsAgedDrug Resistance, NeoplasmFemaleGene AmplificationHumansImmunotherapyMaleMiddle AgedProto-Oncogene Proteins c-mdm2Urinary Bladder NeoplasmsConceptsMDM2</i> amplificationMurine double minute 2Programmed death-ligand 1Programmed death-1Platinum-based chemotherapyUrothelial carcinomaDedifferentiated morphologyClinical outcomesAbundance of CD8<sup>+</sup> T cellsCytotoxic T-lymphocyte-associated protein 4Anti-PD-1/PD-L1 immunotherapyAssociated with inferior overall survivalResponse to platinum-based chemotherapyExpression of immune checkpoint moleculesCD8<sup>+</sup> T cellsMurine double minute 2 amplificationDeath-ligand 1Immune checkpoint moleculesInferior overall survivalTumor immune contextureUbiquitin ligase murine double minute 2Subsets of patientsLethal clinical outcomeIndependent external cohortDouble minute 2
2024
Hypoxia is linked to acquired resistance to immune checkpoint inhibitors in lung cancer
Robles-Oteíza C, Hastings K, Choi J, Sirois I, Ravi A, Expósito F, de Miguel F, Knight J, López-Giráldez F, Choi H, Socci N, Merghoub T, Awad M, Getz G, Gainor J, Hellmann M, Caron É, Kaech S, Politi K. Hypoxia is linked to acquired resistance to immune checkpoint inhibitors in lung cancer. Journal Of Experimental Medicine 2024, 222: e20231106. PMID: 39585348, PMCID: PMC11602551, DOI: 10.1084/jem.20231106.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsNon-small cell lung cancerAcquired resistanceCheckpoint inhibitorsResistant tumorsPatients treated with anti-PD-1/PD-L1 therapyAnti-PD-1/PD-L1 therapyLung cancerResistance to immune checkpoint inhibitorsAssociated with decreased progression-free survivalHypoxia activated pro-drugsTargeting hypoxic tumor regionsTreat non-small cell lung cancerAnti-CTLA-4Anti-PD-1Immune checkpoint inhibitionTumor metabolic featuresProgression-free survivalCell lung cancerResistant cancer cellsHypoxic tumor regionsMHC-II levelsRegions of hypoxiaKnock-outCheckpoint inhibitionTargeting TREX1 induces innate immune response in drug-resistant Small Cell Lung Cancer
Murayama T, Mahadevan N, Meador C, Ivanova E, Pan Y, Knelson E, Tani T, Nakayama J, Ma X, Thai T, Hung Y, Kim W, Watanabe H, Cai K, Hata A, Paweletz C, Barbie D, Cañadas I. Targeting TREX1 induces innate immune response in drug-resistant Small Cell Lung Cancer. Cancer Research Communications 2024, 4: 2399-2414. PMID: 39177280, PMCID: PMC11391691, DOI: 10.1158/2767-9764.crc-24-0360.Peer-Reviewed Original ResearchConceptsSmall-cell lung cancerPatient-derived xenograftsCells to chemotherapyLung cancerInnate immune responseImmune responseSmall cell lung cancerHuman SCLC tumorsSurvival of resistant cellsResponse to chemotherapyCell lung cancerEfficacy of chemotherapyRepair exonuclease 1Postchemotherapy samplesAntitumor immunitySCLC tumorsCold tumorsAvailable therapiesChromatin immunoprecipitation sequencingTransposase-accessible chromatinInduce immunogenicityChemotherapyResistant cellsTherapeutic strategiesTREX1 expressionRethinking the use of germline CHEK2 mutation as a marker for PARP inhibitor sensitivity
Hayman T. Rethinking the use of germline CHEK2 mutation as a marker for PARP inhibitor sensitivity. JNCI Cancer Spectrum 2024, 8: pkae045. PMID: 38950525, PMCID: PMC11216723, DOI: 10.1093/jncics/pkae045.Peer-Reviewed Original ResearchBiomarkers, TumorCheckpoint Kinase 2Drug Resistance, NeoplasmGerm-Line MutationHumansPoly(ADP-ribose) Polymerase InhibitorsHigh-throughput transcriptome profiling indicates ribosomal RNAs to be associated with resistance to immunotherapy in non-small cell lung cancer (NSCLC)
Moutafi M, Bates K, Aung T, Milian R, Xirou V, Vathiotis I, Gavrielatou N, Angelakis A, Schalper K, Salichos L, Rimm D. High-throughput transcriptome profiling indicates ribosomal RNAs to be associated with resistance to immunotherapy in non-small cell lung cancer (NSCLC). Journal For ImmunoTherapy Of Cancer 2024, 12: e009039. PMID: 38857914, PMCID: PMC11168162, DOI: 10.1136/jitc-2024-009039.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerImmune checkpoint inhibitorsProgrammed cell death protein 1Associated with OSCell lung cancerTissue microarray spotsTissue microarrayValidation cohortLung cancerNon-small cell lung cancer treated with immune checkpoint inhibitorsAssociated with resistance to immunotherapyCell death protein 1Resistance to immunotherapyAssociated with PFSProgression-free survivalSecreted frizzled-related protein 2Cox proportional-hazards model analysisCheckpoint inhibitorsImmunotherapy strategiesTumor compartmentsRetrospective cohortDiscovery cohortLong-term benefitsPatientsCD68Unlocking the Potential: Biomarkers of Response to Antibody-Drug Conjugates.
Ascione L, Guidi L, Prakash A, Trapani D, LoRusso P, Lou E, Curigliano G. Unlocking the Potential: Biomarkers of Response to Antibody-Drug Conjugates. American Society Of Clinical Oncology Educational Book 2024, 44: e431766. PMID: 38828973, DOI: 10.1200/edbk_431766.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsBiomarkers, TumorDrug Resistance, NeoplasmHumansImmunoconjugatesMolecular Targeted TherapyNeoplasmsTreatment OutcomeConceptsAntibody-drug conjugatesTumor sitePredictive biomarkersAntigen expressionLack of robust predictive biomarkersSelection of targeted therapiesRobust predictive biomarkersTarget antigen expressionTumor antigen expressionCancer treatment landscapeBiomarkers of responseImprove patient selectionTumor intrinsic featuresBiomarkers of safetyUnique adverse eventsIdentification of patientsPopulation of patientsClinically actionable biomarkersSmall-molecule agentsPatient-centred outcomesTreatment landscapeBiomarker-drivenTreatment resistanceClinical benefitPatient selectionMicrotubule-Targeting Agents: Disruption of the Cellular Cytoskeleton as a Backbone of Ovarian Cancer Therapy
Danziger M, Noble H, Roque D, Xu F, Rao G, Santin A. Microtubule-Targeting Agents: Disruption of the Cellular Cytoskeleton as a Backbone of Ovarian Cancer Therapy. Advances In Experimental Medicine And Biology 2024, 1452: 1-19. PMID: 38805122, DOI: 10.1007/978-3-031-58311-7_1.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCytoskeletonDrug Resistance, NeoplasmFemaleHumansMicrotubulesOvarian NeoplasmsTubulin ModulatorsConceptsOvarian cancer therapyCancer therapyTargets of anti-cancer therapyIntracellular traffickingCellular processesCellular cytoskeletonMicrotubule-active agentsAnti-cancer therapyMicrotubule-stabilizing agentEffective regimenDynamic polymersDevelopment of resistanceB-tubulinTherapeutic challengeMicrotubulesRecurrent settingTherapyEukaryotesCytoskeletonMitosisHeterodimerMotilityTraffickingRegimensReplicationMultiple roles for AU-rich RNA binding proteins in the development of haematologic malignancies and their resistance to chemotherapy
Podszywalow-Bartnicka P, Neugebauer K. Multiple roles for AU-rich RNA binding proteins in the development of haematologic malignancies and their resistance to chemotherapy. RNA Biology 2024, 21: 584-600. PMID: 38798162, PMCID: PMC11135835, DOI: 10.1080/15476286.2024.2346688.Peer-Reviewed Original ResearchConceptsARE-binding proteinsRNA-binding proteinsAU-rich elementsStress granulesBinding proteinTranslational regulation of mRNAsImpact alternative splicingCytoplasmic stress granulesProtein-RNA bindingAdaptation to microenvironmentProtein-RNA networksBinding to AU-rich elementsCancer cell proteomePost-transcriptional regulationAU-rich RNA-binding proteinsRegulation of mRNAsChemotherapy resistanceGene expression levelsSequence motifsProtein-RNAMRNA structureMature mRNATranslational regulationAlternative splicingCell proteomeNetwork-based elucidation of colon cancer drug resistance mechanisms by phosphoproteomic time-series analysis
Rosenberger G, Li W, Turunen M, He J, Subramaniam P, Pampou S, Griffin A, Karan C, Kerwin P, Murray D, Honig B, Liu Y, Califano A. Network-based elucidation of colon cancer drug resistance mechanisms by phosphoproteomic time-series analysis. Nature Communications 2024, 15: 3909. PMID: 38724493, PMCID: PMC11082183, DOI: 10.1038/s41467-024-47957-3.Peer-Reviewed Original ResearchMeSH KeywordsAlgorithmsAntineoplastic AgentsCell Line, TumorColonic NeoplasmsDrug Resistance, NeoplasmHumansPhosphoproteinsPhosphorylationProteomeProteomicsSignal TransductionConceptsMechanism of cell responseResistance mechanismsSignaling pathway responsesDrug resistance mechanismsEnzyme/substrate interactionsAdaptive resistance mechanismsNetwork rewiringPhosphorylation stateSignaling pathway activationDrug perturbationsProteomic technologiesSignaling crosstalkPathway responsesInhibitor designPathway activationCancer drug resistance mechanismsCell adaptive responsesAdaptive responsePhosphatase activityNetwork-based methodologyRewiringTherapeutic efficacyPhosphoproteome coverageCell responsesControl mediumPROTAC EZH2 degrader-1 overcomes the resistance of podophyllotoxin derivatives in refractory small cell lung cancer with leptomeningeal metastasis
Shi M, Ding X, Tang L, Cao W, Su B, Zhang J. PROTAC EZH2 degrader-1 overcomes the resistance of podophyllotoxin derivatives in refractory small cell lung cancer with leptomeningeal metastasis. BMC Cancer 2024, 24: 504. PMID: 38644473, PMCID: PMC11034131, DOI: 10.1186/s12885-024-12244-3.Peer-Reviewed Original ResearchConceptsSmall cell lung cancerCell lung cancerMouse modelLung cancerRefractory small cell lung cancerNude miceIn vivo drug testingCell linesDrug testingLM cellsSensitivity of cisplatinIn vitro drug testingIncreased in vitroBackgroundLeptomeningeal metastasisLeptomeningeal metastasesSevere neurological disordersAssociated with several neurological disordersDrug sensitivityIn vivo live imagingHistological examinationCarotid arteryEffective treatmentMetastasisDrug trialsExpressing luciferaseZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer
Xu Y, Yang Y, Wang Z, Sjostrom M, Jiang Y, Tang Y, Cheng S, Deng S, Wang C, Gonzalez J, Johnson N, Li X, Li X, Metang L, Mukherji A, Xu Q, Tirado C, Wainwright G, Yu X, Barnes S, Hofstad M, Chen Y, Zhu H, Hanker A, Raj G, Zhu G, He H, Wang Z, Arteaga C, Liang H, Feng F, Wang Y, Wang T, Mu P. ZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer. Cancer Discovery 2024, 14: 1496-1521. PMID: 38591846, PMCID: PMC11285331, DOI: 10.1158/2159-8290.cd-23-0539.Peer-Reviewed Original ResearchConceptsLineage plasticityTherapy resistanceProstate cancerCancer cellsAndrogen receptorResistance to AR-targeted therapiesLuminal lineageAR-targeted therapiesOvercome therapy resistanceTransition of cancer cellsEpigenetic regulatory machineryBona fide coactivatorTherapy responseAR signalingEpigenetic rewiringDrug resistanceTherapeutic strategiesEpigenetic reprogrammingProstateTherapyCancerPhenotypic plasticityRegulatory machineryAndrogenTranscriptional programsSomatic gene mutation patterns and burden influence outcomes with enasidenib in relapsed/refractory IDH2-mutated AML
Risueño A, See W, Bluemmert I, de Botton S, DiNardo C, Fathi A, Schuh A, Montesinos P, Vyas P, Prebet T, Gandhi A, Hasan M. Somatic gene mutation patterns and burden influence outcomes with enasidenib in relapsed/refractory IDH2-mutated AML. Leukemia Research 2024, 140: 107497. PMID: 38564986, DOI: 10.1016/j.leukres.2024.107497.Peer-Reviewed Original ResearchConceptsConventional care regimensMutational burdenR/R AMLCo-mutationsIDH2-R172Co-mutation patternsAssociated with decreased overall survivalRelapsed/refractory acute myeloid leukemiaTargeted next-generation sequencingAML patient cohortNewly diagnosed AMLLow mutational burdenEvent-free survivalLimited treatment optionsAcute myeloid leukemiaGene mutation patternsIDH2 variantsIDH2 R140Prognostic impactOverall survivalPrognostic relevanceSurvival benefitMyeloid leukemiaIDH2 mutationsPatient cohort
2023
Delivery of short chain fatty acid butyrate to overcome Fusobacterium nucleatum-induced chemoresistance
Chen L, Zhao R, Kang Z, Cao Z, Liu N, Shen J, Wang C, Pan F, Zhou X, Liu Z, Yang Y, Chen Q. Delivery of short chain fatty acid butyrate to overcome Fusobacterium nucleatum-induced chemoresistance. Journal Of Controlled Release 2023, 363: 43-56. PMID: 37734673, DOI: 10.1016/j.jconrel.2023.09.028.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsButyratesColorectal NeoplasmsDrug Resistance, NeoplasmFusobacterium InfectionsFusobacterium nucleatumLiposomesMiceConceptsShort-chain fatty acid butyrateF. nucleatumFatty acid butyrateColorectal tumorsColorectal cancerInvasion of F. nucleatumTherapeutic efficacy of oxaliplatinEfficacy of oxaliplatinProgression of colorectal cancerEffect of butyrateOrthotopic colorectal tumorsFusobacterium nucleatumClinical application prospectsTherapeutic efficacyDrug resistanceIntravenous administrationColorectal cancer tissuesIntravenous injectionOral administrationCancer resistanceOral deliveryTumorKilling effectCancer tissuesChemoresistanceThe Critical Interplay of CAF Plasticity and Resistance in Prostate Cancer.
Li X, Mu P. The Critical Interplay of CAF Plasticity and Resistance in Prostate Cancer. Cancer Research 2023, 83: 2990-2992. PMID: 37504898, DOI: 10.1158/0008-5472.can-23-2260.Commentaries, Editorials and LettersConceptsCastration-resistant prostate cancerAndrogen deprivation therapyProstate cancerAndrogen receptorCastration-resistant prostate cancer developmentDevelopment of castration-resistant prostate cancerGenetically engineered mouse modelsMyofibroblastic cancer-associated fibroblastsOvercome treatment resistanceCancer-associated fibroblastsIncreased tumor heterogeneityDeprivation therapyCRPC developmentProstate tumorsTumor microenvironmentLineage plasticityTreatment resistanceStromal compartmentStandard treatmentTumor heterogeneityCancer recurrenceDrug resistanceDisease progressionMouse modelSingle-cell RNA sequencingPTEN 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 carcinomaCirculating tumor DNA reveals mechanisms of lorlatinib resistance in patients with relapsed/refractory ALK-driven neuroblastoma
Berko E, Witek G, Matkar S, Petrova Z, Wu M, Smith C, Daniels A, Kalna J, Kennedy A, Gostuski I, Casey C, Krytska K, Gerelus M, Pavlick D, Ghazarian S, Park J, Marachelian A, Maris J, Goldsmith K, Radhakrishnan R, Lemmon M, Mossé Y. Circulating tumor DNA reveals mechanisms of lorlatinib resistance in patients with relapsed/refractory ALK-driven neuroblastoma. Nature Communications 2023, 14: 2601. PMID: 37147298, PMCID: PMC10163008, DOI: 10.1038/s41467-023-38195-0.Peer-Reviewed Original ResearchConceptsAnaplastic lymphoma kinaseLorlatinib resistanceTumor DNAPhase 1 trialCirculating tumor DNAPre-clinical studiesResistance mechanismsTumor DNA samplesALK mutationsDisease progressionHeterogeneity of tumorsClinical utilityRAS-MAPK pathwayTherapeutic strategiesLymphoma kinasePatientsResistance mutationsNeuroblastomaProgressionTrialsMutationsBiochemical assaysDNA samplesPoint mutationsLorlatinib
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