Search results for "targeted therapeutic"

showing 5 items of 5 documents

Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
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Introduction of WT-TP53 into pancreatic cancer cells alters sensitivity to chemotherapeutic drugs, targeted therapeutics and nutraceuticals

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10%. Mutations at the TP53 gene are readily detected in pancreatic tumors isolated from PDAC patients. We have investigated the effects of restoration of wild-type (WT) TP53 activity on the sensitivity of pancreatic cancer cells to: chemotherapy, targeted therapy, as well as, nutraceuticals. Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisp…

0301 basic medicineCancer ResearchPaclitaxelendocrine system diseasesmedicine.medical_treatmentTargeted therapeuticIrinotecanDeoxycytidineTargeted therapyGlycogen Synthase Kinase 303 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumansDoxorubicinTP53Signal transduction inhibitorneoplasmsMolecular BiologyCell ProliferationCisplatinChemotherapybusiness.industryPancreatic Neoplasmmedicine.diseaseGemcitabinedigestive system diseasesGemcitabinePancreatic NeoplasmsOxaliplatin030104 developmental biologyPaclitaxelchemistryFluorouracil030220 oncology & carcinogenesisCancer researchMolecular MedicineFluorouracilCisplatinbusinessDrug sensitivityHumanSignal Transductionmedicine.drug
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Disparity between Inter-Patient Molecular Heterogeneity and Repertoires of Target Drugs Used for Different Types of Cancer in Clinical Oncology

2020

Inter-patient molecular heterogeneity is the major declared driver of an expanding variety of anticancer drugs and personalizing their prescriptions. Here, we compared interpatient molecular heterogeneities of tumors and repertoires of drugs or their molecular targets currently in use in clinical oncology. We estimated molecular heterogeneity using genomic (whole exome sequencing) and transcriptomic (RNA sequencing) data for 4890 tumors taken from The Cancer Genome Atlas database. For thirteen major cancer types, we compared heterogeneities at the levels of mutations and gene expression with the repertoires of targeted therapeutics and their molecular targets accepted by the current guideli…

Gene mutationMedical OncologychemotherapyGenomeTranscriptomelcsh:ChemistryDrug Delivery SystemsProstateNeoplasmstumor heterogeneityMedicineCluster AnalysisMolecular Targeted TherapyPathology MolecularPrecision Medicinelcsh:QH301-705.5targeted therapeuticscancer drugsSpectroscopyExome sequencingGeneral MedicineGenomicspersonalized medicineComputer Science ApplicationsDrug repositioningmedicine.anatomical_structureAntineoplastic AgentsComputational biologyCatalysisArticleInorganic Chemistrymolecular diagnosticsGenetic HeterogeneityDrug TherapyExome SequencingHumansPhysical and Theoretical ChemistryMolecular Biologygenomeclinical oncologybusiness.industryOrganic ChemistryMolecular diagnosticsmutationslcsh:Biology (General)lcsh:QD1-999MutationPersonalized medicinebusinesstranscriptomeInternational Journal of Molecular Sciences
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Sensitivity of pancreatic cancer cells to chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals can be regulated by WT-TP53

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy. Approximately 85% of pancreatic cancers are classified as PDACs. The survival of PDAC patients is very poor and only 5–10% of patients survive 5 years after diagnosis. Mutations at the KRAS and TP53 gene are frequently observed in PDAC patients. The PANC-28 cell line lacks wild-type (WT) TP53. In the following study, we have investigated the effects of restoration of WT TP53 activity on the sensitivity of PANC-28 pancreatic cancer cells to various drugs which are used to treat PDAC patients as well as other cancer patients. In addition, we have examined the effects of signal transduction inhibitors which tar…

Male0301 basic medicineDrugCancer ResearchmiRsendocrine system diseasesmedia_common.quotation_subjectSignal transduction inhibitorsTargeted therapeuticAntineoplastic AgentsMalignancymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineChloroquinePancreatic cancerGeneticsmedicineHumansTP53Molecular BiologyneoplasmsSignal transduction inhibitorTargeted therapeuticsCell Proliferationmedia_commontarget therapeuticsCell growthbusiness.industryCancermedicine.diseasedigestive system diseasesMetforminPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsMutationCancer researchmiRs.Molecular MedicineFemaleKRASTumor Suppressor Protein p53businessSignal Transductionmedicine.drugDrug sensitivity
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Targeting a Targeted Drug: An Approach Toward Hypoxia-Activatable Tyrosine Kinase Inhibitor Prodrugs

2016

Tyrosine kinase inhibitors (TKIs), which have revolutionized cancer therapy over the past 15 years, are limited in their clinical application due to serious side effects. Therefore, we converted two approved TKIs (sunitinib and erlotinib) into 2-nitroimidazole-based hypoxia-activatable prodrugs. Kinetics studies showed very different stabilities over 24 h; however, fast reductive activation via E. coli nitroreductase could be confirmed for both panels. The anticancer activity and signaling inhibition of the compounds against various human cancer cell lines were evaluated in cell culture. These data, together with molecular docking simulations, revealed distinct differences in the impact of …

medicine.drug_classPharmacology010402 general chemistry01 natural sciencesBiochemistryArticleTyrosine-kinase inhibitor03 medical and health sciencesNitroreductase0302 clinical medicinetyrosine kinase inhibitorsDrug DiscoverymedicinecancerEpidermal growth factor receptorGeneral Pharmacology Toxicology and PharmaceuticsPharmacologybiologyhypoxiaSunitinibChemistryOrganic ChemistryProdrugtargeted therapeutic0104 chemical sciencesSettore CHIM/03 - Chimica Generale E InorganicaCell culture030220 oncology & carcinogenesisbiology.proteinMolecular MedicineErlotinibprodrugTyrosine kinasemedicine.drugChemMedChem
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