0000000000529798

AUTHOR

Chiara Mondello

0000-0002-8379-9246

showing 4 related works from this author

Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

2015

As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.

Cancer ResearchReviewHazardous Substanceschemistry.chemical_compoundNeoplasmsAnimalsHumansMedicinebiologyAnimalbusiness.industryMedicine (all)Retinoblastoma proteinContact inhibitionCancerEnvironmental ExposureGeneral MedicineEnvironmental exposureEvasion (ethics)medicine.diseaseCell biologychemistryHazardous SubstanceImmunologyCancer cellbiology.proteinNeoplasmSignal transductionGrowth inhibitionbusinessHumanSignal TransductionCarcinogenesis
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Gene amplification in fibroblasts from ataxia telangiectasia (AT) patients and in X-ray hypersensitive AT-like Chinese hamster mutants

2001

In search of functions involved in the regulation of gene amplification, and given the relevance of chromosome breakage in initiating the process, we analyzed the gene amplification ability of cells hypersensitive to inducers of DNA double-strand breaks and defective in cell cycle control: two human fibroblast strains derived from patients affected by ataxia telangiectasia (AT) and two hamster mutant cell lines belonging to complementation group XRCC8 of the rodent X-ray-sensitive mutants. These mutants are considered hamster models of AT cells. To measure gene amplification, the frequency and the rate of occurrence of N-(phosphonacetyl)-l-aspartate resistant cells were determined. In both …

Settore BIO/18 - GeneticaCancer Research gene amplification DNA repair
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Gene amplification in fibroblasts from ataxia telangiectasia (AT) patients and in X-ray hypersensitive AT-like Chinese hamster mutants.

2001

In search of functions involved in the regulation of gene amplification, and given the relevance of chromosome breakage in initiating the process, we analyzed the gene amplification ability of cells hypersensitive to inducers of DNA double-strand breaks and defective in cell cycle control: two human fibroblast strains derived from patients affected by ataxia telangiectasia (AT) and two hamster mutant cell lines belonging to complementation group XRCC8 of the rodent X-ray-sensitive mutants. These mutants are considered hamster models of AT cells. To measure gene amplification, the frequency and the rate of occurrence of N-(phosphonacetyl)-L-aspartate resistant cells were determined. In both …

Phosphonoacetic AcidCancer ResearchAntimetabolites AntineoplasticMutantHamstermedicine.disease_causeRadiation ToleranceChinese hamsterCell LineAtaxia TelangiectasiaCricetulusMultienzyme ComplexesCricetinaeGene duplicationmedicineAspartate CarbamoyltransferaseAnimalsHumansDihydroorotaseMutationAspartic AcidbiologyX-RaysGenetic Complementation TestGene AmplificationGeneral MedicineCell cycleFibroblastsmedicine.diseasebiology.organism_classificationMolecular biologyDrug Resistance NeoplasmAtaxia-telangiectasiaMutationCarbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)Chromosome breakageCarcinogenesis
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Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead

2015

Goodson, William H. et al.

Cancer ResearchCarcinogenesis[SDV]Life Sciences [q-bio]METHOXYCHLOR-INDUCED ALTERATIONSReviewPharmacologyMESH: Carcinogens EnvironmentalCarcinogenic synergiesChemical mixturesNeoplasmsMESH: AnimalsMESH: NeoplasmsCarcinogenesiRisk assessmentCancerACTIVATED PROTEIN-KINASESMedicine (all)Low dose1. No povertyCumulative effectsBREAST-CANCER CELLSGeneral MedicineEnvironmental exposureMESH: CarcinogenesisBIO/10 - BIOCHIMICAEPITHELIAL-MESENCHYMAL TRANSITION3. Good health[SDV] Life Sciences [q-bio]Environmental CarcinogenesisESTROGEN-RECEPTOR-ALPHARisk assessmentHumanMESH: Environmental ExposureENDOCRINE-DISRUPTING CHEMICALSTARGETING TISSUE FACTOR[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPrototypical chemical disruptorsExposure[SDV.CAN] Life Sciences [q-bio]/CancerEnvironmental healthmedicine[SDV.EE.SANT] Life Sciences [q-bio]/Ecology environment/HealthCarcinogenEnvironmental carcinogenesis[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthMESH: HumansAnimalPOLYBROMINATED DIPHENYL ETHERSCancerEnvironmental Exposuremedicine.diseaseMESH: Hazardous SubstancesCarcinogens EnvironmentalMIGRATION INHIBITORY FACTORVASCULAR ENDOTHELIAL-CELLSHazardous SubstanceNeoplasmCarcinogenesis
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