grant

Par-4 Regulation of Actomyosin Contractility as a Tumor Suppressive Mechanism in Breast Cancer

Organization FRED HUTCHINSON CANCER CENTERLocation SEATTLE, UNITED STATESPosted 1 Jun 2024Deadline 31 May 2029
NIHUS FederalResearch GrantFY20253D cell culture3D cultureActomyosinAnimal ModelAnimal Models and Related StudiesApoptosis Response ProteinApoptoticBiomechanicsBreast CancerBreast Cancer CellBreast Cancer ModelBreast Cancer PatientBreast Cancer PreventionBreast Epithelial CellsBreast Tumor PatientBreast tumor modelCadherin-1Cancer CauseCancer EtiologyCancer GenesCancer-Promoting GeneCancersCause of DeathCell BodyCell DeathCell SurvivalCell ViabilityCellsCessation of lifeClinicalDataDeathDetectable Residual DiseaseDevelopmentDiseaseDisorderDissectionDistantDown-RegulationDuctDuct (organ) structureE-CadherinEpithelial Calcium-Dependent Adhesion ProteinEpithelial-CadherinEventExhibitsGEM modelGEMM modelGeneralized GrowthGenetically Engineered MouseGoalsGrowthHumanInduction TherapyKnock-outKnockoutLaboratoriesLobularMalignantMalignant - descriptorMalignant Breast NeoplasmMalignant CellMalignant NeoplasmsMalignant TumorMeasuresMediatingMetastasisMetastasizeMetastatic LesionMetastatic MassMetastatic NeoplasmMetastatic TumorMinimal Residual DiseaseModelingModern ManNEOADJNeoadjuvantNeoadjuvant TherapyNeoadjuvant TreatmentNeoplasm MetastasisOncogenesPAR4PAWRPAWR genePAWR proteinPRKC, Apoptosis, WT1, RegulatorPathway interactionsPatientsProcessPrognosisProliferatingProstate Apoptosis Response Protein 4RecurrenceRecurrentRecurrent Malignant NeoplasmRecurrent Malignant TumorRecurrent NeoplasmRecurrent diseaseRecurrent tumorRegulationRelapsed DiseaseRelaxationResearchResearch SpecimenResidualResidual CancersResidual NeoplasmResidual TumorsResidual stateRiskRoleSamplingSecondary NeoplasmSecondary TumorSignal PathwaySiteSpecimenTestingTherapeutic InterventionTissue GrowthTranscriptional Repressor PAR4Transforming GenesTumor CellTumor Suppressor ProteinsUvomorulinWT1-Interacting ProteinWomanWomen's mortalityWorkbiomechanicalbreast cancer progressionbreast tumor cellcancer cellcancer metastasiscancer progressioncancer recurrencecohortdeath among femalesdeath among womendeath in femalesdeath in womendeath rate among womendeath rate in womendevelop therapydevelopmentalfemale deathfemale mortalitygenetically engineered mouse modelgenetically engineered murine modelimprovedindividuals with breast cancerinduction therapiesintervention designintervention developmentintervention therapymalignancymalignant breast tumormammary cancer modelmammary cancer preventionmammary epithelial cellsmammary gland epithelial cellsmammary tumor modelmammary tumor preventionmodel of animalmortality among femalesmortality among womenmortality in femalesmortality in womennecrocytosisneoplasm progressionneoplasm recurrenceneoplasm/cancerneoplastic cellneoplastic progressionnovelontogenypar-4par-4 proteinpathwaypatients with breast cancerperson with breast cancerpreventprevent breast cancerpreventingresidual diseaseresistance to therapyresistant to therapyresponsesocial roletargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic resistancetherapy designtherapy developmenttherapy resistantthree dimensional cell culturetreatment designtreatment developmenttreatment resistancetumortumor cell metastasistumor progressiontumor suppressorwomen's deathwomen's death rate
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Project Summary/Abstract
Tumor progression – including resistance to therapy, metastasis, and recurrence – is responsible for the

majority of cancer deaths. Understanding how cancer cells survive treatment, spread to distant sites, persist

as dormant residual cells, and eventually recur is essential to improving the treatment of this disease. The…

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Par-4 Regulation of Actomyosin Contractility as a Tumor Suppressive Mechanism in Breast Cancer — FRED HUTCHINSON CANCER | Dev Procure