Tumor Cell-Microenvironment Interactions in the Molecular Pathogenesis of Multipl

肿瘤细胞-微环境相互作用在多种肿瘤分子发病机制中的作用

• 批准号: 7725606
• 负责人: John Damian Shaughnessy
• 金额: $ 28.61万
• 依托单位: UNIV OF ARKANSAS FOR MED SCIS
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-07-01 至 2014-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7725606
• 关键词: Alleles; Archives; Attenuated; Benign; Binding; Biology; Bone Diseases; Bone Marrow; Bortezomib; CDH1 gene; Cadherins; Carcinoma; Cell Adhesion; Cell Line; Cell Proliferation; Cells; Clinical; Code; Complex; Consensus Sequence; DNA Modification Process; DNA Sequence; Data; Derivation procedure; Disease; Disease Progression; Down-Regulation; Drug resistance; E-Cadherin; Enhancers; Event; Exhibits; Extracellular Matrix; Extramedullary; Foundations; Gene Expression; Gene Expression Profiling; Gene Frequency; Gene Mutation; Genes; Genetic; Genetic Polymorphism; Genetic Transcription; Goals; Growth; Homologous Gene; In Vitro; Instruction; Interleukin-9; Length; Lesion; Link; Longitudinal Studies; Luciferases; Lytic Metastatic Lesion; Magnetic Resonance Imaging; Malignant Neoplasms; Measures; Mediating; Mesenchymal Stem Cells; Messenger RNA; Molecular; Monoclonal gammopathy of uncertain significance; Multiple Myeloma; Mutation; N-Cadherin; Natural History; Neoplasm Metastasis; Nuclear; Nucleotides; Osteoblasts; Osteolytic; Pathogenesis; Pathway interactions; Patients; Pattern; Plasma Cells; Plasmin; Protein Isoforms; Proteins; Publishing; Quality of life; Recombinants; Regulation; Research Personnel; Resistance; Role; SCID-hu Mice; Sampling; Signal Transduction; Site; Solid Neoplasm; Staging; TCF Transcription Factor; Therapeutic; Tissues; Tumor Suppressor Proteins; Up-Regulation; Variant; Western Blotting; Work; Wound Healing; angiogenesis; base; bone; cell growth; chemotherapy; chromatin immunoprecipitation; cyr61 protein; epithelial to mesenchymal transition; gain of function; improved; in vivo; innovation; insight; lenalidomide; loss of function; malignant breast neoplasm; mouse model; neoplastic cell; novel; novel therapeutic intervention; osteoblast differentiation; overexpression; programs; promoter; ranpirnase; syndecan; therapeutic target; transcription factor; tumor; tumor growth; tumor progression