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Prostate Cancer Parasitism of the HSC "niche" as a Molecular Mechanism for Ost

Prostate Cancer Parasitism of the HSC "niche" as a Molecular Mechanism for Ost
前列腺癌 HSC“生态位”的寄生作为 Ost 的分子机制
批准号：
8464645
负责人：
RUSSELL S TAICHMAN
金额：
$20.72万
依托单位：
UNIVERSITY OF MICHIGAN AT ANN ARBOR
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
项目状态：
已结题
起止时间：
2004-06-05 至 2014-04-30
来源：
https://reporter.nih.gov/project-details/8464645
关键词：
ANXA2 geneAccountingAdhesionsAngiogenic SwitchAnimalsAntibodiesAreaBindingBiological AssayBiologyBone MarrowBone Marrow TransplantationCXC ChemokinesCXCR4 ReceptorsCXCR4 geneDataEndothelial CellsEngraftmentEventFoundationsFundingGrowthHematopoietic stem cellsHome environmentHomingHoming BehaviorImplantIndiumInvadedInvestigationLigandsLocationMalignant NeoplasmsMalignant neoplasm of prostateMarrowMetastatic Neoplasm to the BoneMetastatic Prostate CancerModelingMolecularNeoplasm MetastasisOsteoblastsPathway interactionsPeptidesPlayPrimary NeoplasmProstateReceptor SignalingRoleRouteSignal PathwaySignal TransductionSkeletonStromal Cell-Derived Factor 1TestingTherapeutic InterventionTimeTissuesWorkbonecell growthfootin vivometastatic processneoplastic cellnovelparasitismprostate cancer cellreceptorstem cell nichetumor

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中文摘要
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英文摘要
In our previous P01 project we examined the relationship between the expression of CXCR4 by metastatic prostate cancers (PCa) and their bone homing behavior. From these studies we acquired data that suggest that not only do PCa's use the CXCR4/SDF-1 pathway to home to bone - but there is a strong likelihood they use the hematopoietic stem cell (HSC)
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Mechanisms That Regulate Dormancy of Disseminated Tumor Cells in the Bone Marrow
Administrative Core
Prostate Cancer Parasitism of the HSC "niche" as a Molecular Mechanism for Ost
Regulation of the PCa Metastatic Phenotype by the HSC Niche
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