2017
Effect of Longer-Interval vs Standard Dosing of Zoledronic Acid on Skeletal Events in Patients With Bone Metastases: A Randomized Clinical Trial
Himelstein AL, Foster JC, Khatcheressian JL, Roberts JD, Seisler DK, Novotny PJ, Qin R, Go RS, Grubbs SS, O’Connor T, Velasco MR, Weckstein D, O’Mara A, Loprinzi CL, Shapiro CL. Effect of Longer-Interval vs Standard Dosing of Zoledronic Acid on Skeletal Events in Patients With Bone Metastases: A Randomized Clinical Trial. JAMA 2017, 317: 48-58. PMID: 28030702, PMCID: PMC5321662, DOI: 10.1001/jama.2016.19425.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBone and BonesBone Density Conservation AgentsBone NeoplasmsBreast NeoplasmsDiphosphonatesDrug Administration ScheduleFemaleHumansImidazolesMaleMiddle AgedMultiple MyelomaPain MeasurementProstatic NeoplasmsSample SizeSpinal Cord CompressionSpinal FracturesZoledronic AcidConceptsSkeletal morbidity rateProportion of patientsDosing groupZoledronic acidBone metastasesMultiple myelomaProstate cancerBreast cancerSkeletal eventsKidney dysfunctionBone turnoverMorbidity rateClinical trialsEastern Cooperative Oncology Group performance statusOpen-label clinical trialEnd pointIncidence of osteonecrosisYear of randomizationPerformance status scorePrimary end pointSecondary end pointsBrief Pain InventoryMetastatic breast cancerMetastatic prostate cancerAcceptable treatment option
2007
Extrinsic pathway- and cathepsin-dependent induction of mitochondrial dysfunction are essential for synergistic flavopiridol and vorinostat lethality in breast cancer cells
Mitchell C, Park MA, Zhang G, Yacoub A, Curiel DT, Fisher PB, Roberts JD, Grant S, Dent P. Extrinsic pathway- and cathepsin-dependent induction of mitochondrial dysfunction are essential for synergistic flavopiridol and vorinostat lethality in breast cancer cells. Molecular Cancer Therapeutics 2007, 6: 3101-3112. PMID: 18065490, DOI: 10.1158/1535-7163.mct-07-0561.Peer-Reviewed Original ResearchConceptsBcl-xLC-FLIPBreast cancer cellsMitogen-activated protein/ERK kinase 1X-chromosome-linked inhibitorCancer cellsExtracellular signal-regulated kinase 1/2Apoptosis protein levelsSignal-regulated kinase 1/2ERK kinase 1CDK inhibitor roscovitineIntrinsic apoptosis pathwayHistone deacetylase inhibitor suberoylanilide hydroxamic acidForm of AktProtease-dependent pathwayInhibition of AktTreatment of cellsBak functionBcl-xL expressionCell killingCyclin-dependent kinase inhibitor flavopiridolInhibitor suberoylanilide hydroxamic acidKinase inhibitor flavopiridolERK1/2 functionAkt activity
2005
Transient exposure of mammary tumors to PD184352 and UCN-01 causes tumor cell death in vivo and prolonged suppression of tumor re-growth
Hawkins W, Mitchell C, McKinstry R, Gilfor D, Starkey J, Dai Y, Dawson K, Ramakrishnan V, Roberts JD, Yacoub A, Grant S, Dent P. Transient exposure of mammary tumors to PD184352 and UCN-01 causes tumor cell death in vivo and prolonged suppression of tumor re-growth. Cancer Biology & Therapy 2005, 4: 1275-1284. PMID: 16319524, DOI: 10.4161/cbt.4.11.2286.Peer-Reviewed Original ResearchConceptsTumor cell deathTumor growthMDA-MB-231Drug exposureTumor volumeUCN-01Cell deathTumor cellsMCF7 tumor growthMDA-MB-231 tumorsMEK1/2 inhibitorMean tumor volumeMammary tumor growthTransient exposureTumor growth rateHuman mammary carcinoma cellsK-RAS expressionCombination index valuesMammary carcinoma cellsColony formation assaysPhosphorylation of ERK1/2Colony formation studiesEstrogen dependencyMammary tumorsProlonged suppression
1989
Effect of tamoxifen on plasma insulin-like growth factor I in patients with breast cancer.
Colletti RB, Roberts JD, Devlin JT, Copeland KC. Effect of tamoxifen on plasma insulin-like growth factor I in patients with breast cancer. Cancer Research 1989, 49: 1882-4. PMID: 2924327.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBreast NeoplasmsFemaleHumansInsulin-Like Growth Factor IMiddle AgedSomatomedinsTamoxifenConceptsInsulin-like growth factor IBreast cancer patientsGrowth factor ICancer patientsPlasma IGFBreast cancerAmbulatory breast cancer patientsPlasma insulin-like growth factor IFactor IPlasma IGF-I concentrationsPlasma IGF-I levelsAntiestrogen agent tamoxifenRecent weight lossIGF-I levelsEffect of tamoxifenIGF-I concentrationsHuman breast cancer cellsSuppression of IGFGrowth hormone-dependent peptideBreast cancer cellsMetastatic diseasePlasma concentrationsPatientsTamoxifenNutritional status