乳腺癌肿瘤起始细胞的治疗靶向-猫眼课题宝

乳腺癌肿瘤起始细胞的治疗靶向

批准号：

10596215

负责人：

CHARLES M. PEROU

金额：

$41.33万

依托单位：

UNIV OF NORTH CAROLINA CHAPEL HILL

依托单位国家：

美国

项目类别：

财政年份：

2010

资助国家：

美国

项目状态：

未结题

起止时间：

2010-03-17 至 2026-03-31

来源：

https://reporter.nih.gov/project-details/10596215

关键词：

ATAC-seq Adjuvant Affect Antibodies Autopsy Breast Cancer Model Breast Cancer Patient CSF1R gene Cancer Etiology Carboplatin Cells Cessation of life Clinic Complex Mixtures Credentialing Cyclophosphamide Cytometry DNA Structure Disease Drug resistance Drug usage ERBB2 gene Epigenetic Process Epithelial Cells Estrogen Receptors Fatty acid glycerol esters Flow Cytometry Genes Genetically Engineered Mouse Genomics Heterogeneity Histone Deacetylase Human Image Immune Immune checkpoint inhibitor Immunotherapy In Vitro Individual Infiltration Injections Label Liver Luciferases Lung MERTK gene Macrophage Mammary Neoplasms Mesenchymal Metastatic Neoplasm to the Lung Modeling Mus Myelogenous Neoplasm Metastasis Operative Surgical Procedures Organoids Pathway interactions Patients Pharmaceutical Preparations Phenotype Primary Neoplasm Progesterone Receptors Proteins Regimen Reporter Resistance Role Site Specimen Tail Testing Therapeutic Tumor stage United States Veins Visual Woman anti-PD-1 cancer subtypes cancer therapy cancer type cell type chemotherapy clinical subtypes differential expression docetaxel efficacy evaluation epigenetic drug epigenetic therapy immune cell infiltrate improved in vivo in vivo evaluation inhibitor mRNA sequencing malignant breast neoplasm molecular subtypes neoplastic cell novel novel drug combination novel therapeutic intervention patient derived xenograft model prevent primary endpoint programmed cell death ligand 1 programs response single-cell RNA sequencing small molecule standard of care synergism therapeutic target triple-negative invasive breast carcinoma tumor tumor behavior tumor initiation tumor-immune system interactions

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PROJECT ABSTRACT Triple Negative Breast Cancer (TNBC), if considered its own disease type, would rank as the 5th leading cause of cancer deaths in women in the USA. The main systemic treatment option for these patients in the adjuvant setting is multi-agent chemotherapy, and now since early 2019, immunotherapy plus chemotherapy is an option for PDL1-positive metastatic patients. TNBC is also known to be biologically heterogeneous, with multiple genomically-defined subtypes present. We hypothesize that much of this heterogeneity actually represents cellular plasticity, and that some TNBC subtypes can actually morph from one subtype into another. We hypothesize that this plasticity is a key determinant of chemotherapy responsiveness, immune checkpoint inhibitor sensitivity, and metastatic potential. Furthermore, we hypothesize that if we are able to keep, or promote, a tumor into the basal-like state, there may be both a change in the immune microenvironment and increased therapy sensitivity. We will test these hypotheses by using novel combinations of drugs, in vitro screens, and in vivo testing of metastasis vs primary tumor sensitivity using Genetically Engineered Mouse models and human tumor specimens.

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