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PLoS ONE, ISSN 1932-6203, 05/2009, Volume 4, Issue 5, pp. e5622 - e5622
Background: The INK4/ARF locus encodes three tumor suppressor genes (p15(Ink4b), Arf and p16(Ink4a)) and is frequently inactivated in a large number of human... 
BIOLOGY | NIH 3T3 Cells | Myeloid-Lymphoid Leukemia Protein - metabolism | Cellular Senescence | Repressor Proteins - metabolism | Fibroblasts - metabolism | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Cycle Proteins - metabolism | Gene Silencing | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Nuclear Proteins - metabolism | Polycomb-Group Proteins | Enhancer of Zeste Homolog 2 Protein | Polycomb Repressive Complex 2 | Animals | Cyclin-Dependent Kinase Inhibitor p16 - chemistry | Polycomb Repressive Complex 1 | Histone-Lysine N-Methyltransferase - metabolism | Embryo, Mammalian - cytology | Models, Biological | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Protein Binding | DNA Replication Timing | Fibroblasts - cytology | Mice | Histones - metabolism | Methylation | Proteins | Epigenetic inheritance | DNA replication | Senescence | Chromatin | Genes | INK4a protein | Genomes | Recruitment | Cell growth | Transcription activation | Cell cycle | Fibroblasts | Cyclin-dependent kinase inhibitors | Deoxyribonucleic acid--DNA | p16 Protein | INK4 protein | Embryo fibroblasts | Gene expression | Embryos | Loci | DNA biosynthesis | Polycomb group proteins | Replication origins | Pilot projects | Insects | Stem cells | Epigenetics | Tumor suppressor genes | Replication | Embryo, Mammalian | Histone-Lysine N-Methyltransferase | Repressor Proteins | Cell Aging | Nuclear Proteins | Cyclin-Dependent Kinase Inhibitor p16 | Life Sciences | Immunology | Histones | Myeloid-Lymphoid Leukemia Protein | Proto-Oncogene Proteins | Cell Cycle Proteins | Deoxyribonucleic acid | DNA
Journal Article
Genes and Development, ISSN 0890-9369, 05/2013, Volume 27, Issue 10, pp. 1101 - 1114
Tumorigenesis results from dysregulation of oncogenes and tumor suppressors that influence cellular proliferation, differentiation, apoptosis, and/or... 
Huwe1 | c-Myc | Mule | Ras | p21 | Miz1 | DNA-DAMAGE | KERATINOCYTE GROWTH | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | BASE EXCISION-REPAIR | HUWE1 UBIQUITIN LIGASE | NEGATIVE REGULATION | GENETICS & HEREDITY | ARF TUMOR-SUPPRESSOR | DIFFERENTIATION | MIZ-1 | HUMAN CANCER | Protein Inhibitors of Activated STAT - deficiency | Tetradecanoylphorbol Acetate - pharmacology | 9,10-Dimethyl-1,2-benzanthracene - pharmacology | Male | Protein Inhibitors of Activated STAT - metabolism | Cyclin-Dependent Kinase Inhibitor p15 - biosynthesis | Oncogene Protein p21(ras) - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | Oncogene Protein p21(ras) - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Nuclear Proteins - deficiency | Protein Inhibitors of Activated STAT - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Nuclear Proteins - genetics | Protein Inhibitors of Activated STAT - antagonists & inhibitors | Skin Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis | Signal Transduction | Down-Regulation | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Skin Neoplasms - chemically induced | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Skin Neoplasms - metabolism | Keratinocytes - pathology | Animals | Tumor Suppressor Protein p53 | Keratinocytes - drug effects | Keratinocytes - metabolism | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-myc - deficiency | Skin Neoplasms - genetics | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Ubiquitin-Protein Ligases - deficiency | Mice | Proto-Oncogene Proteins c-myc - genetics | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Genes, ras | Ubiquitin-Protein Ligases - genetics | Oncogene Protein p21(ras) - genetics | Carcinogenesis | Ras genes | Analysis | Research Paper
Journal Article
Nature Cell Biology, ISSN 1465-7392, 2009, Volume 11, Issue 8, pp. 973 - 979
Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells(1). Paradoxically, senescent cells also secrete factors that alter... 
TUMOR SUPPRESSION | HUMAN-CELLS | HUMAN FIBROBLASTS | GROWTH-FACTOR | ONCOGENE-INDUCED SENESCENCE | CELLULAR SENESCENCE | CANCER | TUMORIGENESIS | P53 | TELOMERES | CELL BIOLOGY | RNA, Small Interfering - genetics | Humans | Male | Green Fluorescent Proteins - genetics | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Telomerase - genetics | Transfection | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Telomerase - metabolism | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Telomere - genetics | Cell Line | Green Fluorescent Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Enzyme-Linked Immunosorbent Assay | Cell Cycle Proteins - metabolism | Cells, Cultured | Cytokines - secretion | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cellular Senescence - physiology | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Interleukin-6 - secretion | Blotting, Western | Fibroblasts - radiation effects | Checkpoint Kinase 2 | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Signal Transduction - physiology | Fibroblasts - cytology | DNA Damage | Microscopy, Fluorescence | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Cytokines | DNA damage
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 | 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
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
Journal Article
Blood, ISSN 0006-4971, 09/2012, Volume 120, Issue 11, pp. 2280 - 2289
Peripheral T-cell lymphomas (PTCLs) are aggressive malignancies of mature T lymphocytes with 5-year overall survival rates of only similar to 35%. Improvement... 
LUNG-CANCER | OVEREXPRESSION | CANCER DEVELOPMENT | P53 PROTEIN | TRANSLOCATIONS | MUTATIONS | P63 | IDENTIFICATION | HEMATOLOGY | EXPRESSION | CARCINOMA | Oncogene Proteins, Fusion - metabolism | Transcription Factors - chemistry | Oligonucleotide Array Sequence Analysis | United States | Humans | Male | Lymphoma, Large B-Cell, Diffuse - metabolism | Oxidoreductases - chemistry | Tumor Suppressor Protein p53 - genetics | Oncogene Proteins, Fusion - chemistry | WW Domain-Containing Oxidoreductase | DNA Mutational Analysis | Lymphoma, T-Cell, Peripheral - metabolism | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Female | Repressor Proteins - metabolism | Genome-Wide Association Study | Repressor Proteins - chemistry | Tumor Suppressor Proteins - metabolism | Lymphoma, Large B-Cell, Diffuse - pathology | Oxidoreductases - metabolism | Oxidoreductases - genetics | Lymphoma, T-Cell, Peripheral - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Repressor Proteins - genetics | Mutant Proteins - metabolism | Transcription Factors - genetics | Sequence Homology, Nucleic Acid | Lymphoma, Large B-Cell, Diffuse - mortality | Transcription Factors - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - chemistry | Oncogene Proteins, Fusion - genetics | Gene Rearrangement | Lymphoma, T-Cell, Peripheral - pathology | Mutant Proteins - chemistry | Cell Line, Tumor | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Tumor Suppressor Protein p53 - chemistry | Mutation | Lymphoma, Large B-Cell, Diffuse - genetics | Lymphoma, T-Cell, Peripheral - mortality | Lymphoid Neoplasia
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 12/2006, Volume 203, Issue 13, pp. 2793 - 2799
The ataxia telangiectasia mutated (ATM) kinase is a key tumor suppressor that regulates numerous cell cycle checkpoints as well as apoptosis. Here, we report... 
MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | PATHWAY | ATM ACTIVATION | IMMUNOLOGY | CELL-CYCLE CHECKPOINTS | PPM1D | ATAXIA-TELANGIECTASIA | AUTOPHOSPHORYLATION | CANCER | TUMORIGENESIS | P53 | Phosphorylation | Cell Proliferation | Phosphoprotein Phosphatases - metabolism | Apoptosis - genetics | Neoplasm Proteins - metabolism | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Lymphoma - metabolism | Caspases - metabolism | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Lymphoma - pathology | p38 Mitogen-Activated Protein Kinases - metabolism | Neoplasm Proteins - genetics | B-Lymphocytes - metabolism | Protein-Serine-Threonine Kinases - metabolism | Gene Expression | Tumor Suppressor Proteins - metabolism | Heat-Shock Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein Phosphatase 2C | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Lymphoma - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Mice, Transgenic | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Mice, Inbred Strains | Reverse Transcriptase Polymerase Chain Reaction | Caspase Inhibitors | Blotting, Western | Mice, Knockout | Animals | Phosphoprotein Phosphatases - genetics | Models, Biological | Survival Analysis | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Protein Binding | Mice | Proto-Oncogene Proteins c-myc - genetics | HSP27 Heat-Shock Proteins | Brief Definitive Reports
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 09/2015, Volume 465, Issue 1, pp. 71 - 76
Shikonin, a natural naphthoquinone isolated from the Chinese traditional medicine Zi Cao ( ), is known to suppress the growth of several cancer cell types. In... 
Shikonin | p73 | p16INK4A | ICBP90 | Tumor suppressor gene | Apoptosis | p16 | UHRF1 | CCAAT-BINDING-PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | INDUCTION | II-ALPHA EXPRESSION | IN-VITRO | BIOPHYSICS | GENE | PATHWAY | COLORECTAL-CANCER | SRA DOMAIN | p16(INK4A) | Luciferases - metabolism | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Gene Expression Regulation, Neoplastic | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Luciferases - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | DNA-Binding Proteins - metabolism | Proteolysis - drug effects | Proto-Oncogene Proteins c-bcl-2 - metabolism | DNA-Binding Proteins - agonists | MCF-7 Cells | CCAAT-Enhancer-Binding Proteins - antagonists & inhibitors | Tumor Suppressor Proteins - genetics | Caspase 3 - genetics | Female | CCAAT-Enhancer-Binding Proteins - genetics | Nuclear Proteins - genetics | Genes, Reporter | CCAAT-Enhancer-Binding Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Nuclear Proteins - agonists | Signal Transduction | DNA (Cytosine-5-)-Methyltransferase 1 | Cyclin-Dependent Kinase Inhibitor p16 - agonists | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Naphthoquinones - pharmacology | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | DNA (Cytosine-5-)-Methyltransferases - genetics | Poly(ADP-ribose) Polymerases - metabolism | Tumor Protein p73 | Poly(ADP-ribose) Polymerases - genetics | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | HeLa Cells | Antineoplastic Agents, Phytogenic - pharmacology | Proto-Oncogene Proteins c-bcl-2 - genetics | Tumor Suppressor Proteins - agonists | Sugars | Cancer | Monosaccharides | Protein binding
Journal Article
Cancer Research, ISSN 0008-5472, 02/2007, Volume 67, Issue 4, pp. 1626 - 1635
Cervical cancer is a leading cause of death due to cancer among women worldwide. Using transgenic mice to dissect the contributions of the human papillomavirus... 
UTERINE CERVIX | DIFFERENTIAL EXPRESSION | EPITHELIAL-CELLS | ONCOLOGY | UBIQUITIN-PROTEIN LIGASE | HUMAN SCRIBBLE | TYPE-16 E7 ONCOGENE | TUMOR-SUPPRESSOR PROTEIN | MEDIATED DEGRADATION | TRANSGENIC MOUSE MODEL | HUMAN HOMOLOG | Cell Cycle - genetics | Up-Regulation | Tumor Suppressor Protein p53 - biosynthesis | Skin - metabolism | Humans | Uterine Cervical Neoplasms - pathology | Minichromosome Maintenance Complex Component 7 | Oncogenes - physiology | Cyclin E - genetics | Tumor Suppressor Protein p53 - genetics | Retinoblastoma Protein - biosynthesis | Nuclear Proteins - biosynthesis | Uterine Cervical Neoplasms - chemically induced | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis | Female | Oncogene Proteins, Viral - genetics | Nuclear Proteins - genetics | Skin - virology | Estradiol - pharmacology | Repressor Proteins - metabolism | Oncogene Proteins, Viral - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Repressor Proteins - genetics | Mice, Transgenic | Cell Cycle Proteins - biosynthesis | DNA-Binding Proteins - genetics | Oncogene Proteins, Viral - biosynthesis | Cocarcinogenesis | Animals | Repressor Proteins - biosynthesis | Retinoblastoma Protein - genetics | Cyclin E - biosynthesis | Uterine Cervical Neoplasms - virology | Mice | DNA-Binding Proteins - biosynthesis
Journal Article
Cancer Research, ISSN 0008-5472, 08/2006, Volume 66, Issue 15, pp. 7473 - 7481
Glioblastoma multiforme is the most common and lethal form of primary brain cancer. Diagnosis of this advanced glioma has a poor prognosis due to the... 
MAMMALIAN TARGET | ONCOLOGY | TUMOR SUPPRESSION | PHOSPHATASE SHP-2 | GROWTH-FACTORS | JUVENILE MYELOMONOCYTIC LEUKEMIA | C-ROS | PTPN11 MUTATIONS | CELL-LINES | NOONAN-SYNDROME | BRAIN-TUMORS | Protein Kinases - metabolism | Glioblastoma - enzymology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 | Tumor Suppressor Protein p14ARF - deficiency | Protein-Tyrosine Kinases - metabolism | Brain Neoplasms - pathology | Protein Tyrosine Phosphatases - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Proto-Oncogene Proteins - biosynthesis | Recombinant Fusion Proteins - metabolism | Brain Neoplasms - metabolism | Astrocytoma - pathology | Protein-Tyrosine Kinases - genetics | Astrocytoma - enzymology | Glioblastoma - metabolism | Protein Phosphatase 2 | Proto-Oncogene Proteins c-akt - metabolism | Protein-Tyrosine Kinases - biosynthesis | Astrocytoma - metabolism | Proto-Oncogene Proteins - metabolism | Recombinant Fusion Proteins - biosynthesis | Brain Neoplasms - enzymology | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Signal Transduction | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Proto-Oncogene Proteins - genetics | src Homology Domains | Animals | Glioblastoma - pathology | SH2 Domain-Containing Protein Tyrosine Phosphatases | Recombinant Fusion Proteins - genetics | Mice | TOR Serine-Threonine Kinases | Enzyme Activation | Tumor Suppressor Protein p14ARF - genetics
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 12/2006, Volume 12, Issue 23, pp. 6929 - 6936
Purpose: Deregulation of mammalian Polycomb group (PcG) members may contribute to human carcinogenesis. p16INK4a and p14ARF tumor suppressors, human telomerase... 
Polycomb | HODGKINS LYMPHOMA | GROUP GENES | OVEREXPRESSION | ONCOPROTEIN | ONCOLOGY | GROUP PROTEINS | CELL-PROLIFERATION | TRANSCRIPTION FACTOR | CANCER | TRANSGENIC MICE | EZH2 | Humans | Gene Expression Profiling | Neoplasm Proteins - metabolism | Proto-Oncogene Proteins - biosynthesis | Breast Neoplasms - metabolism | DNA-Binding Proteins - metabolism | RNA, Messenger - biosynthesis | Telomerase - genetics | Nuclear Proteins - biosynthesis | Reverse Transcriptase Polymerase Chain Reaction - methods | Female | Telomerase - metabolism | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Neoplasm Proteins - biosynthesis | Down-Regulation | RNA, Messenger - genetics | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | DNA-Binding Proteins - genetics | Proto-Oncogene Proteins c-myc - metabolism | Breast Neoplasms - genetics | Polycomb Repressive Complex 1 | Repressor Proteins - biosynthesis | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Breast Neoplasms - diagnosis | Proto-Oncogene Proteins c-myc - genetics | Tumor Suppressor Protein p14ARF - genetics | Tumor Suppressor Protein p14ARF - metabolism | DNA-Binding Proteins - biosynthesis
Journal Article