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Journal of Clinical Investigation, ISSN 0021-9738, 01/2008, Volume 118, Issue 1, pp. 217 - 228
Loss of the tumor suppressor gene von Hippel-Lindau (VHL) plays a key role in the oncogenesis of clear cell renal cell carcinoma (CCRCC). The loss leads to... 
MEDICINE, RESEARCH & EXPERIMENTAL | HIF-1 | TUMOR SUPPRESSION | CYCLIN D1 | PATHWAY | GENE ALTERATIONS | VHL | KIDNEY | FATE | EXPRESSION | CANCER | Neoplasm Transplantation | RNA, Small Interfering - genetics | Humans | Carcinoma, Renal Cell - genetics | Male | Intracellular Signaling Peptides and Proteins - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Basic Helix-Loop-Helix Transcription Factors - metabolism | Cell Transformation, Neoplastic - genetics | Serrate-Jagged Proteins | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Membrane Proteins - metabolism | Von Hippel-Lindau Tumor Suppressor Protein - genetics | Carcinoma, Renal Cell - drug therapy | Intracellular Signaling Peptides and Proteins - genetics | Von Hippel-Lindau Tumor Suppressor Protein - metabolism | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Carcinoma, Renal Cell - pathology | Membrane Proteins - genetics | RNA, Small Interfering - pharmacology | Intercellular Signaling Peptides and Proteins - genetics | Signal Transduction - genetics | Receptor, Notch1 - metabolism | Cell Transformation, Neoplastic - metabolism | Cyclin-Dependent Kinase Inhibitor p27 | Carcinoma, Renal Cell - metabolism | Animals | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | Cell Transformation, Neoplastic - drug effects | Receptor, Notch1 - antagonists & inhibitors | Cell Transformation, Neoplastic - pathology | Receptor, Notch1 - genetics | Calcium-Binding Proteins - genetics | Care and treatment | Enzyme inhibitors | Tumor suppressor genes | Dosage and administration | Genetic aspects | Carcinoma, Renal cell | Research | Health aspects | Index Medicus | Abridged Index Medicus | RNA; Small Interfering/genetics/pharmacology | Membrane Proteins/genetics/metabolism | Mice; Nude | Signal Transduction/drug effects/genetics | Intracellular Signaling Peptides and Proteins/genetics/metabolism | Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism | Receptor; Notch1/antagonists & inhibitors/genetics/metabolism | Von Hippel-Lindau Tumor Suppressor Protein/genetics/metabolism | Cell Transformation; Neoplastic/drug effects/genetics/metabolism/pathology | Cyclin-Dependent Kinase Inhibitor p21/genetics/metabolism | Cell Line; Tumor | Intercellular Signaling Peptides and Proteins/genetics/metabolism | Calcium-Binding Proteins/genetics/metabolism | Carcinoma; Renal Cell/drug therapy/genetics/metabolism/pathology
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2013, Volume 110, Issue 31, pp. 12655 - 12660
The positive transcription elongation factor b (P-TEFb) is involved in physiological and pathological events including inflammation, cancer, AIDS, and cardiac... 
T lymphocytes | Pathology | RNA | HEK293 cells | Genes | Cell lines | Antibodies | Small nuclear RNA | Gene expression regulation | HIV 1 | 7SK SNRNA | TRANSCRIPTION FACTOR BCL11B | ELONGATION | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | POLYMERASE | HIV-1 TAT | MICROGLIAL CELLS | T-CELL LINEAGE | BROMODOMAIN PROTEIN BRD4 | RNA-Binding Proteins - genetics | Humans | Myosin Heavy Chains - genetics | Cardiomegaly - pathology | Positive Transcriptional Elongation Factor B - metabolism | Positive Transcriptional Elongation Factor B - genetics | Myosin Heavy Chains - metabolism | RNA, Small Nuclear - genetics | Tumor Suppressor Proteins - genetics | HEK293 Cells | Cardiac Myosins - metabolism | Repressor Proteins - metabolism | Promoter Regions, Genetic | Tumor Suppressor Proteins - metabolism | Protein Structure, Secondary | Cyclin-Dependent Kinase 9 - genetics | Cardiac Myosins - genetics | Repressor Proteins - genetics | Transcription Factors - genetics | Transcription Factors - metabolism | Animals | Cyclin-Dependent Kinase 9 - metabolism | Mice | RNA, Small Nuclear - metabolism | Cardiomegaly - genetics | RNA-Binding Proteins - metabolism | Cardiomegaly - metabolism | Physiological aspects | Transcription factors | Genetic aspects | Heart enlargement | Health aspects | Myosin | Proteins | Heart | Acquired immune deficiency syndrome--AIDS | Ribonucleic acid--RNA | Cancer | Index Medicus | Life Sciences | Neurons and Cognition | Biological Sciences
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2008, Volume 118, Issue 1, pp. 79 - 88
Despite great interest in cancer chemoprevention, effective agents are few. Here we show that chloroquine, a drug that activates the stress-responsive Atm-p53... 
MEDICINE, RESEARCH & EXPERIMENTAL | BCL-X-L | SIGNALING PATHWAYS | INDUCED APOPTOSIS | PHOSPHORYLATION | ATM | AUTOPHAGY | CYTOCHROME-C RELEASE | MYC-INDUCED LYMPHOMAGENESIS | TRANSGENIC MICE | P53 | Apoptosis - drug effects | Humans | Apoptosis - genetics | Male | Autophagy - drug effects | Burkitt Lymphoma - pathology | Neoplasms, Experimental - pathology | Chloroquine - pharmacology | Cell Transformation, Neoplastic - genetics | Autophagy - genetics | B-Lymphocytes - pathology | B-Lymphocytes - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | Embryo, Mammalian - pathology | Cell Cycle Proteins - metabolism | Neoplasms, Experimental - prevention & control | bcl-2-Associated X Protein - metabolism | Ataxia Telangiectasia Mutated Proteins | Fibroblasts - pathology | Ataxia Telangiectasia - pathology | Ataxia Telangiectasia - genetics | Mice | Proto-Oncogene Proteins c-myc - genetics | Neoplasms, Experimental - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Embryo, Mammalian - metabolism | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Caspases - metabolism | Lysosomes - metabolism | Burkitt Lymphoma - prevention & control | Mice, Mutant Strains | Tumor Suppressor Proteins - genetics | Neoplasms, Experimental - genetics | Burkitt Lymphoma - genetics | Cell Cycle Proteins - genetics | Female | Lysosomes - pathology | Antirheumatic Agents - pharmacology | bcl-2-Associated X Protein - genetics | Antirheumatic Agents - therapeutic use | Ataxia Telangiectasia - prevention & control | Caspases - genetics | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Burkitt Lymphoma - metabolism | Chloroquine - therapeutic use | Ataxia Telangiectasia - metabolism | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Animals | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Cell Transformation, Neoplastic - pathology | Prevention | Chloroquine | Lysosomes | Dosage and administration | Research | Drug therapy | Health aspects | Cancer | Index Medicus | Abridged Index Medicus
Journal Article
Cellular Signalling, ISSN 0898-6568, 04/2013, Volume 25, Issue 4, pp. 931 - 938
The interleukin-6 (IL-6)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway mediates cell proliferation and migration.... 
Cytoskeleton | p27 | Gastric cancer | Migration | Invasion | Signal transducer and activator of transcription 3 | P27 | ACTIVATION | E-CADHERIN | BETA-CATENIN | INTERLEUKIN-6 | IL-6 | CELL BIOLOGY | OVEREXPRESSION | SIGNALING PATHWAY | SKP2 | CARCINOMA | CYCLE | Up-Regulation | Cell Proliferation | Cadherins - metabolism | Humans | Stomach Neoplasms - metabolism | Sp1 Transcription Factor - metabolism | Stomach Neoplasms - pathology | rhoA GTP-Binding Protein - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Matrix Metalloproteinase 9 - metabolism | Microtubules - metabolism | RNA Interference | Janus Kinase 2 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Focal Adhesion Kinase 1 - metabolism | Interleukin-6 - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Signal Transduction | Matrix Metalloproteinase 2 - metabolism | Down-Regulation | S-Phase Kinase-Associated Proteins - metabolism | Cell Adhesion | GPI-Linked Proteins - metabolism | Cell Line, Tumor | STAT3 Transcription Factor - antagonists & inhibitors | Stathmin - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - genetics | RNA, Small Interfering - metabolism | Phosphates | Enzymes | Cysteine | Analysis | Fluorescein | Cancer cells | Tubulins | Stomach cancer | Enzyme-linked immunosorbent assay | Cancer | Index Medicus
Journal Article
Journal of Immunology, ISSN 0022-1767, 05/2013, Volume 190, Issue 9, pp. 4640 - 4649
Dendritic cells (DC) are professional APCs that regulate innate and adaptive immunity. The role of fatty-acid synthesis in DC development and function is... 
CANCER-CELLS | APOPTOSIS | KAPPA-B ACTIVATION | UNFOLDED PROTEIN RESPONSE | CYTOKINE PRODUCTION | SYNTHASE INHIBITION | ER STRESS | MAP KINASE | MACROPHAGES | ENDOPLASMIC-RETICULUM STRESS | IMMUNOLOGY | Fatty Acids - immunology | Leukocytes, Mononuclear - metabolism | Chemokine CCL2 - immunology | Dendritic Cells - immunology | Humans | Caspase 3 - metabolism | Male | Cyclin B1 - metabolism | Interferon-gamma - metabolism | PPAR gamma - metabolism | CD4-Positive T-Lymphocytes - immunology | Mitogen-Activated Protein Kinase Kinases - metabolism | Liver - immunology | CD8-Positive T-Lymphocytes - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Liver - metabolism | CD4-Positive T-Lymphocytes - metabolism | Interleukin-12 - metabolism | B7-2 Antigen - metabolism | Cell Differentiation - immunology | Intercellular Adhesion Molecule-1 - metabolism | Proto-Oncogene Proteins c-akt - immunology | T-Lymphocytes, Cytotoxic - metabolism | Endoplasmic Reticulum - immunology | Interleukin-12 - immunology | Mice | Killer Cells, Natural - metabolism | CD8-Positive T-Lymphocytes - immunology | bcl-X Protein - metabolism | Fatty Acids - biosynthesis | Mitogen-Activated Protein Kinase Kinases - immunology | Caspase 3 - immunology | Endoplasmic Reticulum - metabolism | Genes, MHC Class II - immunology | PPAR gamma - immunology | Cyclin B1 - immunology | Leukocytes, Mononuclear - immunology | bcl-X Protein - immunology | Killer Cells, Natural - immunology | Chemokine CCL2 - metabolism | B7-2 Antigen - immunology | Fatty Acids - metabolism | Dendritic Cells - metabolism | T-Lymphocytes, Cytotoxic - immunology | B7-1 Antigen - immunology | Intercellular Adhesion Molecule-1 - immunology | Mice, Inbred C57BL | B7-1 Antigen - metabolism | Animals | Apoptosis - immunology | Interferon-gamma - immunology | Dendritic Cells - cytology | Index Medicus | Abridged Index Medicus | Fatty-acid synthesis | ER stress | NK cells | T cells | Bone marrow dendritic cells
Journal Article
Nature, ISSN 0028-0836, 08/2005, Volume 436, Issue 7052, pp. 807 - 811
The c-Myc oncoprotein promotes proliferation and apoptosis, such that mutations that disable apoptotic programmes often cooperate with MYC during... 
APOPTOSIS | ONCOGENE | GENE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | N-TERMINAL DOMAIN | C-MYC | TRANSFORMING ACTIVITY | BURKITT-LYMPHOMA CELLS | TRANSACTIVATION DOMAIN | MUTATIONS | Cell Proliferation | Humans | Adoptive Transfer | Cyclin-Dependent Kinase Inhibitor p16 | Burkitt Lymphoma - pathology | Stem Cell Transplantation | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Burkitt Lymphoma - genetics | Membrane Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Burkitt Lymphoma - metabolism | Mutation - genetics | Proto-Oncogene Proteins c-myc - metabolism | Animals | Apoptosis Regulatory Proteins | Carrier Proteins - metabolism | Genes, myc - genetics | Alleles | Mice | Proto-Oncogene Proteins c-myc - genetics | Tumor Suppressor Protein p14ARF - metabolism | Apoptosis | Proteins | Oncology | Mutation | Cellular biology | Tumors | Index Medicus | Proto-Oncogene Proteins c-myc/genetics/metabolism | Mutation/genetics | Tumor Suppressor Protein p14ARF/metabolism | Cell Cycle Proteins/metabolism | Proto-Oncogene Proteins/metabolism | Tumor Suppressor Protein p53/metabolism | Burkitt Lymphoma/genetics/metabolism/pathology | Genes; myc/genetics | Membrane Proteins/metabolism | Mice; Inbred C57BL | Proto-Oncogene Proteins c-bcl-2/metabolism | Carrier Proteins/metabolism
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
Oncogene, ISSN 0950-9232, 07/2007, Volume 26, Issue 32, pp. 4617 - 4626
Infection with Helicobacter pylori cagA-positive strains is associated with gastric adenocarcinoma. Intestinal metaplasia is a precancerous lesion of the... 
β-catenin | Gastric adenocarcinoma | Helicobacter pylori CagA | E-cadherin | Intestinal metaplasia | beta-catenin | TARGET | ACTIVATION | PROTEIN | CDX1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | CELL BIOLOGY | gastric adenocarcinoma | GENE | ONCOLOGY | intestinal metaplasia | WNT PATHWAY | ATROPHIC GASTRITIS | GENETICS & HEREDITY | INFECTION | EXPRESSION | Intestinal Mucosa - metabolism | Phosphorylation | Adenocarcinoma - pathology | Cadherins - metabolism | beta Catenin - analysis | Adenocarcinoma - etiology | Homeodomain Proteins - metabolism | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Stomach Neoplasms - metabolism | Cytoplasm - metabolism | Gastric Mucosa - pathology | Precancerous Conditions - metabolism | Stomach Neoplasms - pathology | Bacterial Proteins - analysis | Gastric Mucosa - metabolism | Adenocarcinoma - metabolism | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Mucins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Precancerous Conditions - pathology | Stomach Neoplasms - etiology | Cytoplasm - chemistry | Cell Line | Cadherins - analysis | Cell Transformation, Neoplastic - metabolism | Precancerous Conditions - genetics | beta Catenin - metabolism | Homeodomain Proteins - genetics | Mucin-2 | Tyrosine - metabolism | Antigens, Bacterial - analysis | Bacterial Proteins - metabolism | Cell Nucleus - chemistry | Cell Transformation, Neoplastic - pathology | Antigens, Bacterial - metabolism | Intestinal Mucosa - pathology | Index Medicus
Journal Article
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 510, Issue 7506, pp. 547 - 551
Journal Article