0000000000542929

AUTHOR

Antonella Sistigu

showing 3 related works from this author

CHK1-targeted therapy to deplete DNA replication-stressed, p53-deficient, hyperdiploid colorectal cancer stem cells.

2017

ObjectiveCancer stem cells (CSCs) are responsible for tumour formation and spreading, and their targeting is required for tumour eradication. There are limited therapeutic options for advanced colorectal cancer (CRC), particularly for tumours carrying RAS-activating mutations. The aim of this study was to identify novel CSC-targeting strategies.DesignTo discover potential therapeutics to be clinically investigated as single agent, we performed a screening with a panel of FDA-approved or investigational drugs on primary CRC cells enriched for CSCs (CRC-SCs) isolated from 27 patients. Candidate predictive biomarkers of efficacy were identified by integrating genomic, reverse-phase protein mic…

0301 basic medicinep53DNA ReplicationCELL CYCLE CONTROLDNA damageColorectal cancerColonmedicine.medical_treatmentAntineoplastic AgentsBiologyBioinformaticsmedicine.disease_causeDNA DAMAGETargeted therapy03 medical and health sciencesCancer stem cellCell Line TumormedicineHumansCHEK11506DRUG DEVELOPMENTOligonucleotide Array Sequence AnalysisMutationCOLORECTAL CANCERSettore MED/06 - ONCOLOGIA MEDICAGastroenterologyCHEMOTHERAPYmedicine.diseaseImmunohistochemistryPrexasertib030104 developmental biologyPyrazinesCheckpoint Kinase 1MutationCancer researchNeoplastic Stem CellsPyrazolesStem cellTumor Suppressor Protein p53Colorectal NeoplasmsGut
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Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy

2014

International audience; The immune system is routinely confronted with cell death resulting from the physiological turnover of renewable tissues, as well as from pathological insults of several types. We hypothesize the existence of a mechanism that allows the immune system to discriminate between physiological and pathological instances of cell death, but the factors that determine whether cellular demise is perceived as a neutral, tolerogenic or immunogenic event remain unclear 1. Infectious insults are accompanied by so-called microbe-associated molecular patterns (MAMPs), i.e., viral or bacterial products that activate immune cells through a panel of pattern-recognition receptors (PRRs)…

Myxovirus Resistance ProteinsMessengerReceptor Interferon alpha-betaInbred C57BLchemotherapyInterferon alpha-betaMiceInterferonReceptorsAnthracyclinesNeoplasm MetastasisRIG-IPattern recognition receptorAdaptor ProteinsGeneral MedicineNeoadjuvant Therapy3. Good healthGene Expression Regulation NeoplasticTreatment OutcomeReceptors Pattern RecognitionInterferon Type I[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleImmunocompetencemedicine.drugReceptorSignal TransductionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPattern RecognitionSettore BIO/09General Biochemistry Genetics and Molecular BiologyParacrine signallingImmune systemmedicineCXCL10AnimalsHumanscancerRNA MessengerAutocrine signallingNeoplastic[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyToll-Like Receptor 3Mice Inbred C57BLVesicular TransportChemokine CXCL10Adaptor Proteins Vesicular TransportGene Expression RegulationDoxorubicinImmunologyTLR3RNAAdaptor Proteins Vesicular Transport; Animals; Anthracyclines; Breast Neoplasms; Chemokine CXCL10; Doxorubicin; Female; Gene Expression Regulation Neoplastic; Humans; Immunocompetence; Interferon Type I; Mice Inbred C57BL; Myxovirus Resistance Proteins; Neoadjuvant Therapy; Neoplasm Metastasis; RNA; RNA Messenger; Receptor Interferon alpha-beta; Receptors Pattern Recognition; Toll-Like Receptor 3; Treatment Outcome; Signal Transduction
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Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1.

2015

How dying tumor cells get noticed Besides killing tumor cells directly, some chemotherapies, such as anthracyclines, also activate the immune system to kill tumors. Vacchelli et al. discovered that in mice, anthracycline-induced antitumor immunity requires immune cells to express the protein formyl peptide receptor 1 (FPR1). Dendritic cells (DCs) near tumors expressed especially high amounts of FPR1. DCs normally capture fragments of dying tumor cells and use them to activate nearby T cells to kill tumors, but DCs lacking FPR1 failed to do this effectively. Individuals with breast or colon cancer expressing a variant of FPR1 and treated with anthracyclines showed poor metastasis-free and ov…

AnthracyclineColorectal cancermedicine.medical_treatmentT-LymphocytesBreast Neoplasmsmicrofluidic chipchemotherapyPolymorphism Single NucleotideFormyl peptide receptor 1immune responseMiceImmune systemImmunityCell Line TumorNeoplasmsmedicineLeukocytesAnimalsHumansAnthracyclinesAllelesAnnexin A1ChemotherapyMultidisciplinarybusiness.industryDendritic Cellsmedicine.diseaseReceptors Formyl PeptideImmunity InnateChemotherapy AdjuvantCancer cellImmunologyCancer researchFemalebusinessColorectal NeoplasmsAdjuvantFPR1 microfluidicScience (New York, N.Y.)
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