0000000000049843

AUTHOR

Richard A. Franklin

0000-0003-0299-9578

showing 5 related works from this author

Advances in Targeting Signal Transduction Pathways

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Lin Sun 1,2 , Nicole M. Davis 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Lucio Cocco 3 , Camilla Evangelisti 4 , Francesca Chiarini 4 , Alberto M. Martelli 3,4 , Massimo Libra 5 , Saverio Candido 5 , Giovanni Ligresti 5 , Grazia Malaponte 5 , Maria C. Mazzarino 5 , Paolo Fagone 5 , Marco Donia 5 , Ferdinando Nicoletti 5 , Jerry Polesel 6 , Renato Talamini 6 , Jorg Basecke 7 , Sanja Mijatovic 8 , Danijela Maksimovic-Ivanic 8 , Michele Milella 9 , Agostino Tafuri 10 , Joanna Dulinska-Litewka 11 , Piotr Laidler 11 , Antonio B. D’Assoro 12 , Lyudmyla Drobot 13 , Kazuo Umezawa 14 , Giuseppe Montalto 15 , Melchiorre Cer…

cancer stem cellsAMPKtherapy resistanceReviewsLibrary scienceAntineoplastic AgentsrafBiologyPI3Kampk03 medical and health sciences0302 clinical medicineCANCER STEM CELLSNeoplasmsAnimalsHumansUniversity medicalMolecular Targeted TherapyAkt; AMPK; Cancer stem cells; Metformin; MTOR; PI3K; Raf; Targeted therapy; Therapy resistanceTreatment resistanceProtein Kinase Inhibitors030304 developmental biology0303 health sciencesRoswell Park Cancer InstituteAktCancer stem cellAKTMTORAMP-ACTIVATED PROTEIN KINASE (AMPK)Raftargeted therapyMetformin3. Good healthGene Expression Regulation NeoplasticCell stressOncologyDrug Resistance NeoplasmDrug Designtargeted therapy; metformin; therapy resistance; pi3k; akt; ampk; cancer stem cells; raf; mtor030220 oncology & carcinogenesisMutationmTORMolecular targetsCancer researchmetforminSignal Transduction
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: Rationale and importance to inhibiting these pathways in human health

2011

William H. Chappell 1 , Linda S. Steelman 1,2 , Jacquelyn M. Long 2 , Ruth C. Kempf 2 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Jorg Basecke 3 , Franca Stivala 4 , Marco Donia 4 , Paolo Fagone 4 , Graziella Malaponte 4 , Maria C. Mazzarino 4 , Ferdinando Nicoletti 4 , Massimo Libra 4 , Danijela Maksimovic-Ivanic 5 , Sanja Mijatovic 5 , Giuseppe Montalto 6 , Melchiorre Cervello 7 , Piotr Laidler 8 , Michele Milella 9 , Agostino Tafuri 10 , Antonio Bonati 11 , Camilla Evangelisti 12 , Lucio Cocco 12 , Alberto M. Martelli 12,13 , and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University 2 Department of Physics, Greenville, N…

MAPK/ERK pathwayAgingmedicine.medical_treatmentDrug ResistancerafPI3KTargeted therapycombination therapyPhosphatidylinositol 3-Kinases0302 clinical medicineTARGETED THERAPYCANCER STEM CELLSNeoplasmsCancer Stem CellsMedicineExtracellular Signal-Regulated MAP Kinases0303 health sciencesCombination TherapybiologyTOR Serine-Threonine KinasesMTORHuman health Ras inhibitors MEK ERKTargeted TherapyDiscovery and development of mTOR inhibitors3. Good healthDRUG RESISTANCECell Transformation NeoplasticOncology030220 oncology & carcinogenesismTORraf KinasesPremature agingMAP Kinase Signaling SystemReviewsSenescence03 medical and health sciencesCell Line TumorHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyMitogen-Activated Protein Kinase Kinasesbusiness.industryAKTAktagingPTEN PhosphohydrolaseRafTransplantationSENESCENCEImmunologyras Proteinsbiology.proteinCancer researchaging; akt; cancer stem cells; combination therapy; drug resistance; mtor; pi3k; raf; senescence; targeted therapybusinessProto-Oncogene Proteins c-akt
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: How mutations can result in therapy resistance and how to overcome resistance

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Giuseppe Montalto 2 , Melchiorre Cervello 3 , Massimo Libra 4 , Saverio Candido 4 , Grazia Malaponte 4 , Maria C. Mazzarino 4 , Paolo Fagone 4 , Ferdinando Nicoletti 4 , Jorg Basecke 5 , Sanja Mijatovic 6 , Danijela Maksimovic-Ivanic 6 , Michele Milella 7 , Agostino Tafuri 8 , Francesca Chiarini 9 , Camilla Evangelisti 9 , Lucio Cocco 10 , Alberto M. Martelli 9,10 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 3 Consi…

MAPK/ERK pathwaymedicine.medical_treatmentPI3KTargeted therapyTargeted therapyPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsTreatment resistanceExtracellular Signal-Regulated MAP KinasesPhosphoinositide-3 Kinase InhibitorsGenetics0303 health sciencesbiologyCancer stem cellsTOR Serine-Threonine KinasesMAP Kinase Kinase KinasesDiscovery and development of mTOR inhibitorshumanities3. Good healthOncology030220 oncology & carcinogenesismTORSignal TransductionProto-Oncogene Proteins B-rafReviewsAntineoplastic Agents03 medical and health sciencesCell Line TumormedicineHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologybusiness.industryAkt; Cancer stem cells; mTOR; PI3K; Raf; Targeted therapy; Therapy resistanceAktPTEN PhosphohydrolaseTherapy resistanceRafProtein phosphatase 2Targeted Therapy Therapy Resistance Cancer Stem Cells Raf Akt PI3K mTORDrug Resistance NeoplasmMutationras ProteinsCancer researchbiology.proteinbusinessProto-Oncogene Proteins c-akt
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New agents and approaches for targeting the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR cell survival pathways.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have…

MAPK/ERK pathway0303 health sciencesCell signalingbiologyChemistryAKTApoptosisGrowth factorRafOncogens: Signaling pathway3. Good healthMalignant transformation03 medical and health sciences0302 clinical medicineApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinEpidermal growth factor receptorSignal transductionpi3kProtein kinase BRaPI3K/AKT/mTOR pathway030304 developmental biology
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Ectopic NGAL expression can alter sensitivity of breast cancer cells to EGFR, Bcl-2, CaM-K inhibitors and the plant natural product berberine

2012

Neutrophil gelatinase-associated lipocalin (NGAL, a.k.a Lnc2) is a member of the lipocalin family and has diverse roles. NGAL can stabilize matrix metalloproteinase-9 from autodegradation. NGAL is considered as a siderocalin that is important in the transport of iron. NGAL expression has also been associated with certain neoplasias and is implicated in the metastasis of breast cancer. In a previous study, we examined whether ectopic NGAL expression would alter the sensitivity of breast epithelial, breast and colorectal cancer cells to the effects of the chemotherapeutic drug doxorubicin. While abundant NGAL expression was detected in all the cells infected with a retrovirus encoding NGAL, t…

BenzylaminesBerberinemedicine.medical_treatmentDrug ResistanceGene ExpressionBCL-2; Berberine; Breast cancer; Calmodulin kinase; Colorectal cancer; EGFR; Inhibitor sensitivity; Lcn2; Lipocalins; NGAL; Rapamycin; Siderocalins; Targeted therapyPiperazinesMetastasisTargeted therapyNitrophenolsTargeted therapyBreast cancerAntibioticsNGALSulfonamidesAntibiotics AntineoplasticTumorSiderocalinsTyrphostinsAntineoplasticLipocalinsBiphenyl compoundErbB ReceptorsProto-Oncogene Proteins c-bcl-2MCF-7 CellsFemalelipocalinHT29 Cellsmedicine.drugbcl-2; breast cancer; lipocalins; targeted therapy; berberine; lcn2; colorectal cancer; rapamycin; inhibitor sensitivity; siderocalins; egfr; ngal; calmodulin kinaseCalmodulin kinasesiderocalinEGFRBCL-2Breast NeoplasmsSiderocalinBiologyNGAL Lcn2 lipocalins siderocalins targeted therapy inhibitor sensitivity EGFR rapamycin berberine BCL-2 calmodulin kinase breast cancer colorectal cancerCell LineHT29 CellsLcn2Lipocalin-2ReportCell Line TumorProto-Oncogene ProteinsmedicineHumansDoxorubicinRapamycinMolecular BiologyProtein Kinase InhibitorsSirolimusBiphenyl CompoundsCell Biologymedicine.diseaseColorectal cancerCell cultureDoxorubicinDrug Resistance NeoplasmCancer cellCalcium-Calmodulin-Dependent Protein KinasesCancer researchQuinazolinesNeoplasmInhibitor sensitivityDevelopmental BiologyAcute-Phase Proteins
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