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Nature Medicine, ISSN 1078-8956, 09/2017, Volume 23, Issue 9, pp. 1055 - 1062
Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising anticancer therapies. The gene encoding the E3 ubiquitin ligase... 
SELECTIVE-INHIBITION | TARGET | MEDICINE, RESEARCH & EXPERIMENTAL | ANDROGEN RECEPTOR | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACUTE MYELOID-LEUKEMIA | ENHANCERS | CELL BIOLOGY | RNA-SEQ | BROMODOMAIN INHIBITION | MUTATIONS | BRD4 | Prostatic Neoplasms - metabolism | Immunoprecipitation | TOR Serine-Threonine Kinases - metabolism | Humans | Drug Resistance, Neoplasm | Male | Gene Expression Profiling | Molecular Targeted Therapy | Mechanistic Target of Rapamycin Complex 1 | Transcription Factors - drug effects | Multiprotein Complexes - metabolism | Prostatic Neoplasms - genetics | Proteasome Endopeptidase Complex - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Nuclear Proteins - drug effects | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | TOR Serine-Threonine Kinases - drug effects | Multiprotein Complexes - drug effects | Prostatic Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | RNA-Binding Proteins - antagonists & inhibitors | Triazoles - therapeutic use | Cell Survival | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Azepines - therapeutic use | RNA-Binding Proteins - drug effects | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Nuclear Proteins - antagonists & inhibitors | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | RNA-Binding Proteins - metabolism | rac1 GTP-Binding Protein - metabolism | Proto-Oncogene Proteins c-akt - drug effects | rac1 GTP-Binding Protein - genetics | Gene mutations | Physiological aspects | Genetic aspects | Research | Drug resistance | Drug therapy | Prostate cancer | Ubiquitin | Inhibitor drugs | Stabilization | AKT protein | Activation | Biosynthesis | Degradation | Proteins | Ubiquitination | Transcription activation | Bioindicators | Ubiquitin-protein ligase | Binding | Rac1 protein | Tumor cell lines | Gene expression | Cholesterol | Mutants | Inhibitors | Proteasomes | Biomarkers | Bet protein | Prostate | Cancer | Guanosinetriphosphatase
Journal Article
American Journal of Physiology - Endocrinology and Metabolism, ISSN 0193-1849, 2016, Volume 311, Issue 5, pp. E836 - E849
Alcohol ingestion decreases postexercise rates of muscle protein synthesis, but the mechanism( s) (e.g., increased protein breakdown) underlying this... 
Alcohol | Exercise | Autophagy | Protein | Apoptosis | alcohol | ACTIVATION | PHYSIOLOGY | autophagy | MITOCHONDRIAL BIOGENESIS | INCREASES | exercise | apoptosis | HUMAN SKELETAL-MUSCLE | MTOR | CELL-DEATH | DIRECT PHOSPHORYLATION | P53 | MESSENGER-RNA | RESISTANCE EXERCISE | protein | ENDOCRINOLOGY & METABOLISM | Molecular Chaperones - metabolism | Apoptosis - drug effects | Humans | Male | Autophagy - physiology | Alcohol Drinking | Carrier Proteins - drug effects | Autophagy - drug effects | Electron Transport Complex IV - metabolism | Transcription Factors - drug effects | Central Nervous System Depressants - pharmacology | Mitochondrial Proteins - drug effects | Young Adult | Organelle Biogenesis | Mitochondrial Proteins - metabolism | Dietary Proteins - pharmacology | Nuclear Respiratory Factor 1 - metabolism | Mitochondrial Proton-Translocating ATPases - drug effects | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - drug effects | Voltage-Dependent Anion Channel 1 - drug effects | Mitochondrial Degradation - physiology | Mitochondrial Proton-Translocating ATPases - metabolism | Cross-Over Studies | Signal Transduction - drug effects | Mitochondrial Degradation - drug effects | Adolescent | Electron Transport Complex IV - drug effects | Membrane Proteins - drug effects | Exercise - physiology | RNA-Binding Proteins - metabolism | Protein Kinases - metabolism | Muscle Fibers, Skeletal - drug effects | Healthy Volunteers | DNA-Binding Proteins - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism | Adult | Molecular Chaperones - drug effects | Membrane Proteins - metabolism | DNA Fragmentation - drug effects | Muscle Fibers, Skeletal - physiology | Proto-Oncogene Proteins - metabolism | Protein Kinases - drug effects | Proto-Oncogene Proteins - drug effects | Dietary Carbohydrates - pharmacology | DNA-Binding Proteins - drug effects | Tumor Suppressor Protein p53 - metabolism | Voltage-Dependent Anion Channel 1 - metabolism | Tumor Suppressor Protein p53 - drug effects | Nuclear Respiratory Factor 1 - drug effects | RNA-Binding Proteins - drug effects | Transcription Factors - metabolism | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - drug effects | Ethanol - pharmacology | Carrier Proteins - metabolism | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Apoptosis - physiology | Autophagy (Cytology) | Cell research | Alcoholic beverages | Physiological aspects | Cellular signal transduction | Research
Journal Article
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 10/2013, Volume 188, Issue 7, pp. 770 - 775
The remarkable success of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors in patients with EGFR... 
Molecular targeted therapy | Lung cancer | Cancer genomics | RET | GEFITINIB | EML4-ALK FUSION GENE | KINASE INHIBITOR | ALK INHIBITOR | SOMATIC MUTATIONS | EGFR | CHEMOTHERAPY | lung cancer | PHASE-II TRIAL | RESPIRATORY SYSTEM | CRIZOTINIB | cancer genomics | molecular targeted therapy | CRITICAL CARE MEDICINE | Lung Neoplasms - drug therapy | Oncogene Proteins - genetics | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Adenocarcinoma of Lung | Receptor, ErbB-2 - genetics | Genomics | Humans | ErbB Receptors - genetics | Antineoplastic Agents - therapeutic use | ErbB Receptors - therapeutic use | Anaplastic Lymphoma Kinase | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adenocarcinoma - genetics | ras Proteins - drug effects | Receptor, ErbB-2 - drug effects | Molecular Targeted Therapy - methods | Lung Neoplasms - genetics | Proto-Oncogene Proteins - drug effects | Carcinoma, Non-Small-Cell Lung - genetics | Proto-Oncogene Proteins c-met - drug effects | Proto-Oncogene Proteins - genetics | Mutation - genetics | Adenocarcinoma - drug therapy | Oncogene Proteins - drug effects | Proto-Oncogene Proteins c-met - genetics | Mutation - drug effects | Receptor Protein-Tyrosine Kinases - genetics | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - drug effects | Proto-Oncogene Proteins B-raf - genetics | Receptor Protein-Tyrosine Kinases - therapeutic use | Proto-Oncogene Proteins c-ret - drug effects | Carcinoma, Non-Small-Cell Lung - drug therapy | Proto-Oncogene Proteins c-ret - genetics | Pulmonary
Journal Article
Cancer Treatment Reviews, ISSN 0305-7372, 2014, Volume 40, Issue 6, pp. 750 - 759
Abstract The hedgehog (Hh) pathway is aberrantly activated in a number of tumors. In medulloblastoma, basal cell carcinoma, and rhabdomyosarcoma, mutations in... 
Hematology, Oncology and Palliative Medicine | Hedgehog | Smoothened | Combination chemotherapy | Targeted therapy | Novel antitumor agents | Cell signaling | STEM-CELLS | ACTIVATED PROTEIN-KINASE | SELF-RENEWAL | CHRONIC MYELOID-LEUKEMIA | EPITHELIAL-MESENCHYMAL TRANSITION | GLI TRANSCRIPTION FACTORS | ONCOLOGY | BASAL-CELL CARCINOMA | PROSTATE-CANCER | TARGETING HEDGEHOG | SONIC-HEDGEHOG | Hedgehog Proteins - drug effects | Neoplasms - metabolism | TOR Serine-Threonine Kinases - metabolism | Receptors, Notch - metabolism | Humans | Hedgehog Proteins - metabolism | Receptor, Epidermal Growth Factor - drug effects | Phosphatidylinositol 3-Kinases - metabolism | raf Kinases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Receptor, Epidermal Growth Factor - metabolism | Phosphatidylinositol 3-Kinases - drug effects | Proto-Oncogene Proteins c-akt - metabolism | TOR Serine-Threonine Kinases - drug effects | Janus Kinase 2 - antagonists & inhibitors | Molecular Targeted Therapy - methods | Proto-Oncogene Proteins p21(ras) - metabolism | Receptors, Notch - drug effects | Fusion Proteins, bcr-abl - drug effects | Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - drug effects | Animals | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | raf Kinases - drug effects | Fusion Proteins, bcr-abl - metabolism | Proto-Oncogene Proteins c-akt - drug effects | Receptor Cross-Talk - drug effects | Care and treatment | Health aspects | Leukemia | Analysis | Cancer
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2016, Volume 113, Issue 50, pp. E8051 - E8058
Protein–protein interactions play a central role in cellular function. Improving the understanding of complex formation has many practical applications,... 
Druggable surface | Direct coupling analysis | Drug design | Protein-protein interface | Hot spots | drug design | MULTIDISCIPLINARY SCIENCES | DRUG DISCOVERY | DIMERIZATION | protein-protein interface | INHIBITION | CONSERVATION | hot spots | CDK1 | HOT-SPOTS | direct coupling analysis | HIV-1 PROTEASE | BINDING-SITES | WEB SERVER | druggable surface | COMPUTATIONAL PREDICTION | Histone Deacetylase 1 - chemistry | Molecular Probes | HIV Protease - drug effects | Humans | Proto-Oncogene Proteins c-mdm2 - chemistry | CDC2-CDC28 Kinases - antagonists & inhibitors | Repressor Proteins - antagonists & inhibitors | HIV Protease Inhibitors - pharmacology | Proto-Oncogene Proteins c-mdm2 - drug effects | CDC2 Protein Kinase - drug effects | Drug Design | Histone Deacetylase 1 - drug effects | CDC2 Protein Kinase - chemistry | Histone Deacetylase 1 - antagonists & inhibitors | Binding Sites | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Molecular Docking Simulation - methods | Repressor Proteins - chemistry | Protein Interaction Domains and Motifs - drug effects | CDC2 Protein Kinase - antagonists & inhibitors | HIV-1 - drug effects | CDC2-CDC28 Kinases - chemistry | CDC2-CDC28 Kinases - drug effects | Histone Deacetylases - chemistry | HIV Protease Inhibitors - chemistry | Tumor Necrosis Factor-alpha - chemistry | Tumor Necrosis Factor-alpha - drug effects | HIV-1 - enzymology | Histone Deacetylases - drug effects | Repressor Proteins - drug effects | HIV Protease - chemistry | Protein Multimerization - drug effects | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Evolution, Molecular | Observations | Protein-protein interactions | Biological Sciences | PNAS Plus | protein−protein interface
Journal Article
Nature Communications, ISSN 2041-1723, 07/2017, Volume 8, Issue 1, p. 16078
BCL-2 family proteins are central regulators of mitochondrial apoptosis and validated anticancer targets. Using small cell lung cancer (SCLC) as a model, we... 
CELL LUNG-CANCER | SELECTIVE-INHIBITION | BAK ACTIVATION | POTENT | MULTIDISCIPLINARY SCIENCES | BIM | TRANSCRIPTION | DEATH | CDK INHIBITOR | ABT-263 | BH3 DOMAIN | Lung Neoplasms - drug therapy | Apoptosis - drug effects | Humans | Lung Neoplasms - metabolism | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Drug Resistance, Neoplasm | Molecular Targeted Therapy | Apoptosis Regulatory Proteins - drug effects | Myeloid Cell Leukemia Sequence 1 Protein - drug effects | Small Cell Lung Carcinoma - drug therapy | Small Cell Lung Carcinoma - metabolism | bcl-X Protein - drug effects | Proto-Oncogene Proteins c-bcl-2 - metabolism | bcl-X Protein - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Myeloid Cell Leukemia Sequence 1 Protein - antagonists & inhibitors | Aniline Compounds - pharmacology | Cyclin-Dependent Kinase 9 - antagonists & inhibitors | Sulfonamides - pharmacology | Apoptosis Regulatory Proteins - metabolism | Drug Synergism | Pyridinium Compounds - pharmacology | Bridged Bicyclo Compounds, Heterocyclic - pharmacology | High-Throughput Screening Assays | Apoptosis Regulatory Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-bcl-2 - drug effects | Cell Line, Tumor | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | bcl-X Protein - metabolism | Doxorubicin - pharmacology | Regulators | Bax protein | Bcl-2 protein | Small cell lung carcinoma | Lung cancer | High-throughput screening | Doxorubicin | BAK protein | Mcl-1 protein | Proteins | Mitochondria | Inhibitors | Bcl-x protein | Anthracycline | Addiction | Cell death | Sequestering | Cancer | Apoptosis
Journal Article
Cell, ISSN 0092-8674, 2005, Volume 122, Issue 6, pp. 927 - 939
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 10/2009, Volume 101, Issue 19, pp. 1308 - 1324
The monoclonal antibodies panitumumab and cetuximab that target the epidermal growth factor receptor (EGFR) have expanded the range of treatment options for... 
CELL LUNG-CANCER | PHASE-III TRIAL | TYROSINE KINASE INHIBITORS | COLON-CANCER | KRAS MUTATIONS | K-RAS MUTATIONS | PROGRESSION-FREE-SURVIVAL | ONCOLOGY | CETUXIMAB PLUS IRINOTECAN | IN-SITU HYBRIDIZATION | GENE COPY NUMBER | PTEN Phosphohydrolase - drug effects | Predictive Value of Tests | Proto-Oncogene Proteins p21(ras) - genetics | Colorectal Neoplasms - genetics | Humans | Antibodies, Monoclonal - therapeutic use | Antibodies, Monoclonal, Humanized | Receptor, Epidermal Growth Factor - metabolism | Colorectal Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - drug effects | Biomarkers, Tumor - metabolism | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Cetuximab | Odds Ratio | PTEN Phosphohydrolase - genetics | Proto-Oncogene Proteins - drug effects | Antibodies, Monoclonal - pharmacology | Proto-Oncogene Proteins - genetics | Randomized Controlled Trials as Topic | Phosphatidylinositol 3-Kinases - genetics | Disease-Free Survival | Proto-Oncogene Proteins p21(ras) - drug effects | Animals | Class I Phosphatidylinositol 3-Kinases | Mutation - drug effects | Proto-Oncogene Proteins B-raf - drug effects | Proto-Oncogene Proteins B-raf - genetics | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Colorectal Neoplasms - pathology | Neoplasm Staging | Research Design | Usage | Care and treatment | Prognosis | Gene mutations | Colorectal cancer | Monoclonal antibodies | Development and progression | Genetic aspects | Research | Biological markers | Health aspects | Review
Journal Article
Leukemia, ISSN 0887-6924, 07/2011, Volume 25, Issue 7, pp. 1064 - 1079
It has become apparent that regulation of protein translation is an important determinant in controlling cell growth and leukemic transformation. The... 
mTOR | translation | sensitivity | PI3K | therapy | resistance | TUMOR-SUPPRESSOR CANDIDATE | PROTEIN-KINASE | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | GROWTH-FACTOR RECEPTOR | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | AKT/PROTEIN-KINASE-B | ACUTE LYMPHOBLASTIC-LEUKEMIA | HEMATOPOIETIC STEM-CELLS | CHRONIC LYMPHOCYTIC-LEUKEMIA | HEMATOLOGY | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Neoplasm Proteins - physiology | PTEN Phosphohydrolase - physiology | Apoptosis - genetics | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - genetics | Gene Expression Regulation, Leukemic - genetics | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | Transcription Factors - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | PTEN Phosphohydrolase - antagonists & inhibitors | TOR Serine-Threonine Kinases - genetics | Protein Processing, Post-Translational - drug effects | Drug Design | TOR Serine-Threonine Kinases - physiology | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Leukemia - genetics | Multiprotein Complexes - drug effects | PTEN Phosphohydrolase - genetics | Proteins - physiology | Transcription Factors - physiology | RNA, Messenger - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Transcription Factors - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - physiology | Multiprotein Complexes - physiology | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | Pseudogenes | Signal Transduction - drug effects | Phosphatidylinositol 3-Kinases - physiology | Proteins - drug effects | RNA, Neoplasm - genetics | Protein Biosynthesis - drug effects | MicroRNAs - genetics | Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Genes | Leukemia | Physiological aspects | Development and progression | Genetic aspects | Research | Antineoplastic agents | Drug therapy | Health aspects
Journal Article