2019
PI3K oncogenic mutations mediate resistance to afatinib in HER2/neu overexpressing gynecological cancers
Bonazzoli E, Cocco E, Lopez S, Bellone S, Zammataro L, Bianchi A, Manzano A, Yadav G, Manara P, Perrone E, Haines K, Espinal M, Dugan K, Menderes G, Altwerger G, Han C, Zeybek B, Litkouhi B, Ratner E, Silasi DA, Huang GS, Azodi M, Schwartz PE, Santin AD. PI3K oncogenic mutations mediate resistance to afatinib in HER2/neu overexpressing gynecological cancers. Gynecologic Oncology 2019, 153: 158-164. PMID: 30630630, PMCID: PMC6430698, DOI: 10.1016/j.ygyno.2019.01.002.Peer-Reviewed Original ResearchMeSH KeywordsAdultAfatinibAgedAnimalsAntineoplastic AgentsCell Line, TumorClass I Phosphatidylinositol 3-KinasesClass Ia Phosphatidylinositol 3-KinaseDrug Resistance, NeoplasmFemaleGenital Neoplasms, FemaleHumansMiceMice, SCIDMiddle AgedMutationPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsReceptor, ErbB-2TransfectionXenograft Model Antitumor AssaysConceptsHER2/neuAKT/mTOR pathwayPIK3CA mutationsMTOR pathwayActivity of afatinibEffect of afatinibPI3K/AKT/mTOR pathwayPotential mechanismsPIK3CA/AKT/mTOR pathwayRapid tumor growthGreater compensatory increasePI3K mutationsAmplification/mutationOncogenic PIK3CA mutationsAfatinib exposurePIK3CA H1047RGynecological cancerClinical trialsMTOR inhibitorsAfatinibTumor growthCompensatory increasePhosphorylated Akt proteinPIK3CA geneC-erb
2010
Inhibition of the c-fms proto-oncogene autocrine loop and tumor phenotype in glucocorticoid stimulated human breast carcinoma cells
Toy EP, Lamb T, Azodi M, Roy WJ, Woo HH, Chambers SK. Inhibition of the c-fms proto-oncogene autocrine loop and tumor phenotype in glucocorticoid stimulated human breast carcinoma cells. Breast Cancer Research And Treatment 2010, 129: 411-419. PMID: 21063905, DOI: 10.1007/s10549-010-1247-7.Peer-Reviewed Original ResearchMeSH KeywordsAutocrine CommunicationBreast NeoplasmsCarcinomaCell AdhesionCell Line, TumorCell MovementDexamethasoneDose-Response Relationship, DrugFemaleGlucocorticoidsHumansMacrophage Colony-Stimulating FactorNeoplasm InvasivenessOligonucleotides, AntisensePhenotypePhenylurea CompoundsProtein Kinase InhibitorsProto-Oncogene MasReceptor, Macrophage Colony-Stimulating FactorRNA InterferenceThiazolesTransfectionConceptsC-fms signalingBreast cancer cellsAntisense oligonucleotide therapyBreast cancerGC stimulationC-fms expressionCancer cellsBreast cancer cell invasionTargeted molecular therapiesHuman breast cancer cellsCo-expressed receptorsAutocrine feedback loopDose-response mannerC-fms mRNAHuman breast carcinoma cellsBreast tumor behaviorReceptor/ligand pairsBreast carcinoma cellsCancer cell invasionInhibition of glucocorticoidsC-fmsAutocrine pathwayClinical utilityParacrine mannerTumor behavior