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Nature (London), ISSN 1476-4687, 2018, Volume 562, Issue 7725, pp. 69 - 75
.... Here we show that the hepatic microenvironment epigenetically shapes lineage commitment in mosaic mouse models of liver tumorigenesis... 
PATHOGENESIS | HEPATOCELLULAR-CARCINOMA | INTRAHEPATIC CHOLANGIOCARCINOMA | READ ALIGNMENT | HEPATOCYTES | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | SEQUENCING DATA | EXPRESSION | DISCOVERY | CELL-DEATH | Humans | Tumor Microenvironment | Apoptosis - genetics | Hepatocytes - pathology | Male | Gene Expression Profiling | Genes, myc | Hepatocytes - metabolism | Proto-Oncogene Proteins c-akt - genetics | DNA-Binding Proteins - metabolism | Carcinoma, Hepatocellular - genetics | DNA Transposable Elements - genetics | Female | Liver Neoplasms - pathology | Cell Differentiation | Cell Lineage - genetics | Disease Models, Animal | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Cytokines - metabolism | Liver Neoplasms - genetics | Carcinogenesis - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Transcription Factors - metabolism | Cholangiocarcinoma - pathology | Animals | Epigenesis, Genetic - genetics | Carcinoma, Hepatocellular - pathology | Cholangiocarcinoma - genetics | Mosaicism | Mice | Necrosis - genetics | Genes, ras | Liver cancer | Research | Carcinogenesis | Oncology, Experimental | Apoptosis | Cancer | Animal models | Cytokines | Liver | Hepatocellular carcinoma | Genomes | Metastasis | Risk analysis | Gene expression | Risk factors | Metastases | Hepatocytes | Morphology | DNA methylation | Tumorigenesis | Bioinformatics | Cholangiocarcinoma | Deoxyribonucleic acid--DNA | Tumors | T-Box Domain Proteins/metabolism | Hepatocytes/pathology | DNA-Binding Proteins/metabolism | Life Sciences | Cholangiocarcinoma/pathology | Transcription Factors/metabolism | Necrosis/genetics | Cytokines/metabolism | Epigenesis, Genetic/genetics | Cyclin-Dependent Kinase Inhibitor p16/deficiency | Carcinoma, Hepatocellular/pathology | DNA Transposable Elements/genetics | Cell Lineage/genetics | T-Box Domain Proteins/genetics | Transcription Factors/genetics | Apoptosis/genetics | Proto-Oncogene Proteins c-akt/genetics | Liver Neoplasms/genetics | Cholangiocarcinoma/genetics | Liver Neoplasms/pathology | DNA-Binding Proteins/genetics | Hepatocytes/metabolism | Carcinoma, Hepatocellular/genetics | Carcinogenesis/genetics
Journal Article
Journal Article
Journal Article
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2017, Volume 355, Issue 6320, pp. 84 - 88
Journal Article
Journal Article
Nature genetics, ISSN 1546-1718, 2017, Volume 49, Issue 10, pp. 1522 - 1528
Journal Article
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2017, Volume 355, Issue 6320, pp. 78 - 83
Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology with altered lineage marker expression, suggesting that lineage plasticity facilitates therapeutic resistance... 
PATHWAY | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | SMALL-CELL CARCINOMA | PTEN | GENERATION | TUMORIGENESIS | EXPRESSION | DEFICIENCY | DELETION | EZH2 | Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors | Epigenesis, Genetic | Humans | SOXB1 Transcription Factors - antagonists & inhibitors | Male | Retinoblastoma-Like Protein p107 - genetics | Tumor Suppressor Protein p53 - genetics | Neoplasms, Experimental - pathology | Neoplasm Metastasis | Prostatic Neoplasms - genetics | SOXB1 Transcription Factors - genetics | Neoplasms, Experimental - genetics | Adenocarcinoma - genetics | Prostatic Neoplasms - drug therapy | Neuroendocrine Tumors - pathology | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Enhancer of Zeste Homolog 2 Protein - genetics | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Neuroendocrine Tumors - genetics | Cell Lineage | Drug Resistance, Neoplasm - genetics | Animals | Androgen Antagonists - therapeutic use | Cell Line, Tumor | Neuroendocrine Tumors - drug therapy | Cell Plasticity | Mice | Mutation | Neoplasms, Experimental - drug therapy | Prevention | Antimitotic agents | Epigenetic inheritance | Development and progression | Genetic aspects | Dosage and administration | Metastasis | Gene expression | Antineoplastic agents | Drug resistance | Health aspects | Prostate cancer | Drugs | Therapy | Deprivation | Histology | Hormones | Suppressors | Switching | Signal transduction | Sensitivity | Androgens | Inhibitors | Rodents | Plasticity | Epigenetics | Tumor suppressor genes | Plastic properties | Prostate | Cancer | Tumors | Mutations
Journal Article
Circulation (New York, N.Y.), ISSN 1524-4539, 2018, Volume 138, Issue 25, pp. 2931 - 2939
... investigated. METHODS:Here we generated Ly6a gene–targeted mice containing either a constitutive or an inducible Cre recombinase to perform genetic lineage tracing of Sca-1 cells in vivo... 
stem cells | endothelial cells | cell lineage | regeneration | myocardial infarction | CARDIAC & CARDIOVASCULAR SYSTEMS | MULTIPOTENT | HEMATOPOIETIC STEM-CELL | ISCHEMIA | CARDIOMYOCYTES | ADULT | CARDIAC REGENERATION | RENEWAL | PROGENITOR-CELL | C-KIT(+) CELLS | PERIPHERAL VASCULAR DISEASE | EXPRESSION | Linkage (Genetics) | Research | Analysis | Stem cells | Endothelium | lineage tracing |