0000000000445522

AUTHOR

Maitane Asensio

0000-0002-8723-6053

showing 3 related works from this author

Isopetasin and S-isopetasin as novel P-glycoprotein inhibitors against multidrug-resistant cancer cells

2019

Abstract Background A major problem of cancer treatment is the development of multidrug resistance (MDR) to chemotherapy. MDR is caused by different mechanisms such as the expression of the ABC-transporters P-glycoprotein (P-gp, MDR1, ABCB1) and breast cancer resistance protein (BCRP, ABCG2). These transporters efflux xenobiotic toxins, including chemotherapeutics, and they were found to be overexpressed in different cancer types. Purpose Identification of novel molecules that overcome MDR by targeting ABC-transporters. Methods Resazurin reduction assay was used for cytotoxicity test. AutoDock 4.2. was used for molecular docking. The function of P-gp and BCRP was tested using a doxorubicin …

ATP Binding Cassette Transporter Subfamily BAbcg2Pharmaceutical Science03 medical and health sciences0302 clinical medicineCell Line TumorDrug DiscoverymedicineHumansCytotoxic T cell030304 developmental biologyP-glycoproteinPharmacology0303 health sciencesbiologyChemistryCancermedicine.diseaseDrug Resistance MultipleNeoplasm ProteinsMolecular Docking SimulationMultiple drug resistanceComplementary and alternative medicineDrug Resistance NeoplasmApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchMolecular MedicineEffluxSesquiterpenesPhytomedicine
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Molecular bases of the poor response of liver cancer to chemotherapy

2018

Summary A characteristic shared by most frequent types of primary liver cancer, i.e., hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) in adults, and in a lesser extent hepatoblastoma (HB) mainly in children, is their high refractoriness to chemotherapy. This is the result of synergic interactions among complex and diverse mechanisms of chemoresistance (MOC) in which more than 100 genes are involved. Pharmacological treatment, although it can be initially effective, frequently stimulates the expression of MOC genes, which results in the relapse of the tumor, usually with a more aggressive and less chemosensitive phenotype. Identification of the MOC genetic signature accounting fo…

0301 basic medicineHepatoblastomaCarcinoma HepatocellularGenetic enhancementmedicine.medical_treatmentCholangiocarcinoma03 medical and health sciences0302 clinical medicineHumansMedicinecholangiocarcinoma; hepatoblastoma; hepatocellular carcinoma; multidrug resistance; targeted therapies; hepatology; gastroenterologyChemotherapyHepatologybusiness.industryLiver NeoplasmsGastroenterologymedicine.diseasePhenotypeResistome030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisHepatocellular carcinomaCancer cellCancer researchbusinessLiver cancerClinics and Research in Hepatology and Gastroenterology
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Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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