2016
The HIV-protease inhibitor saquinavir reduces proliferation, invasion and clonogenicity in cervical cancer cell lines
Bandiera E, Todeschini P, Romani C, Zanotti L, Erba E, Colmegna B, Bignotti E, Santin AD, Sartori E, Odicino FE, Pecorelli S, Tassi RA, Ravaggi A. The HIV-protease inhibitor saquinavir reduces proliferation, invasion and clonogenicity in cervical cancer cell lines. Oncology Letters 2016, 12: 2493-2500. PMID: 27698818, PMCID: PMC5038480, DOI: 10.3892/ol.2016.5008.Peer-Reviewed Original ResearchCC cell linesCervical cancerCell linesCell proliferationHIV protease inhibitor saquinavirProteasomal activityActive antiretroviral therapyHuman immunodeficiency virusCell invasionDirect antitumor activityCervical cancer cell linesHIV protease inhibitorsAntiretroviral therapyCancer cell linesSaquinavir concentrationsImmunodeficiency virusPropidium iodide stainingInhibitor saquinavirMatrigel chamberAntineoplastic effectsInnovative therapiesClinical modelSaquinavirCytometric analysisTherapeutic agents
2014
The PD-1 pathway as a therapeutic target to overcome immune escape mechanisms in cancer
Henick BS, Herbst RS, Goldberg SB. The PD-1 pathway as a therapeutic target to overcome immune escape mechanisms in cancer. Expert Opinion On Therapeutic Targets 2014, 18: 1407-1420. PMID: 25331677, DOI: 10.1517/14728222.2014.955794.Peer-Reviewed Original ResearchConceptsPD-1 pathwayEarly clinical trialsClinical trialsTumor typesDeath-1 pathway inhibitorsPD-1 pathway inhibitionImmune escape mechanismsOngoing clinical trialsEarly-stage cancerTreatment of cancerCure rateLikely respondersCancer immunotherapyPreclinical dataAntineoplastic effectsTherapeutic targetPathway inhibitionPathway inhibitorCancer typesBiological rationaleCancer treatmentMonoclonal antibodiesEscape mechanismsUpcoming trialsTrials
2013
Human Vγ2Vδ2 T cells limit breast cancer growth by modulating cell survival‐, apoptosis‐related molecules and microenvironment in tumors
Aggarwal R, Lu J, Kanji S, Das M, Joseph M, Lustberg M, Ray A, Pompili V, Shapiro C, Das H. Human Vγ2Vδ2 T cells limit breast cancer growth by modulating cell survival‐, apoptosis‐related molecules and microenvironment in tumors. International Journal Of Cancer 2013, 133: 2133-2144. PMID: 23595559, PMCID: PMC3939063, DOI: 10.1002/ijc.28217.Peer-Reviewed Original ResearchConceptsΓδ T cellsVγ2Vδ2 T cellsT cellsApoptosis-related moleculesAntineoplastic effectsVγ2Vδ2 T-cell subsetTumor cellsInfiltration of tumorsMICA/BT cell subsetsHuman Vγ2Vδ2 T cellsBreast cancer growthExpression levelsInnate immune systemMolecular signalingBreast tumor cellsMDA-MB-231Resistant cell linesCell subsetsSurface expression levelsCancer growthImmune systemTumor growthMalignant transformationTumor progression
2003
The effects of fish oil, olive oil, oleic acid and linoleic acid on colorectal neoplastic processes
LLOR X, PONS E, ROCA A, ÀLVAREZ M, MAÑÉ J, FERNÁNDEZ-BAÑARES F, GASSULL MA. The effects of fish oil, olive oil, oleic acid and linoleic acid on colorectal neoplastic processes. Clinical Nutrition 2003, 22: 71-79. PMID: 12553953, DOI: 10.1054/clnu.2002.0627.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCaco-2 CellsCells, CulturedCyclooxygenase 2Fish OilsGenes, bcl-2HT29 CellsHumansIsoenzymesKeratin-8KeratinsLinoleic AcidMembrane ProteinsMicroscopy, FluorescenceOleic AcidOlive OilPlant OilsProstaglandin-Endoperoxide SynthasesReverse Transcriptase Polymerase Chain ReactionSucrase-Isomaltase ComplexThymidineConceptsColorectal cancer developmentCOX-2Bcl-2 expressionFish oilCancer developmentHT-29 colorectal cancer cellsCell proliferationLinoleic acidColorectal cancer cellsMain dietary sourceFatty acidsLate effectsColorectal carcinogenesisAntineoplastic effectsNeoplastic processInduction of apoptosisEarly downregulationImportant mediatorOlive oilCancer cellsCaco-2Dietary sourcesBcl-2Different fatsApoptosis induction
1987
Effects of the mode of administration of mitomycin on tumor and marrow response and on the therapeutic ratio.
Rockwell S, Nierenburg M, Irvin C. Effects of the mode of administration of mitomycin on tumor and marrow response and on the therapeutic ratio. Journal Of The National Cancer Institute 1987, 71: 927-34. PMID: 3652056.Peer-Reviewed Original ResearchConceptsDoses of mitomycinTherapeutic ratioSingle injectionDaily injectionsAntineoplastic effectsSurvival curvesEMT6 mouse mammary tumorsHost toxicityBALB/c miceLarge single doseTumor growth assaysEffect of mitomycinLess host toxicityMouse mammary tumorsResponse of tumorsBone marrow stem cellsMode of administrationMarrow stem cellsSublethal lesionsMarrow responseDaily fractionsSingle doseTumor responseC miceClinical impression
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