2021
Treatment scheduling effects on the evolution of drug resistance in heterogeneous cancer cell populations
Patwardhan GA, Marczyk M, Wali VB, Stern DF, Pusztai L, Hatzis C. Treatment scheduling effects on the evolution of drug resistance in heterogeneous cancer cell populations. Npj Breast Cancer 2021, 7: 60. PMID: 34040000, PMCID: PMC8154902, DOI: 10.1038/s41523-021-00270-4.Peer-Reviewed Original ResearchHeterogeneous cancer cell populationsCancer cell populationsTriple-negative breast cancerSingle-cell RNA sequencingCell populationsFitness advantageRNA sequencingMDA-MB-231 TNBC cellsDrug resistanceMechanisms of resistanceVitro screening assaysClonal dynamicsTNBC cellsScreening assaysResistant clonesPatterns of resistanceConcomitant treatmentTherapy combinationsBreast cancerClinical studiesTreatment doseTreatment scheduleBarcodesSequencingTreatment
2015
The broad‐spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF‐mutant melanoma cells in combination with other signaling pathway inhibitors
Langdon CG, Held MA, Platt JT, Meeth K, Iyidogan P, Mamillapalli R, Koo AB, Klein M, Liu Z, Bosenberg MW, Stern DF. The broad‐spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF‐mutant melanoma cells in combination with other signaling pathway inhibitors. Pigment Cell & Melanoma Research 2015, 28: 417-430. PMID: 25854919, PMCID: PMC5215495, DOI: 10.1111/pcmr.12376.Peer-Reviewed Original ResearchConceptsBRAF-mutant melanomaBRAF inhibitorsCell linesCombination of dovitinibBRAF inhibitor treatmentBRAF mutant melanoma cellsBRAF inhibitor resistanceColorectal carcinoma cell linesBRAF-mutant melanoma cell linesMelanoma cell linesCarcinoma cell linesMetastatic melanomaEffective therapyWild-type BRAF cellsInhibitor treatmentAgent inhibitsPathway inhibitorDovitinibInhibitor resistanceMelanoma cellsMelanomaSecond agentInhibitorsTreatment