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Kidney International, ISSN 0085-2538, 08/2012, Volume 82, Issue 4, pp. 412 - 427
Endothelial progenitor cells are known to reverse acute kidney injury by paracrine mechanisms. We previously found that microvesicles released from these... 
exosome | ischemia–reperfusion | acute kidney injury | ischemia-reperfusion | HORIZONTAL TRANSFER | STEM-CELLS | CONTRIBUTE | REGENERATION | FAILURE | EXPERIMENTAL GLOMERULONEPHRITIS | REPAIR | EPITHELIAL-CELLS | MESSENGER-RNA | UROLOGY & NEPHROLOGY | PLATELET-ACTIVATING-FACTOR | Chemotaxis, Leukocyte | Cell Proliferation | Epithelial Cells - metabolism | Kidney - blood supply | Capillaries - pathology | Kidney - pathology | Rats, Wistar | Endothelial Cells - transplantation | Cell-Derived Microparticles - transplantation | Male | MicroRNAs - metabolism | Acute Kidney Injury - genetics | Stem Cells - metabolism | Cell Hypoxia | Stem Cell Transplantation | Kidney - metabolism | Transfection | RNA Interference | Time Factors | Cell-Derived Microparticles - pathology | Cell-Derived Microparticles - metabolism | Kidney Tubules - pathology | Kidney Tubules - metabolism | Capillaries - metabolism | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Disease Models, Animal | Ribonuclease III - genetics | Ribonuclease III - metabolism | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Endothelial Cells - metabolism | Cells, Cultured | Gene Expression Regulation | Rats | Epithelial Cells - pathology | Acute Kidney Injury - prevention & control | Regeneration | Oligonucleotides - metabolism | Animals | Reperfusion Injury - prevention & control | Fibrosis | Stem Cells - pathology | Acute Kidney Injury - metabolism | Endothelial Cells - pathology | Apoptosis | Index Medicus | Cell proliferation | Intravenous administration | Paracrine signalling | mRNA | Leukocytes | Ribonuclease | Endothelial cells | Kidney | Angiogenesis | Ischemia | Stem cells | Hypoxia | miRNA | Capillaries | Injuries
Journal Article
Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7571, pp. 131 - 135
Despite major advances in understanding the molecular and genetic basis of cancer, metastasis remains the cause of >90% of cancer-related mortality(1).... 
INHIBITION | COMMITMENT | MULTIDISCIPLINARY SCIENCES | GROWTH | GENES | MARKERS | IDENTIFICATION | FATE | TUMORS | TRANSCRIPTOME ANALYSIS | MAMMARY-GLAND | Neoplastic Stem Cells - drug effects | Epithelial Cells - drug effects | Humans | Gene Expression Profiling | Epithelial-Mesenchymal Transition - genetics | Cell Differentiation - genetics | Flow Cytometry | Neoplasm Metastasis - drug therapy | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Cyclin-Dependent Kinases - antagonists & inhibitors | Single-Cell Analysis | Disease Models, Animal | Cell Separation | Epithelial Cells - pathology | Mice, SCID | Breast Neoplasms - drug therapy | Disease Progression | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Cell Differentiation - drug effects | Neoplasm Metastasis - pathology | Genes, myc - genetics | Cell Line, Tumor | Mice, Inbred NOD | Cell Proliferation - drug effects | Mesoderm - metabolism | Mice | Cell Transformation, Neoplastic - drug effects | Cell Cycle - drug effects | Cell Transformation, Neoplastic - pathology | Mesoderm - pathology | Stem cells | Cancer cells | Development and progression | Breast cancer | Metastasis | Observations | Health aspects | Bone marrow | Principal components analysis | Gene expression | Tumors | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 506, Issue 7488, pp. 328 - 333
In acute myeloid leukaemia (AML), the cell of origin, nature and biological consequences of initiating lesions, and order of subsequent mutations remain poorly... 
BREAST-CANCER | RELAPSE | ACUTE NONLYMPHOCYTIC LEUKEMIA | MULTIDISCIPLINARY SCIENCES | ACUTE LYMPHOBLASTIC-LEUKEMIA | PANCREATIC-CANCER | DNA METHYLTRANSFERASE | CLONAL EVOLUTION | ACUTE MYELOID-LEUKEMIA | DNMT3A MUTATIONS | MYELODYSPLASTIC SYNDROMES | Clone Cells - cytology | Neoplasm Transplantation | Neoplastic Stem Cells - cytology | Neoplastic Stem Cells - drug effects | Humans | Hematopoietic Stem Cells - pathology | DNA (Cytosine-5-)-Methyltransferases - metabolism | Heterografts | Neoplastic Stem Cells - metabolism | T-Lymphocytes - metabolism | Hematopoiesis | Cell Division | Leukemia, Myeloid, Acute - drug therapy | Neoplastic Stem Cells - pathology | Female | Cell Differentiation | T-Lymphocytes - pathology | Nuclear Proteins - genetics | Hematopoietic Stem Cells - drug effects | Leukemia, Myeloid, Acute - pathology | Isocitrate Dehydrogenase - genetics | Hematopoietic Stem Cells - metabolism | Mice, SCID | Mutation - genetics | Clone Cells - metabolism | Remission Induction | Cell Lineage | DNA (Cytosine-5-)-Methyltransferases - genetics | Animals | Clone Cells - pathology | Leukemia, Myeloid, Acute - diagnosis | Hematopoietic Stem Cells - cytology | Mice, Inbred NOD | Mice | Drug Resistance, Neoplasm - drug effects | Leukemia, Myeloid, Acute - genetics | Acute leukemia | Genetic aspects | Diagnosis | Identification and classification | Hematopoietic stem cells | Index Medicus
Journal Article
Journal Article
Cancer Cell, ISSN 1535-6108, 12/2015, Volume 28, Issue 6, pp. 800 - 814
The regulation and stem cell origin of normal and neoplastic gastric glands are uncertain. Here, we show that Mist1 expression marks quiescent stem cells in... 
CARCINOMA-CELLS | PROGENITOR CELLS | CHIEF CELLS | MAINTENANCE | ONCOLOGY | MOUSE STOMACH | INNATE LYMPHOID-CELLS | E-CADHERIN | BONE | INTRAEPITHELIAL NEOPLASIA | CANCER | CELL BIOLOGY | Epithelial Cells - metabolism | Cadherins - metabolism | Neoplastic Stem Cells - drug effects | Epithelial Cells - drug effects | Humans | Stomach Neoplasms - metabolism | Tumor Microenvironment | Gastric Mucosa - pathology | Male | Stomach Neoplasms - pathology | Wnt-5a Protein | Gastric Mucosa - metabolism | Wnt Proteins - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Neoplastic Stem Cells - metabolism | Time Factors | Cell Transformation, Neoplastic - genetics | Cellular Senescence | Bone Marrow Transplantation | Gastric Mucosa - drug effects | Neoplastic Stem Cells - pathology | Antineoplastic Agents - pharmacology | Wnt Signaling Pathway | Lymphocytes - metabolism | Stomach Neoplasms - genetics | Basic Helix-Loop-Helix Transcription Factors - genetics | Stem Cell Niche | Signal Transduction | Endothelial Cells - metabolism | Cell Communication | Epithelial Cells - pathology | Mice, Transgenic | Stomach Neoplasms - drug therapy | Cell Transformation, Neoplastic - metabolism | Receptors, CXCR4 - metabolism | Cell Lineage | Lymphocytes - pathology | Animals | Chemokine CXCL12 - metabolism | rho GTP-Binding Proteins - metabolism | Cell Line, Tumor | Anoikis | Mice | Cell Transformation, Neoplastic - pathology | Endothelial Cells - pathology | Antimitotic agents | Medical colleges | Antineoplastic agents | Liver | Stem cells | Microbiology | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2017, Volume 543, Issue 7647, pp. 676 - 680
Journal Article
Aging Cell, ISSN 1474-9718, 08/2015, Volume 14, Issue 4, pp. 644 - 658
The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous... 
dasatinib | plasminogen‐activated inhibitor | dependence receptors | quercetin | ephrins | 3K delta | p21 | Dasatinib | Dependence receptors | Ephrins | Plasminogen-activated inhibitor | Quercetin | PI3K delta | P21 | ENDOTHELIAL DYSFUNCTION | PLASMINOGEN-ACTIVATOR INHIBITOR-1 | EXPRESSION PROFILES | plasminogen-activated inhibitor | CELLULAR SENESCENCE | CANCER-THERAPY | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | LUNG-CANCER | SET ENRICHMENT ANALYSIS | GENE-EXPRESSION | IONIZING-RADIATION | TUMOR-GROWTH | Carotid Arteries - drug effects | Endonucleases - genetics | Plasminogen Activator Inhibitor 2 - genetics | Transcriptome | Gene Expression Profiling | Adipocytes - drug effects | Aging - genetics | Osteoporosis - metabolism | Ephrins - metabolism | Plasminogen Activator Inhibitor 2 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Osteoporosis - genetics | Intervertebral Disc - pathology | Fibroblasts - metabolism | Endothelial Cells - metabolism | Intervertebral Disc - chemistry | Fibroblasts - pathology | Mesenchymal Stem Cells - pathology | Mice, Knockout | Dasatinib - pharmacology | Osteoporosis - pathology | Ephrins - genetics | Fibroblasts - drug effects | Mice | Endothelial Cells - pathology | bcl-X Protein - metabolism | Aging - metabolism | Aging - drug effects | bcl-X Protein - genetics | Cellular Senescence - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Endonucleases - metabolism | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Mesenchymal Stem Cells - drug effects | Mesenchymal Stem Cells - metabolism | Heart - physiopathology | Cellular Senescence - genetics | Osteoporosis - prevention & control | DNA-Binding Proteins - genetics | Adipocytes - pathology | Aging - pathology | Phosphatidylinositol 3-Kinases - genetics | Animals | Quercetin - pharmacology | Adipocytes - metabolism | Heart - drug effects | Carotid Arteries - pathology | Intervertebral Disc - drug effects | Drug Combinations | Endothelial Cells - drug effects | Index Medicus | Original
Journal Article
Nature Cell Biology, ISSN 1465-7392, 03/2010, Volume 12, Issue 3, pp. 299 - 305
For most types of cancers, the cell at the origin of tumour initiation is still unknown. Here, we used mouse genetics to identify cells at the origin of basal... 
POPULATION | STEM-CELLS | SONIC HEDGEHOG | EPIDERMIS | HAIR FOLLICLE BULGE | KERATINOCYTES | CANCER | EXPRESSION | HUMAN HOMOLOG | MOUSE SKIN | CELL BIOLOGY | Epithelial Cells - metabolism | Cadherins - metabolism | Receptors, G-Protein-Coupled - metabolism | Skin - metabolism | Cell Count | Ear, External - pathology | Integrin beta4 - metabolism | Tail - pathology | Hair Follicle - pathology | Hedgehog Proteins - genetics | Neoplastic Stem Cells - metabolism | Kruppel-Like Transcription Factors - metabolism | Smoothened Receptor | Neoplastic Stem Cells - pathology | Cell Differentiation | Patched Receptors | Skin - pathology | Keratin-10 - metabolism | Epidermis - metabolism | Epidermis - pathology | RNA, Untranslated | Bacterial Proteins - genetics | Receptors, Cell Surface - metabolism | Epithelial Cells - pathology | Genes, Reporter - genetics | Mice, Transgenic | Carcinoma, Basal Cell - pathology | Mice, Inbred Strains | Clone Cells - metabolism | Keratin-14 - genetics | Carcinoma, Basal Cell - metabolism | Keratin-15 - metabolism | Keratin-19 - genetics | Proteins - genetics | Cell Lineage | Animals | Clone Cells - pathology | Proteins - metabolism | Models, Biological | Hair Follicle - metabolism | Bacterial Proteins - metabolism | Luminescent Proteins - genetics | Mice | Receptors, G-Protein-Coupled - genetics | Integrases - genetics | Keratin-15 - genetics | Luminescent Proteins - metabolism | Basal cell carcinoma | Stem cells | Genetic aspects | Cellular signal transduction | Research | Health aspects | Risk factors | Index Medicus
Journal Article