2025
Neoadjuvant cabozantinib for locally advanced nonmetastatic clear cell renal cell carcinoma: a phase 2 trial
Bilen M, Vo B, Liu Y, Greenwald R, Davarpanah A, McGuire D, Shiradkar R, Li L, Midya A, Nazha B, Brown J, Williams S, Session W, Russler G, Caulfield S, Joshi S, Narayan V, Filson C, Ogan K, Kucuk O, Carthon B, Del Balzo L, Cohen A, Boyanton A, Prokhnevska N, Cardenas M, Sobierajska E, Jansen C, Patil D, Nicaise E, Osunkoya A, Kissick H, Master V. Neoadjuvant cabozantinib for locally advanced nonmetastatic clear cell renal cell carcinoma: a phase 2 trial. Nature Cancer 2025, 6: 432-444. PMID: 40016487, DOI: 10.1038/s43018-025-00922-5.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnilidesCarcinoma, Renal CellFemaleHumansKidney NeoplasmsMaleMiddle AgedNeoadjuvant TherapyProtein Kinase InhibitorsPyridinesQuality of LifeTreatment OutcomeConceptsNonmetastatic clear cell renal cell carcinomaRenal cell carcinomaClear cell renal cell carcinomaCell renal cell carcinomaCD8+ T cellsT cellsCell carcinomaAdverse eventsStem-like CD8+ T cellsMetastatic renal cell carcinomaPalmar-plantar erythrodysesthesia syndromeSingle-arm clinical trialOral multikinase inhibitorDisease-free survivalPhase 2 trialSecondary end pointsCabozantinib treatmentNeoadjuvant settingStable diseaseBiopsy-provenPartial responseSurgical resectionOverall survivalMultikinase inhibitorMyeloid populationsFAK 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 cellsContinued Treatment with Nintedanib in Patients with Progressive Pulmonary Fibrosis: Data from INBUILD-ON
Wuyts W, Bonella F, Chaudhuri N, Varone F, Antin-Ozerkis D, Song J, Miede C, Dumistracel M, Coeck C, Cottin V. Continued Treatment with Nintedanib in Patients with Progressive Pulmonary Fibrosis: Data from INBUILD-ON. Lung 2025, 203: 25. PMID: 39789408, PMCID: PMC11717875, DOI: 10.1007/s00408-024-00778-z.Peer-Reviewed Original ResearchConceptsProgressive pulmonary fibrosisForced vital capacityAdverse eventsSafety profilePulmonary fibrosisConclusionThe safety profileDiscontinuation of nintedanibExposure to nintedanibSafety of nintedanibOpen-label extensionBaseline to weekFrequent adverse eventsFatal adverse eventsLong-term treatmentLonger-term treatmentNintedanib groupGastrointestinal eventsINBUILD trialNintedanibMethodsAdverse eventsModerate severityPatientsContinuous treatmentVital capacityINBUILD
2024
A Phase 2 study of Savolitinib in Patients with MET Amplified Metastatic Colorectal Cancer
Jia J, Moyer A, Lowe M, Bolch E, Kortmansky J, Cho M, Lenz H, Kalyan A, Niedzwiecki D, Strickler J. A Phase 2 study of Savolitinib in Patients with MET Amplified Metastatic Colorectal Cancer. Journal Of Gastrointestinal Cancer 2024, 56: 29. PMID: 39652198, DOI: 10.1007/s12029-024-01156-x.Peer-Reviewed Original ResearchMeSH KeywordsAgedColorectal NeoplasmsFemaleGene AmplificationHumansMaleMiddle AgedProtein Kinase InhibitorsProto-Oncogene Proteins c-metTriazinesConceptsTreatment-emergent adverse eventsMetastatic colorectal cancerPhase 2 studyEpidermal growth factor receptorAnti-tumor activityStable diseaseProgressive diseaseChemotherapy refractory metastatic colorectal cancerOral small-molecule tyrosine kinase inhibitorColorectal cancerResistance to epidermal growth factor receptorSmall molecule tyrosine kinase inhibitorsRefractory metastatic colorectal cancerBest overall responseRAS wild-typeAdvanced solid tumorsBiomarker-selected patientsTyrosine kinase inhibitorsWild-typeGrowth factor receptorResultsFive patientsPrimary endpointSecondary endpointsSolid tumorsSavolitinibSequencing of Checkpoint or BRAF/MEK Inhibitors on Brain Metastases in Melanoma.
Ascierto P, Mandalà M, Ferrucci P, Guidoboni M, Rutkowski P, Ferraresi V, Arance A, Guida M, Maiello E, Gogas H, Richtig E, Quaglino P, Lebbé C, Helgadottir H, Queirolo P, Spagnolo F, Tucci M, Del Vecchio M, Gonzalez-Cao M, Minisini A, De Placido S, Sanmamed M, Casula M, Bulgarelli J, Pisano M, Piccinini C, Piccin L, Cossu A, Mallardo D, Paone M, Vitale M, Melero I, Grimaldi A, Giannarelli D, Palmieri G, Dummer R, Sileni V. Sequencing of Checkpoint or BRAF/MEK Inhibitors on Brain Metastases in Melanoma. NEJM Evidence 2024, 3: evidoa2400087. PMID: 39315864, DOI: 10.1056/evidoa2400087.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitionBrain metastasesBRAF/MEK inhibitorsArm BArm AProgressive diseaseCheckpoint inhibitionBrain metastases-free survivalImmune checkpoint inhibitor ipilimumabMetastases-free survival ratesDevelopment of brain metastasesCheckpoint inhibitor ipilimumabMetastases-free survivalUnresectable metastatic melanomaV600-mutant melanomaCheckpoint inhibitorsInhibitor ipilimumabMetastatic melanomaBRAF/MEK inhibitionArm CReviewed patientsBRAF/MEKThree-arm trialEncorafenibFollow-upClass 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 strategiesPreclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer
Hartwich T, Mansolf M, Demirkiran C, Greenman M, Bellone S, McNamara B, Nandi S, Alexandrov L, Yang‐Hartwich Y, Coma S, Pachter J, Santin A. Preclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer. Cancer Medicine 2024, 13: e70210. PMID: 39240189, PMCID: PMC11378359, DOI: 10.1002/cam4.70210.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBenzamidesCarcinoma, EndometrioidCell Line, TumorCell ProliferationEndometrial NeoplasmsExome SequencingFemaleFocal Adhesion Kinase 1HumansImidazolesMiceNeoplasm GradingOxazepinesProtein Kinase InhibitorsPyrazinesSulfonamidesXenograft Model Antitumor AssaysConceptsFocal adhesion kinaseWhole-exome sequencingEndometrial cancer cell linesVS-4718Cell linesRas/MAPK pathwayPhosphorylated focal adhesion kinaseWestern blot assayWhole-exome sequencing resultsRAF/MEK inhibitionEAC cell linesBlot assayP-FAKGenetic landscapeCell cycleEndometrial cancerGenetic derangementsDefactinibP-MEKGrowth inhibitionRAF/MEKRas/MAPKCell viabilityP-ERKHigh-grade endometrial cancerCell-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 sensitivityGastrointestinal Cancer Therapy and Cardiotoxicity
Leiva O, Zarif T, Alvarez-Cardona J. Gastrointestinal Cancer Therapy and Cardiotoxicity. Current Treatment Options In Oncology 2024, 25: 1203-1209. PMID: 39102169, DOI: 10.1007/s11864-024-01236-x.Peer-Reviewed Original ResearchConceptsTyrosine kinase inhibitorsGastrointestinal cancerAnti-vascular endothelial growth factorHeterogeneous group of cancersCancer-specific outcomesEndothelial growth factorGroup of cancersConventional chemotherapyCardiotoxic therapiesTargeted therapyPotential cardiotoxicityKinase inhibitorsRisk factorsCardiovascular diseaseGrowth factorCancerHeterogeneous groupTherapyCardiotoxicityImmunotherapyChemotherapyPatientsEmerging therapeutic options for follicular-derived thyroid cancer in the era of immunotherapy
Turner N, Hamidi S, Ouni R, Rico R, Henderson Y, Puche M, Alekseev S, Colunga-Minutti J, Zafereo M, Lai S, Kim S, Cabanillas M, Nurieva R. Emerging therapeutic options for follicular-derived thyroid cancer in the era of immunotherapy. Frontiers In Immunology 2024, 15: 1369780. PMID: 38868771, PMCID: PMC11167082, DOI: 10.3389/fimmu.2024.1369780.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma, FollicularAnimalsHumansImmunotherapyIodine RadioisotopesProtein Kinase InhibitorsThyroid NeoplasmsConceptsAnaplastic thyroid cancerFollicular-derived thyroid cancersAdvanced thyroid cancerThyroid cancerFood and Drug AdministrationManagement of advanced thyroid cancerEra of immunotherapyTargeted kinase inhibitorsU.S Food and Drug AdministrationImmune milieuRefractory diseaseExcellent prognosisTherapeutic optionsTreatment optionsKinase inhibitorsDrug AdministrationGenetic driversTherapeutic avenuesCancerImmunotherapyGenetic landscapeRadioiodineTreatmentMolecular basisOptionsTransformation to small cell lung cancer is irrespective of EGFR and accelerated by SMAD4-mediated ASCL1 transcription independently of RB1 in non-small cell lung cancer
Ding X, Shi M, Liu D, Cao J, Zhang K, Zhang R, Zhang L, Ai K, Su B, Zhang J. Transformation to small cell lung cancer is irrespective of EGFR and accelerated by SMAD4-mediated ASCL1 transcription independently of RB1 in non-small cell lung cancer. Cell Communication And Signaling 2024, 22: 45. PMID: 38233864, PMCID: PMC10795321, DOI: 10.1186/s12964-023-01260-8.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerSmall cell lung cancerSmall cell lung cancer transformationCell lung cancerTransformation to small cell lung cancerLung cancerEGFR-mutant non-small cell lung cancerMYC inhibitorsNon-small cell lung cancer patientsMechanisms of TKI resistanceEGFR mutation statusResistant lung cancerNon-small cell lung cancer cellsDriver gene statusPhenotype in vitroCancer-related genesPotential functional genesPutative gene functionsCRISPR-Cas 9SCLC transformationTKI resistanceMutation statusNeuroendocrine phenotypeRB1 statusClinical characteristicsSequential immunotherapy and targeted therapy for metastatic BRAF V600 mutated melanoma: 4-year survival and biomarkers evaluation from the phase II SECOMBIT trial
Ascierto P, Casula M, Bulgarelli J, Pisano M, Piccinini C, Piccin L, Cossu A, Mandalà M, Ferrucci P, Guidoboni M, Rutkowski P, Ferraresi V, Arance A, Guida M, Maiello E, Gogas H, Richtig E, Fierro M, Lebbe C, Helgadottir H, Queirolo P, Spagnolo F, Tucci M, Del Vecchio M, Cao M, Minisini A, De Placido S, Sanmamed M, Mallardo D, Paone M, Vitale M, Melero I, Grimaldi A, Giannarelli D, Dummer R, Sileni V, Palmieri G. Sequential immunotherapy and targeted therapy for metastatic BRAF V600 mutated melanoma: 4-year survival and biomarkers evaluation from the phase II SECOMBIT trial. Nature Communications 2024, 15: 146. PMID: 38167503, PMCID: PMC10761671, DOI: 10.1038/s41467-023-44475-6.Peer-Reviewed Original ResearchConceptsOverall survivalSurvival outcomesNoncomparative phase II trialTotal progression-free survivalLong-term survival outcomesMEK inhibitionBRAF/MEK inhibitionFirst-line treatment approachFirst-line treatment optionBRAF/MEK inhibitorsT-lymphocyte antigen-4Cell death protein 1BRAFV600-mutant melanomaDual checkpoint blockadeFirst-line immunotherapyMetastatic BRAF V600Serum interferon gammaPhase II trialProgression-free survivalDeath protein 1BRAFV600-mutant metastatic melanomaLow baseline levelsBiomarker analysisCombination BRAFSequential immunotherapyReal‐world analysis of adverse event rates after initiation of ibrutinib among Medicare beneficiaries with chronic lymphocytic leukemia
Huntington S, de Nigris E, Puckett J, Kamal‐Bahl S, Farooqui M, Ryland K, Sarpong E, Leng S, Yang X, Doshi J. Real‐world analysis of adverse event rates after initiation of ibrutinib among Medicare beneficiaries with chronic lymphocytic leukemia. Cancer Medicine 2024, 13: e6953. PMID: 38348963, PMCID: PMC10832339, DOI: 10.1002/cam4.6953.Peer-Reviewed Original ResearchMeSH KeywordsAdenineAgedHumansLeukemia, Lymphocytic, Chronic, B-CellMedicarePiperidinesProtein Kinase InhibitorsUnited StatesConceptsChronic lymphocytic leukemiaRate of adverse eventsIncidence rate of adverse eventsAdverse eventsPatient-monthsLymphocytic leukemiaIncidence ratePatients treated with ibrutinibTreatment of chronic lymphocytic leukemiaStandard-of-care therapyNon-discontinuationInitiation of ibrutinibBTK inhibitor ibrutinibAdverse event ratesPotential side effectsInhibitor ibrutinibMedicare beneficiariesReal-world analysisAtrial fibrillationFollow-upIbrutinibSide effectsReal-world outcomesEvent ratesLeukemiaCombined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1
Hu R, Hou H, Li Y, Zhang M, Li X, Chen Y, Guo Y, Sun H, Zhao S, Liao M, Cao D, Yan Q, Chen X, Yin M. Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1. Theranostics 2024, 14: 593-607. PMID: 38169595, PMCID: PMC10758063, DOI: 10.7150/thno.85437.Peer-Reviewed Original ResearchConceptsMEK inhibitor resistanceMEK inhibitor trametinibTrametinib treatmentInhibitor resistanceInhibitor trametinibMelanoma patientsYAP1 expressionMEK inhibitionBRAF-mutant melanoma patientsResistance to MEK inhibitionYAP1 inhibitionResistance to trametinibMelanoma growth <i>inInhibition of BRD4Trametinib resistanceAntitumor effectMelanoma growthTrametinibNHWD-870YAP1 inhibitorDrug resistanceMelanomaMelanoma samplesMelanoma cellsBRD4 depletion
2023
Elimusertib has anti-tumor activity in preclinical patient-derived pediatric solid tumor models
Pusch F, García H, Xu R, Gürgen D, Bei Y, Brückner L, Röefzaad C, von Stebut J, Bardinet V, Gonzalez R, Eggert A, Schulte J, Hundsdörfer P, Seifert G, Haase K, Schäfer B, Wachtel M, Kühl A, Ortiz M, Wengner A, Scheer M, Henssen A. Elimusertib has anti-tumor activity in preclinical patient-derived pediatric solid tumor models. Molecular Cancer Therapeutics 2023, 23: 507-519. PMID: 38159110, PMCID: PMC10985474, DOI: 10.1158/1535-7163.mct-23-0094.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsBiomarkersCell Line, TumorChildHumansNeoplasmsProtein Kinase InhibitorsXenograft Model Antitumor AssaysConceptsPatient-derived xenograftsPediatric solid tumor modelsPreclinical antitumor activitySolid tumor modelsTumor modelStandard-of-care chemotherapyAntitumor activityInhibitor of ataxia telangiectasiaSolid tumor entitiesClinically meaningful responseAnti-tumor activityPreclinical activityRad3-related proteinTumor entitiesPediatric malignanciesAntitumor effectCancer entitiesResponse biomarkersSmall molecule inhibitorsClinical trialsElimusertibMeaningful responseAtaxia telangiectasiaResponse rateCell linesALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells
Bergaggio E, Tai W, Aroldi A, Mecca C, Landoni E, Nüesch M, Mota I, Metovic J, Molinaro L, Ma L, Alvarado D, Ambrogio C, Voena C, Blasco R, Li T, Klein D, Irvine D, Papotti M, Savoldo B, Dotti G, Chiarle R. ALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells. Cancer Cell 2023, 41: 2100-2116.e10. PMID: 38039964, PMCID: PMC10793157, DOI: 10.1016/j.ccell.2023.11.004.Peer-Reviewed Original ResearchMeSH KeywordsAnaplastic Lymphoma KinaseAntigens, NeoplasmCell Line, TumorHumansNeuroblastomaProtein Kinase InhibitorsT-LymphocytesConceptsALK inhibitorsALK expressionChimeric antigen receptor TBest tumor antigensPromising clinical activityExpression of ALKMost normal tissuesHematologic malignanciesClinical activityMost neuroblastomasAnaplastic lymphoma kinase (ALK) receptorTherapeutic successTumor antigensPotent efficacySolid tumorsTherapeutic efficacyNeuroblastomaTumor growthOncogenic driversNeuroblastoma cellsNormal tissuesALKKinase receptorsMonotherapyInhibitorsHOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway by regulating MSK1 and PPP2R2B
Malvi P, Chava S, Cai G, Hu K, Zhu L, Edwards Y, Green M, Gupta R, Wajapeyee N. HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway by regulating MSK1 and PPP2R2B. Cell Reports Medicine 2023, 4: 101285. PMID: 37951219, PMCID: PMC10694669, DOI: 10.1016/j.xcrm.2023.101285.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, Pancreatic DuctalCell ProliferationMammalsMiceNeoplasm ProteinsPancreatic NeoplasmsProtein Kinase InhibitorsTOR Serine-Threonine KinasesConceptsPancreatic ductal adenocarcinomaHomeobox C6PDAC growthInsulin-like growth factor 1 receptorGrowth factor 1 receptorKinase MSK1Factor 1 receptorTranscription factorsPancreatic cancer growthMSK1Tumor growthPDAC tumor growthMost pancreatic ductal adenocarcinomasMammalian targetIGF1R inhibitorsTherapeutic vulnerabilitiesRapamycin (mTOR) pathway activationMEK inhibitor trametinibMetastasis pathwaysPDAC mouse modelPDAC cellsMTOR inhibitionPharmacological inhibitionPathway activationInhibition blocksTheoretical analysis reveals a role for RAF conformational autoinhibition in paradoxical activation
Mendiratta G, Stites E. Theoretical analysis reveals a role for RAF conformational autoinhibition in paradoxical activation. ELife 2023, 12: e82739. PMID: 37823369, PMCID: PMC10627510, DOI: 10.7554/elife.82739.Peer-Reviewed Original ResearchInhibition of a lower potency target drives the anticancer activity of a clinical p38 inhibitor
Bhattacharjee D, Bakar J, Chitnis S, Sausville E, Ashtekar K, Mendelson B, Long K, Smith J, Heppner D, Sheltzer J. Inhibition of a lower potency target drives the anticancer activity of a clinical p38 inhibitor. Cell Chemical Biology 2023, 30: 1211-1222.e5. PMID: 37827156, PMCID: PMC10715717, DOI: 10.1016/j.chembiol.2023.09.013.Peer-Reviewed Original ResearchMeSH KeywordsErbB ReceptorsHumansLung NeoplasmsMitogen-Activated Protein Kinase 14MutationProtein Kinase InhibitorsLarotrectinib efficacy and safety in adult patients with tropomyosin receptor kinase fusion sarcomas
Kummar S, Shen L, Hong D, McDermott R, Keedy V, Casanova M, Demetri G, Dowlati A, Melcón S, Lassen U, Leyvraz S, Liu T, Moreno V, Patel J, Patil T, Mallick A, Sousa N, Tahara M, Ziegler D, Norenberg R, Arvis P, Brega N, Drilon A, Tan D. Larotrectinib efficacy and safety in adult patients with tropomyosin receptor kinase fusion sarcomas. Cancer 2023, 129: 3772-3782. PMID: 37769113, PMCID: PMC11265530, DOI: 10.1002/cncr.35036.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultBone NeoplasmsChildGene FusionHumansNeoplasmsOncogene Proteins, FusionProtein Kinase InhibitorsPyrazolesReceptor, trkASarcomaSoft Tissue NeoplasmsTropomyosinConceptsTropomyosin receptor kinaseNTRK gene fusionsAdult patientsFusion sarcomaAdverse eventsData cutoffGrade 3 treatment-emergent adverse eventsTropomyosin receptor kinase fusion cancerCohort of adult patientsClinical management of adult patientsExtended survival benefitSafety of larotrectinibManagement of adult patientsGastrointestinal stromal tumorsSoft tissue sarcomasTreatment of patientsFirst-in-classGene fusionsInvestigator-assessedNTRK genesReceptor kinaseStromal tumorsSurvival benefitPediatric patientsSolid tumors
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