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2008, Cancer drug discovery and development, ISBN 9781597453561, xi, 393
The epidermal growth factor (EGF) receptor and its downstream signal transduction networks have been implicated in the ontology and maintenance of tumor... 
drug therapy | Signal Transduction | drug effects | metabolism | Neoplasms | antagonists & inhibitors | Receptor, Epidermal Growth Factor | Clinical & internal medicine | Cancer | Chemotherapy | Treatment | Medicine & Public Health | Cancer Research | Oncology
Book
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2013, Volume 8, Issue 1, pp. e53510 - e53510
Background: There is increasing evidence that opioid analgesics may interfere with tumour growth. It is currently thought that these effects are mediated by... 
ACTIVATED PROTEIN-KINASE | INHIBITION | CARCINOMA CELLS | TYROSINE KINASE | DESENSITIZATION | MULTIDISCIPLINARY SCIENCES | DOWN-REGULATION | RESISTANCE | OPIOID RECEPTORS | MECHANISMS | EGF RECEPTOR | Receptor, ErbB-3 - metabolism | Receptor, ErbB-2 - genetics | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Receptor, ErbB-2 - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Neuregulin-1 - genetics | Proto-Oncogene Proteins c-akt - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Receptors, Opioid, kappa - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Morphine - pharmacology | Receptors, Opioid, mu - metabolism | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Receptors, Opioid, kappa - metabolism | Receptor, ErbB-3 - genetics | Adenocarcinoma - drug therapy | Breast Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Neuregulin-1 - metabolism | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Receptors, Opioid, mu - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Tyrosine | Morphine | Breast cancer | Growth | Protein kinases | Cancer cells | Adenocarcinoma | Phosphorylation | Immunoprecipitation | Laboratories | Switching theory | AKT protein | Feedback loops | Heregulin | Kinases | Receptors | Cell growth | Epidermal growth factor | Analgesics | Protein-tyrosine kinase receptors | Metalloproteinase | Protein-tyrosine kinase | ErbB-1 protein | Opioid receptors | ErbB protein | Extracellular signal-regulated kinase | ErbB-3 protein | Protein kinase inhibitors | ErbB-2 protein | 1-Phosphatidylinositol 3-kinase | Signaling | Breast | Sensitivity enhancement | Control theory | Cancer | Tumors | Apoptosis | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 04/2016, Volume 29, Issue 4, pp. 477 - 493
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2012, Volume 7, Issue 9, pp. e44471 - e44471
Journal Article
Molecular Cancer, ISSN 1476-4598, 06/2012, Volume 11, Issue 1, pp. 38 - 38
Background: Tri- and tetra-nucleotide repeats in mammalian genomes can induce formation of alternative non-B DNA structures such as triplexes and guanine... 
EXON | HUMAN BREAST | GENE | SEQUENCES | ONCOLOGY | U2AF | BIOCHEMISTRY & MOLECULAR BIOLOGY | INVOLVEMENT | IDENTIFICATION | EXPRESSION | SPLICING FACTOR | PRE-MESSENGER-RNA | RNA-Binding Proteins - genetics | Lymph Nodes - pathology | RecQ Helicases - metabolism | Humans | Werner Syndrome Helicase | Gene Expression Regulation, Neoplastic | Male | RecQ Helicases - genetics | DNA-Binding Proteins - metabolism | Splicing Factor U2AF | Neoplasm Metastasis | Octamer Transcription Factors - genetics | Female | Ribonucleoproteins - genetics | Exodeoxyribonucleases - genetics | Nuclear Proteins - genetics | Colorectal Neoplasms - metabolism | Octamer Transcription Factors - metabolism | Colorectal Neoplasms - mortality | Nuclear Matrix-Associated Proteins - metabolism | Nuclear Proteins - metabolism | Ribonucleoproteins - metabolism | DNA - metabolism | DNA-Binding Proteins - genetics | beta Catenin - metabolism | PTB-Associated Splicing Factor | beta Catenin - genetics | Nuclear Matrix-Associated Proteins - genetics | Exodeoxyribonucleases - metabolism | Proteomics | Protein Binding | Colorectal Neoplasms - pathology | Neoplasm Staging | RNA-Binding Proteins - metabolism | Lymphatic diseases | Patient outcomes | Genomics | Colorectal cancer | Antibodies | Genomes | Metastasis | Viral antibodies | Cancer patients | Gastrointestinal diseases | DNA | Binding proteins | Intermediate filament proteins | Protein binding | Studies | Proteins | Medical research | Mutation | Deoxyribonucleic acid--DNA | Index Medicus | DNA structure | TOR protein | catenin | c-Myc protein | Cyclin-dependent kinase 4 | Guanine | Lymph nodes | Western blotting | Genomic instability | Metastases | DNA-binding protein | ErbB-1 protein | splicing factors | streptavidin | proteomics | Stat5 protein | Survival | Chromosome translocations | Protein arrays | Mutagenesis | cyclin D1 | PTEN protein | Tumors
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2013, Volume 8, Issue 5, pp. e64672 - e64672
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2012, Volume 7, Issue 5, pp. e36828 - e36828
Background: Growth factors activating the ErbB receptors have been described in prostate tumors. The androgen dependent prostate cancer cell line, LNCaP,... 
GROWTH-FACTOR RECEPTOR | COMPLEX | PROTEIN | BECLIN-1 | C-ERBB-2 | PHOSPHORYLATION | BIOLOGY | HYDROGEN-PEROXIDE | DEATH | CARCINOMA | EXPRESSION | Reactive Oxygen Species - metabolism | Humans | Male | Autophagy - physiology | Prostatic Neoplasms - physiopathology | Neoplasms, Hormone-Dependent - physiopathology | Autophagy - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-bcl-2 - metabolism | Apoptosis Regulatory Proteins - genetics | TOR Serine-Threonine Kinases - physiology | Membrane Proteins - metabolism | Cell Death - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Prostatic Neoplasms - drug therapy | Beclin-1 | Prostatic Neoplasms - pathology | Adenine - analogs & derivatives | Membrane Proteins - genetics | Neuregulins - physiology | Adenine - pharmacology | Recombinant Proteins - pharmacology | Anthracenes - pharmacology | Apoptosis Regulatory Proteins - metabolism | MAP Kinase Signaling System - drug effects | Cell Death - physiology | Membrane Proteins - antagonists & inhibitors | Signal Transduction - drug effects | Neoplasms, Hormone-Dependent - pathology | Neuregulins - pharmacology | Acetylcysteine - pharmacology | Apoptosis Regulatory Proteins - antagonists & inhibitors | Cell Line, Tumor | Neoplasms, Hormone-Dependent - drug therapy | Tyrosine | Acetylcysteine | Epidermal growth factor | Cell death | Prostate cancer | Phosphotransferases | TOR protein | Phosphorylation | Bcl-2 protein | AKT protein | Kinases | Signal transduction | Receptors | Neuregulin | Inhibition | Growth factors | ErbB-1 protein | Cell survival | ErbB protein | Mortality | JNK protein | Rapamycin | ErbB-3 protein | Ribonucleic acid--RNA | ErbB-2 protein | 1-Phosphatidylinositol 3-kinase | Signaling | Androgens | Dimers | Prostate | Phagocytosis | Tumors | Cancer | Apoptosis | Index Medicus | RNA | Ribonucleic acid
Journal Article
Molecular Systems Biology, ISSN 1744-4292, 2012, Volume 8, Issue 1, pp. 570 - n/a
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, pp. e70608 - e70608
The presence of the Philadelphia chromosome in patients with acute lymphoblastic leukemia (Ph(+)ALL) is a negative prognostic indicator. Tyrosine kinase... 
CANCER-CELLS | ACTIVATION | PHARMACOKINETICS | PH PLUS | MULTIDISCIPLINARY SCIENCES | ACUTE MYELOGENOUS LEUKEMIA | IMATINIB | BIM | HER2 | LAPATINIB GW572016 | ARRAYS | Apoptosis - drug effects | Humans | Middle Aged | Caspase 3 - metabolism | Male | Molecular Targeted Therapy | Young Adult | Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Protein Kinase Inhibitors - chemistry | Receptor, Epidermal Growth Factor - metabolism | Aged, 80 and over | Adult | Female | Gene Expression Regulation, Neoplastic - drug effects | Philadelphia Chromosome - drug effects | Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology | Enzyme Activation - drug effects | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Signal Transduction - drug effects | Protein Kinase Inhibitors - therapeutic use | Adolescent | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism | Cell proliferation | Cellular signal transduction | Acute lymphocytic leukemia | Research | Apoptosis | Philadelphia chromosome | BCR protein | Pediatrics | Biotechnology | Phosphorylation | Target recognition | Laboratories | Leukemia | Abl gene | Antibodies | Biology | BCR gene | Kinases | Caspase-3 | Proteins | Cell activation | Epidermal growth factor | Protein-tyrosine kinase | Bioinformatics | ErbB-1 protein | Tyrosine | Imatinib | Acute lymphatic leukemia | ErbB protein | Caspase | Lymphatic leukemia | Patients | ErbB-2 protein | Ribosomal protein S6 kinase | Signaling | Protein arrays | Inhibitors | Cell death | Biopsy | Cell lines | Response rates | Arrays | BIM protein | Cancer | Index Medicus
Journal Article
Cancer, ISSN 0008-543X, 10/2017, Volume 123, Issue 19, pp. 3681 - 3690
To the authors' knowledge, no data exist regarding the prevalence of next‐generation sequencing‐detected mutations in patients with early‐stage lung... 
lung adenocarcinomas | stereotactic body radiotherapy | targeted therapy | next‐generation sequencing | lung mutations | next-generation sequencing | PLACEBO | CANCER | SOMATIC MUTATIONS | RADIATION-THERAPY | TRIAL | NONSMALL CELL LUNG | ONCOLOGY | RANDOMIZED PHASE-II | PROGNOSTIC-SIGNIFICANCE | ERLOTINIB | Adenocarcinoma - pathology | Adenocarcinoma of Lung | Lung Neoplasms - mortality | Humans | Middle Aged | Radiosurgery | Lung Neoplasms - radiotherapy | Lung Neoplasms - pathology | Male | Molecular Targeted Therapy | fms-Like Tyrosine Kinase 3 - genetics | Genes, p53 | Anaplastic Lymphoma Kinase | Smad4 Protein - genetics | Aged, 80 and over | Adult | Female | Adenocarcinoma - genetics | High-Throughput Nucleotide Sequencing - methods | Adenocarcinoma - radiotherapy | Lung Neoplasms - genetics | PTEN Phosphohydrolase - genetics | Neoplasm Recurrence, Local | In Situ Hybridization, Fluorescence | Proto-Oncogene Proteins c-met - genetics | Genes, erbB-1 | Analysis of Variance | Receptor Protein-Tyrosine Kinases - genetics | Proto-Oncogene Proteins B-raf - genetics | Gene Rearrangement | Chromosome Aberrations | Aged | Genes, ras | Adenocarcinoma - mortality | Proto-Oncogene Proteins c-ret - genetics | Usage | Care and treatment | Lung cancer | Patient outcomes | Genetic aspects | Nucleotide sequencing | Radiotherapy | DNA sequencing | Adenocarcinoma | Smad protein | p53 Protein | Lung | Fluorescence | Homology | Population genetics | Smad4 protein | Genetic screening | Clinical outcomes | K-Ras protein | Epidermal growth factor | Fluorescence in situ hybridization | Protein-tyrosine kinase | Tensin | Sequences | Epidermal growth factor receptors | Histology | Radiation therapy | Disease control | Patients | Lymphoma | Amplification | Mutation | Aberration | PTEN protein | Tumors | Cancer | Index Medicus | Abridged Index Medicus
Journal Article
Cancer Research, ISSN 0008-5472, 12/2010, Volume 70, Issue 24, pp. 10402 - 10410
The molecular mechanism by which epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI) induce apoptosis in non-small cell-lung cancer (NSCLC)... 
GROWTH-FACTOR RECEPTOR | ACTIVATION | AMPLIFICATION | THERAPY | GENE | ONCOLOGY | PROLIFERATION | INDUCTION | GEFITINIB RESISTANCE | EXPRESSION | ERLOTINIB | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Microtubule-Associated Proteins - genetics | Apoptosis - drug effects | Humans | Oncogene Protein v-akt - antagonists & inhibitors | Lung Neoplasms - pathology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - biosynthesis | Gene Knockdown Techniques | RNA, Messenger - biosynthesis | Receptor, Epidermal Growth Factor - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - genetics | Oncogene Protein v-akt - metabolism | Apoptosis Regulatory Proteins - biosynthesis | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Lung Neoplasms - enzymology | Inhibitor of Apoptosis Proteins | Carcinoma, Non-Small-Cell Lung - genetics | Membrane Proteins - genetics | RNA, Messenger - genetics | Proto-Oncogene Proteins - genetics | Down-Regulation - drug effects | Microtubule-Associated Proteins - biosynthesis | Genes, erbB-1 | Membrane Proteins - biosynthesis | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Apoptosis - physiology | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Mutation | Quinazolines - pharmacology | Index Medicus
Journal Article