2025
Weight Loss Is Protective in Preclinical Breast Cancer Models: Interactions with the Anticancer Immune Response.
Sassoon R, Perry R. Weight Loss Is Protective in Preclinical Breast Cancer Models: Interactions with the Anticancer Immune Response. Cancer Prevention Research 2025, of1-of2. PMID: 40421602, DOI: 10.1158/1940-6207.capr-25-0168.Peer-Reviewed Original ResearchICR miceIntermittent calorie restrictionE0771 breast cancer cellsPreclinical breast cancer modelsRate of tumor growthTriple-negative breast cancerAnticancer immune responseBreast cancer modelBreast cancer cellsCancer prevention researchAntitumor immunityHigh-fat dietTumor sizeImmune dysfunctionPreclinical evidenceLean controlsPoor prognosisCancer modelsBreast cancerTumor growthOld miceObesogenic dietAdvanced ageIncreased riskImmune response
2024
Modeling epithelial-mesenchymal transition in patient-derived breast cancer organoids
Bar-Hai N, Ben-Yishay R, Arbili-Yarhi S, Herman N, Avidan-Noy V, Menes T, Mansour A, Awwad F, Balint-Lahat N, Goldinger G, Hout-Siloni G, Adileh M, Berger R, Ishay-Ronen D. Modeling epithelial-mesenchymal transition in patient-derived breast cancer organoids. Frontiers In Oncology 2024, 14: 1470379. PMID: 39469640, PMCID: PMC11513879, DOI: 10.3389/fonc.2024.1470379.Peer-Reviewed Original ResearchEpithelial-mesenchymal transitionPatient-derived breast cancer modelsCancer patientsCell plasticityTGF-bBreast cancer organoidsCancer cell plasticityBreast cancer modelBreast cancer patientsEMT-like featuresE-cadherin downregulationEMT-like processCancer modelsOrganoid linesCancer organoidsEpithelial plasticityInvasive phenotypeCellular plasticityE-cadherinOrganoidsPatientsCancerDedifferentiation processMorphological changesCytoskeletal reorganizationProgestogen-driven B7-H4 contributes to onco-fetal immune tolerance
Yu J, Yan Y, Li S, Xu Y, Parolia A, Rizvi S, Wang W, Zhai Y, Xiao R, Li X, Liao P, Zhou J, Okla K, Lin H, Lin X, Grove S, Wei S, Vatan L, Hu J, Szumilo J, Kotarski J, Freeman Z, Skala S, Wicha M, Cho K, Chinnaiyan A, Schon S, Wen F, Kryczek I, Wang S, Chen L, Zou W. Progestogen-driven B7-H4 contributes to onco-fetal immune tolerance. Cell 2024, 187: 4713-4732.e19. PMID: 38968937, PMCID: PMC11344674, DOI: 10.1016/j.cell.2024.06.012.Peer-Reviewed Original ResearchB7-H4Immune toleranceProgesterone receptorCD8<sup>+</sup> T cell exhaustionImmune tolerance checkpointB7-H4 expressionT cell exhaustionImmune tolerance mechanismsMaternal-fetal interfaceBreast cancer modelFemale sex hormonesBreast cancer progressionBreast cancer cellsTolerance checkpointsFetal resorptionHuman cancer typesHormonal screeningImmune activationPregnancy modelCancer modelsSex hormonesCell exhaustionPR antagonistsGenetic deficiencyCancer cells
2023
The tumor-derived cytokine Chi3l1 induces neutrophil extracellular traps that promote T cell exclusion in triple-negative breast cancer
Taifour T, Attalla S, Zuo D, Gu Y, Sanguin-Gendreau V, Proud H, Solymoss E, Bui T, Kuasne H, Papavasiliou V, Lee C, Kamle S, Siegel P, Elias J, Park M, Muller W. The tumor-derived cytokine Chi3l1 induces neutrophil extracellular traps that promote T cell exclusion in triple-negative breast cancer. Immunity 2023, 56: 2755-2772.e8. PMID: 38039967, DOI: 10.1016/j.immuni.2023.11.002.Peer-Reviewed Original ResearchTriple-negative breast cancerImmune checkpoint blockadeBreast cancerAnti-tumor immune responseHuman triple-negative breast cancerNeutrophil extracellular trap formationT cell exclusionAnti-tumor immunityPoor clinical outcomeImmunosuppressive tumor microenvironmentMammary tumor onsetNeutrophil extracellular trapsExtracellular trap formationBreast cancer modelMurine breast tumorsClinical outcomesNeutrophil recruitmentCell infiltrationCHI3L1 expressionTumor infiltrationExtracellular trapsTranscription factor STAT3Immune responseLack of responsivenessSolid tumorsRadiation Synergizes with IL2/IL15 Stimulation to Enhance Innate Immune Activation and Antitumor Immunity.
Li X, Huntoon K, Wang Y, Lee D, Dong S, Antony A, Walkey C, Kim B, Jiang W. Radiation Synergizes with IL2/IL15 Stimulation to Enhance Innate Immune Activation and Antitumor Immunity. Molecular Cancer Therapeutics 2023, 23: 330-342. PMID: 37956421, DOI: 10.1158/1535-7163.mct-23-0236.Peer-Reviewed Original ResearchTumor growth inhibitionDendritic cellsAnti-PD-1 checkpoint inhibitorsAntigen-specific T cellsIL-2/ILGreater tumor infiltrationImmune stimulatory mechanismsMurine breast cancer modelAntitumor immune responseCombination of radiotherapyInnate immune activationType I interferon productionImmune-modulatory propertiesIL-15 receptorBreast cancer modelI interferon productionSuperior tumor growth inhibitionGrowth inhibitionInterferon genes (STING) pathwaySystemic immunotherapyWestern blot analysisCheckpoint inhibitorsMetastatic settingAntitumor immunitySurvival benefit
2022
Pharmacological targeting of androgen receptor elicits context-specific effects in estrogen receptor-positive breast cancer
Wei L, Gao H, Yu J, Zhang H, Nguyen T, Gu Y, Passow M, Carter J, Qin B, Boughey J, Goetz M, Weinshilboum R, Ingle J, Wang L. Pharmacological targeting of androgen receptor elicits context-specific effects in estrogen receptor-positive breast cancer. Cancer Research 2022, 83: 456-470. PMID: 36469363, PMCID: PMC9896025, DOI: 10.1158/0008-5472.can-22-1016.Peer-Reviewed Original ResearchConceptsER+ breast cancerAR-targeted therapiesBreast cancer modelAndrogen receptorBreast cancerAR agonistsCancer modelsAR/ER ratioEstrogen receptor-positive breast cancerReceptor-positive breast cancerAssociated with improved prognosisAR-targeted drugsAlterations of global gene expressionRelationship of ARBinding of ARER+ tumorsAR expressionCell growth inhibitionAR signalingImprove prognosisEstrogen receptorER levelsTumor growthTreatment strategiesEnz treatmentPTHrP induces STAT5 activation, secretory differentiation and accelerates mammary tumor development
Grinman DY, Boras-Granic K, Takyar FM, Dann P, Hens JR, Marmol C, Lee J, Choi J, Chodosh LA, Sola MEG, Wysolmerski JJ. PTHrP induces STAT5 activation, secretory differentiation and accelerates mammary tumor development. Breast Cancer Research 2022, 24: 30. PMID: 35440032, PMCID: PMC9020078, DOI: 10.1186/s13058-022-01523-1.Peer-Reviewed Original ResearchConceptsOverexpression of PTHrPSecretory differentiationEpithelial cellsPTHrP overexpressionTumor latencyBreast cancerMammary epithelial cellsType 1 PTH/PTHrP receptorMMTV-PyMT breast cancer modelPTH/PTHrP receptorMMTV-PyMT miceMammary tumor developmentBreast cancer riskBreast cancer biologyExpression of PTHrPHormone-related proteinHuman breast cancerBreast cancer modelE74-like factor 5Normal mammary epithelial cellsBreast cancer progressionMouse mammary tumorsExpression of markersAlveolar epithelial cellsLuminal epithelial cells
2020
Targeted glycan degradation potentiates the anticancer immune response in vivo
Gray MA, Stanczak MA, Mantuano NR, Xiao H, Pijnenborg JFA, Malaker SA, Miller CL, Weidenbacher PA, Tanzo JT, Ahn G, Woods EC, Läubli H, Bertozzi CR. Targeted glycan degradation potentiates the anticancer immune response in vivo. Nature Chemical Biology 2020, 16: 1376-1384. PMID: 32807964, PMCID: PMC7727925, DOI: 10.1038/s41589-020-0622-x.Peer-Reviewed Original ResearchMeSH KeywordsAllograftsAnimalsAntibodies, MonoclonalB7-H1 AntigenCell Line, TumorHumansHydrolysisImmunoconjugatesImmunotherapyKiller Cells, NaturalMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutModels, MolecularMolecular Targeted TherapyNeuraminidasePolysaccharidesProgrammed Cell Death 1 ReceptorProtein BindingProtein Interaction Domains and MotifsProtein Structure, SecondaryReceptor, ErbB-2Sialic Acid Binding Immunoglobulin-like LectinsSurvival AnalysisT-LymphocytesConceptsImmune checkpoint inhibitor therapyTumor-infiltrating myeloid cellsCheckpoint inhibitor therapyImmune cell infiltrationPowerful treatment optionAnticancer immune responseSurvival of miceSyngeneic breast cancer modelImmune cell activationBreast cancer modelBreast cancer cellsCheckpoint therapyMost patientsInhibitor therapyPD-1Checkpoint receptorsImmune suppressionTreatment optionsCell infiltrationImmune responseMyeloid cellsCancer modelCell activationCertain cancersCancer types
2019
Evaluating the role of the COX2/PGE2 pathway in anti-melanoma immunity.
Ferreira M, Krykbaeva I, Damsky W, Kluger H, Bosenberg M. Evaluating the role of the COX2/PGE2 pathway in anti-melanoma immunity. Journal Of Clinical Oncology 2019, 37: e14114-e14114. DOI: 10.1200/jco.2019.37.15_suppl.e14114.Peer-Reviewed Original ResearchC57BL6/J micePD-L1 upregulationT cell exhaustionTumor implantationJ miceCell exhaustionDay 7Male C57BL6/J miceCOX2/PGE2 pathwayDay 32Anti-melanoma immunityBreast cancer modelSafety of inhibitorsAttractive pharmacologic targetML/daySyngeneic cell linesCheckpoint inhibitorsPartial responseMelanoma patientsComplete regressionSafety profileMetastatic melanomaPathway blockadePGE2 pathwayCOX2 inhibitors
2018
Optoacoustics delineates murine breast cancer models displaying angiogenesis and vascular mimicry
Quiros-Gonzalez I, Tomaszewski M, Aitken S, Ansel-Bollepalli L, McDuffus L, Gill M, Hacker L, Brunker J, Bohndiek S. Optoacoustics delineates murine breast cancer models displaying angiogenesis and vascular mimicry. British Journal Of Cancer 2018, 118: 1098-1106. PMID: 29576623, PMCID: PMC5931091, DOI: 10.1038/s41416-018-0033-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiological MimicryBreast NeoplasmsCell Line, TumorDrug MonitoringFemaleHumansMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred BALB CMice, NudeNeoplasm StagingNeovascularization, PathologicOxygen ConsumptionPhotoacoustic TechniquesSensitivity and SpecificityTomographyTumor HypoxiaXenograft Model Antitumor AssaysConceptsMDA-MB-231Breast cancer modelCancer modelsVascular mimicryOrthotopic breast cancer xenograftsVascular phenotypeMurine breast cancer modelMDA-MB-231 tumorsMCF-7Consistent with angiogenesisMCF-7 tumorsTotal hemoglobinBreast cancer xenograftsBreast tumor modelEx vivo analysisNO serum levelsTumor oxygenationEstrogen-independentCancer xenograftsSerum levelsEstrogen-dependentTherapeutic responseBreast tumorsTumor modelClinical trialsAllele-Specific Chromatin Recruitment and Therapeutic Vulnerabilities of ESR1 Activating Mutations
Jeselsohn R, Bergholz JS, Pun M, Cornwell M, Liu W, Nardone A, Xiao T, Li W, Qiu X, Buchwalter G, Feiglin A, Abell-Hart K, Fei T, Rao P, Long H, Kwiatkowski N, Zhang T, Gray N, Melchers D, Houtman R, Liu XS, Cohen O, Wagle N, Winer EP, Zhao J, Brown M. Allele-Specific Chromatin Recruitment and Therapeutic Vulnerabilities of ESR1 Activating Mutations. Cancer Cell 2018, 33: 173-186.e5. PMID: 29438694, PMCID: PMC5813700, DOI: 10.1016/j.ccell.2018.01.004.Peer-Reviewed Original ResearchConceptsChromatin recruitmentLigand-independent functionsER mutationsPro-metastatic phenotypeGenetic screenTranscriptional networksTranscriptional programsWild-type ERTherapeutic vulnerabilitiesPotential therapeutic targetMutationsMutantsDomain mutationsLigand-binding domain mutationsActivating mutationsTherapeutic targetTherapy resistanceUnique recruitmentRecruitmentGenetic vulnerabilityCancer modelGenesBreast cancer modelERPhenotype
2017
A Phase I/Ib Study of Enzalutamide Alone and in Combination with Endocrine Therapies in Women with Advanced Breast Cancer
Schwartzberg LS, Yardley D, Elias A, Patel M, LoRusso P, Burris HA, Gucalp A, Peterson A, Blaney M, Steinberg J, Gibbons J, Traina TA. A Phase I/Ib Study of Enzalutamide Alone and in Combination with Endocrine Therapies in Women with Advanced Breast Cancer. Clinical Cancer Research 2017, 23: 4046-4054. PMID: 28280092, DOI: 10.1158/1078-0432.ccr-16-2339.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnastrozoleAntineoplastic Agents, HormonalAntineoplastic Combined Chemotherapy ProtocolsAromatase InhibitorsBenzamidesBreast NeoplasmsCytochrome P-450 CYP3ADose-Response Relationship, DrugDrug-Related Side Effects and Adverse ReactionsFemaleHumansMiddle AgedNeoplasm StagingNitrilesPhenylthiohydantoinPostmenopauseReceptors, EstrogenReceptors, ProgesteroneTriazolesConceptsEndocrine therapyEnzalutamide monotherapyBreast cancerEstrogen receptor-positive/progesterone receptor-positive breast cancerProgesterone receptor-positive breast cancerCytochrome P450 3A4 inducerRandomized phase II studyReceptor-positive breast cancerDose-expansion cohortsEffect of enzalutamidePhase II studyAdvanced breast cancerAndrogen receptor signalingBreast cancer modelClin Cancer ResDose modificationII studyPharmacokinetic interactionsPreclinical dataProstate cancerIb studyAdditional cohortMonotherapyCancer modelExemestaneCombination Epigenetic Therapy in Advanced Breast Cancer with 5-Azacitidine and Entinostat: A Phase II National Cancer Institute/Stand Up to Cancer Study
Connolly RM, Li H, Jankowitz RC, Zhang Z, Rudek MA, Jeter SC, Slater SA, Powers P, Wolff AC, Fetting JH, Brufsky A, Piekarz R, Ahuja N, Laird PW, Shen H, Weisenberger DJ, Cope L, Herman JG, Somlo G, Garcia AA, Jones PA, Baylin SB, Davidson NE, Zahnow CA, Stearns V. Combination Epigenetic Therapy in Advanced Breast Cancer with 5-Azacitidine and Entinostat: A Phase II National Cancer Institute/Stand Up to Cancer Study. Clinical Cancer Research 2017, 23: 2691-2701. PMID: 27979916, PMCID: PMC5457329, DOI: 10.1158/1078-0432.ccr-16-1729.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerObjective response rateCombination epigenetic therapyEstrogen receptorEndocrine therapyPrimary endpointPartial responseMulticenter phase II studyEpigenetic therapyAdditional partial responsesHormone-resistant diseasePhase II studyTime of progressionBreast cancer modelClin Cancer ResHistone deacetylase inhibitorsImportant therapeutic targetPosttreatment biopsiesTNBC cohortII studyBreast cancerDNA methyltransferase inhibitorTherapeutic targetResponse rateCancer model
2016
PlGF/VEGFR-1 Signaling Promotes Macrophage Polarization and Accelerated Tumor Progression in Obesity
Incio J, Tam J, Rahbari NN, Suboj P, McManus DT, Chin SM, Vardam TD, Batista A, Babykutty S, Jung K, Khachatryan A, Hato T, Ligibel JA, Krop IE, Puchner SB, Schlett CL, Hoffmman U, Ancukiewicz M, Shibuya M, Carmeliet P, Soares R, Duda DG, Jain RK, Fukumura D. PlGF/VEGFR-1 Signaling Promotes Macrophage Polarization and Accelerated Tumor Progression in Obesity. Clinical Cancer Research 2016, 22: 2993-3004. PMID: 26861455, PMCID: PMC4911258, DOI: 10.1158/1078-0432.ccr-15-1839.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsDiet, High-FatFemaleGlucoseHumansHypoglycemic AgentsMacrophagesMetforminMiceMice, Inbred C57BLMice, KnockoutMice, ObeseNeovascularization, PathologicObesityPancreatic NeoplasmsPlacenta Growth FactorPrognosisSignal TransductionVascular Endothelial Growth Factor Receptor-1ConceptsMouse modelTumor progressionTumor-associated macrophage recruitmentDiet-induced obese mouse modelTumor angiogenesisVEGFR-1Breast cancer mouse modelRole of PlGFBreast cancer patientsTumor immune microenvironmentObese mouse modelPlacental growth factorWild-type C57BL/6Addition of metforminHigh-fat dietTumor immune environmentCancer mouse modelReceptors VEGFR-1Breast cancer modelBreast cancer progressionAntitumor immunityTAM infiltrationImmune environmentInsulin levelsImmune microenvironment
2015
AIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis
Ji W, Li Y, He Y, Yin M, Zhou HJ, Boggon TJ, Zhang H, Min W. AIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis. Cancer Research 2015, 75: 3492-3504. PMID: 26139244, PMCID: PMC4558200, DOI: 10.1158/0008-5472.can-15-0088.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGuanylate KinasesHumansMelanoma, ExperimentalMiceNeoplasm MetastasisNeovascularization, PathologicProtein Kinase InhibitorsSignal TransductionTumor MicroenvironmentVascular Endothelial Growth Factor Receptor-2ConceptsEpithelial-mesenchymal transitionPremetastatic niche formationTumor growthAugments tumor growthBreast cancer modelSuppresses tumor progressionVascular endothelial cellsNiche formationSystemic administrationCancer modelVEGFR2 kinase inhibitorTumor neovascularizationTumor progressionTumor angiogenesisTumor microenvironmentTumor cellsEndothelial cellsMetastasisKinase inhibitorsTumor nicheVascular ECsSpecific deletionVascular environmentEMT switchAIP1 gene
2012
A phase I/IB dose-escalation study of BEZ235 in combination with trastuzumab in patients with PI3-kinase or PTEN altered HER2+ metastatic breast cancer.
Krop I, Saura C, Rodon Ahnert J, Becerra C, Britten C, Isakoff S, Demanse D, Hackl W, Quadt C, Silva A, Burris H, Abu-Khalaf M, Baselga J. A phase I/IB dose-escalation study of BEZ235 in combination with trastuzumab in patients with PI3-kinase or PTEN altered HER2+ metastatic breast cancer. Journal Of Clinical Oncology 2012, 30: 508-508. DOI: 10.1200/jco.2012.30.15_suppl.508.Peer-Reviewed Original ResearchMetastatic breast cancerPI3K pathway alterationsBreast cancerG3 nauseaResistant HER2Disease stabilizationPathway alterationsPI3K/AKT/mTOR pathwayAcceptable safety profileDose-escalation studyAdvanced solid tumorsAKT/mTOR pathwayBreast cancer modelLogistic regression modelsPI3K pathwayG3 fatigueObserved DLTsBrain metastasesPartial responseSkin rashAdverse eventsLiver metastasesDose escalationSafety profileDose levels
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply