International Journal of Hematology, ISSN 0925-5710, 10/2018, Volume 108, Issue 4, pp. 416 - 422
Hairy cell leukemia (HCL) is a rare B-cell lymphoid malignancy that is difficult to distinguish from other morphological variants. The frequency of HCL has not...
BRAF V600E | Hairy cell leukemia | Medicine & Public Health | Hematology | Quenching probe | Japan | Oncology | Low-grade B-cell malignancy | DIAGNOSIS | NEOPLASMS | EFFICACY | RETROSPECTIVE SURVEY | CHINESE | VARIANT | FEATURES | ERDHEIM-CHESTER DISEASE | MELANOMA | HEMATOLOGY | VEMURAFENIB | Japan - epidemiology | Humans | Middle Aged | Leukemia, Hairy Cell - epidemiology | Leukemia, Hairy Cell - genetics | Male | Mutation, Missense | Nucleic Acid Probes | Asian Continental Ancestry Group | Leukemia, Hairy Cell - metabolism | Proto-Oncogene Proteins B-raf - genetics | Aged, 80 and over | Adult | Female | Aged | Polymorphism, Single Nucleotide | Proto-Oncogene Proteins B-raf - metabolism | Amino Acid Substitution | Medical research | Interleukins | Gene mutations | Analysis | Leukemia, Hairy cell | Detectors | Genetic research | Medicine, Experimental | Genetic aspects | Methods | Genetic polymorphisms | Thrombocytopenia | Chronic lymphatic leukemia | Leukemia | Interleukin | Single-nucleotide polymorphism | Malignancy | Lymphatic leukemia | Patients | Cell surface | Quenching | Diseases | Lymphocytes B | Interleukin 2 | Probe method (forecasting) | Mutation | Surface markers | Polymorphism | Neutropenia
BRAF V600E | Hairy cell leukemia | Medicine & Public Health | Hematology | Quenching probe | Japan | Oncology | Low-grade B-cell malignancy | DIAGNOSIS | NEOPLASMS | EFFICACY | RETROSPECTIVE SURVEY | CHINESE | VARIANT | FEATURES | ERDHEIM-CHESTER DISEASE | MELANOMA | HEMATOLOGY | VEMURAFENIB | Japan - epidemiology | Humans | Middle Aged | Leukemia, Hairy Cell - epidemiology | Leukemia, Hairy Cell - genetics | Male | Mutation, Missense | Nucleic Acid Probes | Asian Continental Ancestry Group | Leukemia, Hairy Cell - metabolism | Proto-Oncogene Proteins B-raf - genetics | Aged, 80 and over | Adult | Female | Aged | Polymorphism, Single Nucleotide | Proto-Oncogene Proteins B-raf - metabolism | Amino Acid Substitution | Medical research | Interleukins | Gene mutations | Analysis | Leukemia, Hairy cell | Detectors | Genetic research | Medicine, Experimental | Genetic aspects | Methods | Genetic polymorphisms | Thrombocytopenia | Chronic lymphatic leukemia | Leukemia | Interleukin | Single-nucleotide polymorphism | Malignancy | Lymphatic leukemia | Patients | Cell surface | Quenching | Diseases | Lymphocytes B | Interleukin 2 | Probe method (forecasting) | Mutation | Surface markers | Polymorphism | Neutropenia
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2015, Volume 10, Issue 11, p. e0141946
2-Hydroxypropyl-beta-cyclodextrin (HP-beta-CyD) is a cyclic oligosaccharide that is widely used as an enabling excipient in pharmaceutical formulations, but...
METHYL-BETA-CYCLODEXTRIN | CANCER-CELLS | CHOLESTEROL DEPLETION | MULTIDISCIPLINARY SCIENCES | LIPID RAFTS | BCR-ABL | IN-VIVO | MYELOGENOUS LEUKEMIA | TYROSINE KINASE INHIBITOR | CELL-LINE | CHRONIC MYELOID-LEUKEMIA | 2-Hydroxypropyl-beta-cyclodextrin | Apoptosis - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Transplantation, Heterologous | Antineoplastic Agents - therapeutic use | Colorimetry | Antineoplastic Agents - toxicity | G2 Phase Cell Cycle Checkpoints - drug effects | Cholesterol - analysis | Leukemia, Myeloid, Acute - drug therapy | Lung - pathology | M Phase Cell Cycle Checkpoints - drug effects | Cholesterol - metabolism | Mice, SCID | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Mice, Nude | beta-Cyclodextrins - therapeutic use | K562 Cells | Cell Line, Tumor | Mice, Inbred NOD | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | beta-Cyclodextrins - toxicity | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Cell proliferation | BCR protein | Niemann-Pick disease | Animal models | Leukemia | Medical services | Stem cell transplantation | Lipids | Cyclodextrins | Kinases | Anticancer properties | Graduate studies | Inhibition | Lipid metabolism | Fusion protein | Protein-tyrosine kinase | Formulations | Tyrosine | Cell survival | Acute lymphatic leukemia | Myeloid leukemia | Medical treatment | Abl protein | Chronic myeloid leukemia | Lymphatic leukemia | Metabolism | Cholesterol | Cyclodextrin | Human performance | Cell lines | Stem cells | Hypoxia | Acute myeloid leukemia | Apoptosis
METHYL-BETA-CYCLODEXTRIN | CANCER-CELLS | CHOLESTEROL DEPLETION | MULTIDISCIPLINARY SCIENCES | LIPID RAFTS | BCR-ABL | IN-VIVO | MYELOGENOUS LEUKEMIA | TYROSINE KINASE INHIBITOR | CELL-LINE | CHRONIC MYELOID-LEUKEMIA | 2-Hydroxypropyl-beta-cyclodextrin | Apoptosis - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Transplantation, Heterologous | Antineoplastic Agents - therapeutic use | Colorimetry | Antineoplastic Agents - toxicity | G2 Phase Cell Cycle Checkpoints - drug effects | Cholesterol - analysis | Leukemia, Myeloid, Acute - drug therapy | Lung - pathology | M Phase Cell Cycle Checkpoints - drug effects | Cholesterol - metabolism | Mice, SCID | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Mice, Nude | beta-Cyclodextrins - therapeutic use | K562 Cells | Cell Line, Tumor | Mice, Inbred NOD | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | beta-Cyclodextrins - toxicity | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Cell proliferation | BCR protein | Niemann-Pick disease | Animal models | Leukemia | Medical services | Stem cell transplantation | Lipids | Cyclodextrins | Kinases | Anticancer properties | Graduate studies | Inhibition | Lipid metabolism | Fusion protein | Protein-tyrosine kinase | Formulations | Tyrosine | Cell survival | Acute lymphatic leukemia | Myeloid leukemia | Medical treatment | Abl protein | Chronic myeloid leukemia | Lymphatic leukemia | Metabolism | Cholesterol | Cyclodextrin | Human performance | Cell lines | Stem cells | Hypoxia | Acute myeloid leukemia | Apoptosis
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2014, Volume 9, Issue 12, p. e111881
Overcoming metastasis is one of the most important issues with lung cancer. Since metastasis arises through complex steps, a suitable animal model is...
CELLS | CIRCULATING DNA | METASTASIS | EVOLUTION | THERAPY | SCID MICE | MULTIDISCIPLINARY SCIENCES | HUMAN LUNG-CANCER | INTRATUMOR HETEROGENEITY | ACQUIRED-RESISTANCE | DETECTION SYSTEM | Carcinoma, Non-Small-Cell Lung - pathology | Neoplasm Transplantation | Receptor, Epidermal Growth Factor - genetics | Liver - pathology | Lung - pathology | Body Weight | Lymph Nodes - pathology | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Mice, SCID | Neoplasm Metastasis | Animals | Neoplasms - blood | DNA, Neoplasm - blood | DNA Mutational Analysis | Cell Line, Tumor | Mice, Inbred NOD | Mice | Mutation | Disease Models, Animal | Liver cancer | Dendritic cells | Lung cancer | DNA | Diagnosis | Intermediate filament proteins | Cancer | Tumors | Macrophages | E-cadherin
CELLS | CIRCULATING DNA | METASTASIS | EVOLUTION | THERAPY | SCID MICE | MULTIDISCIPLINARY SCIENCES | HUMAN LUNG-CANCER | INTRATUMOR HETEROGENEITY | ACQUIRED-RESISTANCE | DETECTION SYSTEM | Carcinoma, Non-Small-Cell Lung - pathology | Neoplasm Transplantation | Receptor, Epidermal Growth Factor - genetics | Liver - pathology | Lung - pathology | Body Weight | Lymph Nodes - pathology | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Mice, SCID | Neoplasm Metastasis | Animals | Neoplasms - blood | DNA, Neoplasm - blood | DNA Mutational Analysis | Cell Line, Tumor | Mice, Inbred NOD | Mice | Mutation | Disease Models, Animal | Liver cancer | Dendritic cells | Lung cancer | DNA | Diagnosis | Intermediate filament proteins | Cancer | Tumors | Macrophages | E-cadherin
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 11/2011, Volume 29, Issue 33, pp. 4410 - 4416
Purpose To explore a more effective treatment for newly diagnosed stage IV, relapsed, or refractory extranodal natural killer/T-cell lymphoma, nasal type...
L-ASPARAGINASE | DEXAMETHASONE | NEOPLASMS | ONCOLOGY | NON-HODGKINS-LYMPHOMAS | METHOTREXATE | MALIGNANCIES | T-CELL | IFOSFAMIDE | EXPRESSION | TRANSPLANTATION | Recurrence | Nose Neoplasms - pathology | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Male | Asparaginase - administration & dosage | Lymphoma, Extranodal NK-T-Cell - drug therapy | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Lymphoma, Extranodal NK-T-Cell - pathology | Nose Neoplasms - drug therapy | Adolescent | Lymphoma, Extranodal NK-T-Cell - mortality | Adult | Female | Aged | Neoplasm Staging
L-ASPARAGINASE | DEXAMETHASONE | NEOPLASMS | ONCOLOGY | NON-HODGKINS-LYMPHOMAS | METHOTREXATE | MALIGNANCIES | T-CELL | IFOSFAMIDE | EXPRESSION | TRANSPLANTATION | Recurrence | Nose Neoplasms - pathology | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Male | Asparaginase - administration & dosage | Lymphoma, Extranodal NK-T-Cell - drug therapy | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Lymphoma, Extranodal NK-T-Cell - pathology | Nose Neoplasms - drug therapy | Adolescent | Lymphoma, Extranodal NK-T-Cell - mortality | Adult | Female | Aged | Neoplasm Staging
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, p. e57833
Hypoxia-inducible factor-1alpha (HIF-1 alpha) plays an essential role in the regulation of various genes associated with low oxygen consumption. Elevated...
FACTOR 1-ALPHA | OVEREXPRESSION | HIF-1 | STEM-CELLS | FACTOR-1-ALPHA | MULTIDISCIPLINARY SCIENCES | ALPHA | HIF-1-ALPHA | CANCER | EXPRESSION | CELL CARCINOMA | Lymphocytes - metabolism | Cell Proliferation | Receptors, Antigen, T-Cell - metabolism | Cell Survival | Humans | Transgenes - genetics | Lymphoid Tissue - metabolism | Mice, Transgenic | Cell Transformation, Neoplastic - metabolism | Lymphoproliferative Disorders - pathology | Lymphoproliferative Disorders - metabolism | Lymphoid Tissue - pathology | Lymphocytes - pathology | Phenotype | Animals | Hematopoietic System - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Survival Analysis | Mice | Receptors, Antigen, T-Cell - genetics | Cell Transformation, Neoplastic - pathology | Hematopoietic System - pathology | RNA | Genes | Stem cells | Development and progression | Lymphomas | Genetic aspects | Genetic engineering | Metastasis | B cells | Hypoxia-inducible factor 1 | Mesenchyme | Mucosa | Gene regulation | Cytotoxicity | Biology | mRNA | Birth | Kinases | Cancer therapies | Metastases | Proteins | Angiogenesis | Hypoxia-inducible factor 1a | Lymphocytes | Intestine | Rodents | Animal tissues | Fibroblasts | Tumorigenesis | Age | Constitution | Hypoxia-inducible factors | Cytomegalovirus | Cell survival | Internal medicine | Research & development--R&D | Immunoproliferative diseases | Transgenic mice | Organs | Etoposide | Oxygen consumption | Breast cancer | Gene expression | Survival | Lymphoma | Medicine | Lungs | Medical prognosis | Hypoxia | Tumors | Research & development | R&D
FACTOR 1-ALPHA | OVEREXPRESSION | HIF-1 | STEM-CELLS | FACTOR-1-ALPHA | MULTIDISCIPLINARY SCIENCES | ALPHA | HIF-1-ALPHA | CANCER | EXPRESSION | CELL CARCINOMA | Lymphocytes - metabolism | Cell Proliferation | Receptors, Antigen, T-Cell - metabolism | Cell Survival | Humans | Transgenes - genetics | Lymphoid Tissue - metabolism | Mice, Transgenic | Cell Transformation, Neoplastic - metabolism | Lymphoproliferative Disorders - pathology | Lymphoproliferative Disorders - metabolism | Lymphoid Tissue - pathology | Lymphocytes - pathology | Phenotype | Animals | Hematopoietic System - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Survival Analysis | Mice | Receptors, Antigen, T-Cell - genetics | Cell Transformation, Neoplastic - pathology | Hematopoietic System - pathology | RNA | Genes | Stem cells | Development and progression | Lymphomas | Genetic aspects | Genetic engineering | Metastasis | B cells | Hypoxia-inducible factor 1 | Mesenchyme | Mucosa | Gene regulation | Cytotoxicity | Biology | mRNA | Birth | Kinases | Cancer therapies | Metastases | Proteins | Angiogenesis | Hypoxia-inducible factor 1a | Lymphocytes | Intestine | Rodents | Animal tissues | Fibroblasts | Tumorigenesis | Age | Constitution | Hypoxia-inducible factors | Cytomegalovirus | Cell survival | Internal medicine | Research & development--R&D | Immunoproliferative diseases | Transgenic mice | Organs | Etoposide | Oxygen consumption | Breast cancer | Gene expression | Survival | Lymphoma | Medicine | Lungs | Medical prognosis | Hypoxia | Tumors | Research & development | R&D
Journal Article
Pathology & Oncology Research, ISSN 1219-4956, 1/2017, Volume 23, Issue 1, pp. 181 - 188
BRAF gene mutations have been observed in 30–50 % of malignant melanoma patients. Recent development of therapeutic intervention using BRAF inhibitors requires...
Biomedicine, general | Pathology | Molecular targeted therapy | Biomedicine | Immunology | B-raf | Melanoma | Cancer Research | Oncology | Tyrosine kinase inhibitors | METASTATIC MELANOMA | BRAF GENE | PLUS DACARBAZINE | ONCOLOGY | PHASE-III | MALIGNANT-MELANOMA | PATHOLOGY | CANCER | Skin Neoplasms - pathology | Humans | Middle Aged | Asian Continental Ancestry Group - genetics | Genotype | Male | Melanoma - pathology | DNA Mutational Analysis - methods | Mutation - genetics | Melanoma - genetics | Proto-Oncogene Proteins B-raf - genetics | Skin Neoplasms - genetics | Cell Line, Tumor | Female | Aged | Tyrosine | Purines | Gene mutations | Genes | Detectors | Genetic research | Genetic aspects
Biomedicine, general | Pathology | Molecular targeted therapy | Biomedicine | Immunology | B-raf | Melanoma | Cancer Research | Oncology | Tyrosine kinase inhibitors | METASTATIC MELANOMA | BRAF GENE | PLUS DACARBAZINE | ONCOLOGY | PHASE-III | MALIGNANT-MELANOMA | PATHOLOGY | CANCER | Skin Neoplasms - pathology | Humans | Middle Aged | Asian Continental Ancestry Group - genetics | Genotype | Male | Melanoma - pathology | DNA Mutational Analysis - methods | Mutation - genetics | Melanoma - genetics | Proto-Oncogene Proteins B-raf - genetics | Skin Neoplasms - genetics | Cell Line, Tumor | Female | Aged | Tyrosine | Purines | Gene mutations | Genes | Detectors | Genetic research | Genetic aspects
Journal Article
Rinsho byori. The Japanese journal of clinical pathology, ISSN 0047-1860, 02/2017, Volume 65, Issue 2, p. 190
A biobank is a facility that collects and manages biological specimens such as tissues, cells, and blood de- rived from living organisms. In addition to these...
Biological Specimen Banks | Genomics | Humans | Japan | Biomedical Research | Precision Medicine
Biological Specimen Banks | Genomics | Humans | Japan | Biomedical Research | Precision Medicine
Journal Article
Journal of Cancer Research and Clinical Oncology, ISSN 0171-5216, 12/2017, Volume 143, Issue 12, pp. 2401 - 2412
Our previous experiments show that the main constituent of green-tea catechins, (−)-epigallocatechin gallate (EGCG), completely prevents tumor promotion on...
Stemness | Self-renewal | Medicine & Public Health | Hematology | EGCG | Oncology | Cancer Research | Internal Medicine | Parental cells | CSCs | GROWTH-INHIBITION | PANCREATIC-CANCER | DRINKING GREEN TEA | BHLH FACTORS | EPITHELIAL-MESENCHYMAL TRANSITION | LUNG-CANCER | ONCOLOGY | PROSTATE-CANCER | EPIGALLOCATECHIN GALLATE | NF-KAPPA-B | Neoplasms - metabolism | Animals | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - drug effects | Humans | Biomarkers, Tumor - metabolism | Neoplastic Stem Cells - pathology | Neoplasms - prevention & control | Catechin - analogs & derivatives | Neoplasms - pathology | Prevention | Catechin | Green tea | Stem cells | Cancer | Review – Cancer Research
Stemness | Self-renewal | Medicine & Public Health | Hematology | EGCG | Oncology | Cancer Research | Internal Medicine | Parental cells | CSCs | GROWTH-INHIBITION | PANCREATIC-CANCER | DRINKING GREEN TEA | BHLH FACTORS | EPITHELIAL-MESENCHYMAL TRANSITION | LUNG-CANCER | ONCOLOGY | PROSTATE-CANCER | EPIGALLOCATECHIN GALLATE | NF-KAPPA-B | Neoplasms - metabolism | Animals | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - drug effects | Humans | Biomarkers, Tumor - metabolism | Neoplastic Stem Cells - pathology | Neoplasms - prevention & control | Catechin - analogs & derivatives | Neoplasms - pathology | Prevention | Catechin | Green tea | Stem cells | Cancer | Review – Cancer Research
Journal Article
Journal of Cancer Research and Clinical Oncology, ISSN 0171-5216, 10/2013, Volume 139, Issue 10, pp. 1603 - 1614
The classic two-stage chemical carcinogenesis in rodents is not directly linked to multistage carcinogenesis in humans. In light of our findings that tumor...
Tipα | Medicine & Public Health | Hematology | TNF-α | TPA | Reiztheorie | Cytokine | Oncology | Cancer Research | Internal Medicine | Okadaic acid | Keywords: Cytokine | Tipa | TNF-alpha | NECROSIS-FACTOR-ALPHA | KINASE-C | CANCER | OKADAIC ACID CLASS | MOUSE SKIN TUMORS | GREEN TEA | GLANDULAR STOMACH | ONCOLOGY | HELICOBACTER-PYLORI | PHORBOL ESTERS | Gastrointestinal Neoplasms - prevention & control | Inflammation - chemically induced | Okadaic Acid - pharmacology | Skin Neoplasms - immunology | Humans | Neoplasms, Experimental - enzymology | Helicobacter Infections - complications | Helicobacter Infections - immunology | Neoplasms, Experimental - chemically induced | Skin Neoplasms - chemically induced | Organ Specificity | Gastrointestinal Neoplasms - etiology | Gastrointestinal Neoplasms - immunology | Animals | Carcinogens - pharmacology | Skin Neoplasms - enzymology | Neoplasms, Experimental - immunology | Catechin - analogs & derivatives | Catechin - pharmacology | Anticarcinogenic Agents - pharmacology | Inflammation Mediators - physiology | Phorbol esters | Care and treatment | Stem cells | Development and progression | Inflammation | Green tea | Tumors | Cancer | Index Medicus
Tipα | Medicine & Public Health | Hematology | TNF-α | TPA | Reiztheorie | Cytokine | Oncology | Cancer Research | Internal Medicine | Okadaic acid | Keywords: Cytokine | Tipa | TNF-alpha | NECROSIS-FACTOR-ALPHA | KINASE-C | CANCER | OKADAIC ACID CLASS | MOUSE SKIN TUMORS | GREEN TEA | GLANDULAR STOMACH | ONCOLOGY | HELICOBACTER-PYLORI | PHORBOL ESTERS | Gastrointestinal Neoplasms - prevention & control | Inflammation - chemically induced | Okadaic Acid - pharmacology | Skin Neoplasms - immunology | Humans | Neoplasms, Experimental - enzymology | Helicobacter Infections - complications | Helicobacter Infections - immunology | Neoplasms, Experimental - chemically induced | Skin Neoplasms - chemically induced | Organ Specificity | Gastrointestinal Neoplasms - etiology | Gastrointestinal Neoplasms - immunology | Animals | Carcinogens - pharmacology | Skin Neoplasms - enzymology | Neoplasms, Experimental - immunology | Catechin - analogs & derivatives | Catechin - pharmacology | Anticarcinogenic Agents - pharmacology | Inflammation Mediators - physiology | Phorbol esters | Care and treatment | Stem cells | Development and progression | Inflammation | Green tea | Tumors | Cancer | Index Medicus
Journal Article
Journal of Thoracic Oncology, ISSN 1556-0864, 09/2012, Volume 7, Issue 9, pp. 1369 - 1381
Detection of ( mutations is indispensable to determine an appropriate lung cancer treatment. Although retreatment often prolongs survival, how to select the...
Monitoring system | EGFR activating/sensitive mutations | EGFR-TKI | Lung cancer | Plasma DNA | GEFITINIB | TYROSINE KINASE | ADENOCARCINOMAS | ACQUIRED-RESISTANCE | EGFR MUTATION | CHEMOTHERAPY | CELL LUNG-CANCER | ONCOLOGY | RESPIRATORY SYSTEM | NEVER SMOKERS | INHIBITOR | ERLOTINIB | Lung Neoplasms - genetics | Oligonucleotides - genetics | Receptor, Epidermal Growth Factor - genetics | Sequence Deletion | Adenocarcinoma - pathology | Prognosis | Humans | Exons - genetics | Lung Neoplasms - pathology | Male | Mutation - genetics | DNA, Neoplasm - blood | Polymerase Chain Reaction | Female | Adenocarcinoma - genetics | Aged | DNA, Neoplasm - analysis | DNA, Neoplasm - genetics | Neoplasm Staging
Monitoring system | EGFR activating/sensitive mutations | EGFR-TKI | Lung cancer | Plasma DNA | GEFITINIB | TYROSINE KINASE | ADENOCARCINOMAS | ACQUIRED-RESISTANCE | EGFR MUTATION | CHEMOTHERAPY | CELL LUNG-CANCER | ONCOLOGY | RESPIRATORY SYSTEM | NEVER SMOKERS | INHIBITOR | ERLOTINIB | Lung Neoplasms - genetics | Oligonucleotides - genetics | Receptor, Epidermal Growth Factor - genetics | Sequence Deletion | Adenocarcinoma - pathology | Prognosis | Humans | Exons - genetics | Lung Neoplasms - pathology | Male | Mutation - genetics | DNA, Neoplasm - blood | Polymerase Chain Reaction | Female | Adenocarcinoma - genetics | Aged | DNA, Neoplasm - analysis | DNA, Neoplasm - genetics | Neoplasm Staging
Journal Article
Rinsho byori. The Japanese journal of clinical pathology, ISSN 0047-1860, 08/2016, Volume 64, Issue 8, p. 965
The knowledge and skills of clinical hematology necessary for clinical laboratory medicine are different from the knowledge required for the hematological...
Journal Article
Lung Cancer, ISSN 0169-5002, 2017, Volume 110, pp. 35 - 41
Highlights • Endogenous DDR2 protein expression levels were high in 29% of lung SQCC patients. • A DDR2 mutation (T681I) identified in a lung SQCC clinical...
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | Overexpression | Mutation | MMP-1 | DDR2 | Lung squamous cell carcinoma | INVASION | ONCOLOGY | RESPIRATORY SYSTEM | REGISTRY | Immunohistochemistry | Lung Neoplasms - genetics | Gene Expression | Phosphorylation | Cell Proliferation | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Lung Neoplasms - metabolism | Discoidin Domain Receptor 2 - metabolism | Lung Neoplasms - pathology | Male | Cell Movement - genetics | Animals | Proto-Oncogene Proteins c-jun - metabolism | Alleles | Cell Line, Tumor | Mice | Matrix Metalloproteinase 1 - metabolism | Discoidin Domain Receptor 2 - genetics | Disease Models, Animal | Memory (Computers) | RNA | Lung cancer | Analysis | Respiratory agents | Genetic aspects | Metastasis | Animal experimentation | Squamous cell carcinoma | Development and progression
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | Overexpression | Mutation | MMP-1 | DDR2 | Lung squamous cell carcinoma | INVASION | ONCOLOGY | RESPIRATORY SYSTEM | REGISTRY | Immunohistochemistry | Lung Neoplasms - genetics | Gene Expression | Phosphorylation | Cell Proliferation | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Lung Neoplasms - metabolism | Discoidin Domain Receptor 2 - metabolism | Lung Neoplasms - pathology | Male | Cell Movement - genetics | Animals | Proto-Oncogene Proteins c-jun - metabolism | Alleles | Cell Line, Tumor | Mice | Matrix Metalloproteinase 1 - metabolism | Discoidin Domain Receptor 2 - genetics | Disease Models, Animal | Memory (Computers) | RNA | Lung cancer | Analysis | Respiratory agents | Genetic aspects | Metastasis | Animal experimentation | Squamous cell carcinoma | Development and progression
Journal Article
Journal of Thoracic Oncology, ISSN 1556-0864, 10/2011, Volume 6, Issue 10, pp. 1639 - 1648
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors are widely used to treat lung adenocarcinomas with -activating mutations. However, half of...
Monitoring system | T790M | EGFR-TKI | Lung cancer | Plasma DNA | DIAGNOSIS | GEFITINIB | ACQUIRED-RESISTANCE | T790M MUTATION | PERIPHERAL-BLOOD | DRUG-RESISTANCE | EGFR T790M | CELL LUNG-CANCER | CIRCULATING TUMOR-CELLS | ONCOLOGY | RESPIRATORY SYSTEM | ERLOTINIB | Erlotinib Hydrochloride | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Follow-Up Studies | Humans | Middle Aged | Male | Antineoplastic Agents - therapeutic use | Case-Control Studies | DNA, Neoplasm - blood | DNA Mutational Analysis | Sensitivity and Specificity | Polymerase Chain Reaction | Female | Adenocarcinoma - genetics | Tumor Cells, Cultured | Lung Neoplasms - genetics | Adenocarcinoma - blood | Survival Rate | Treatment Outcome | Mutation - genetics | Adenocarcinoma - drug therapy | Drug Resistance, Neoplasm - genetics | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Lung Neoplasms - blood | DNA, Neoplasm - genetics | Neoplasm Staging
Monitoring system | T790M | EGFR-TKI | Lung cancer | Plasma DNA | DIAGNOSIS | GEFITINIB | ACQUIRED-RESISTANCE | T790M MUTATION | PERIPHERAL-BLOOD | DRUG-RESISTANCE | EGFR T790M | CELL LUNG-CANCER | CIRCULATING TUMOR-CELLS | ONCOLOGY | RESPIRATORY SYSTEM | ERLOTINIB | Erlotinib Hydrochloride | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Follow-Up Studies | Humans | Middle Aged | Male | Antineoplastic Agents - therapeutic use | Case-Control Studies | DNA, Neoplasm - blood | DNA Mutational Analysis | Sensitivity and Specificity | Polymerase Chain Reaction | Female | Adenocarcinoma - genetics | Tumor Cells, Cultured | Lung Neoplasms - genetics | Adenocarcinoma - blood | Survival Rate | Treatment Outcome | Mutation - genetics | Adenocarcinoma - drug therapy | Drug Resistance, Neoplasm - genetics | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Lung Neoplasms - blood | DNA, Neoplasm - genetics | Neoplasm Staging
Journal Article
Anticancer research, ISSN 0250-7005, 01/2016, Volume 36, Issue 1, pp. 95 - 102
Background: Torin2 is a second-generation ATP-competitive inhibitor of the mammalian target of rapamycin (mTOR). Dysregulation of mTOR signaling pathway,...
Adult T-cell leukemia/lymphoma | mammalian target of rapamycin | AKT | growth inhibition | LEUKEMIA-LYMPHOMA | TRANSFORMATION | ACTIVATION | KINASE | TAX | CANCER | THERAPY | MTOR INHIBITION | ONCOLOGY | GROWTH | Cell Survival - drug effects | Phosphorylation | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | Etoposide - pharmacology | Leukemia-Lymphoma, Adult T-Cell - pathology | Mechanistic Target of Rapamycin Complex 2 | Sirolimus - pharmacology | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | Dose-Response Relationship, Drug | TOR Serine-Threonine Kinases - antagonists & inhibitors | Multiprotein Complexes - metabolism | Leukemia-Lymphoma, Adult T-Cell - drug therapy | Signal Transduction - drug effects | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | G1 Phase Cell Cycle Checkpoints - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Leukemia-Lymphoma, Adult T-Cell - enzymology | Naphthyridines - pharmacology
Adult T-cell leukemia/lymphoma | mammalian target of rapamycin | AKT | growth inhibition | LEUKEMIA-LYMPHOMA | TRANSFORMATION | ACTIVATION | KINASE | TAX | CANCER | THERAPY | MTOR INHIBITION | ONCOLOGY | GROWTH | Cell Survival - drug effects | Phosphorylation | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | Etoposide - pharmacology | Leukemia-Lymphoma, Adult T-Cell - pathology | Mechanistic Target of Rapamycin Complex 2 | Sirolimus - pharmacology | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | Dose-Response Relationship, Drug | TOR Serine-Threonine Kinases - antagonists & inhibitors | Multiprotein Complexes - metabolism | Leukemia-Lymphoma, Adult T-Cell - drug therapy | Signal Transduction - drug effects | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | G1 Phase Cell Cycle Checkpoints - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Leukemia-Lymphoma, Adult T-Cell - enzymology | Naphthyridines - pharmacology
Journal Article
Lung Cancer, ISSN 0169-5002, 2011, Volume 75, Issue 1, pp. 89 - 94
Abstract MET, a receptor tyrosine kinase for hepatocyte growth factor, is associated with tumor progression and acquired resistance to epidermal growth factor...
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | EGFR mutation | FISH | Prognosis | BAC | MET | Lung cancer | CANCER PATIENTS | GEFITINIB | ACTIVATION | ACQUIRED-RESISTANCE | TYROSINE KINASE INHIBITORS | GROWTH-FACTOR RECEPTOR | BRONCHIOLOALVEOLAR CARCINOMA | AMPLIFICATION | ONCOLOGY | RESPIRATORY SYSTEM | C-MET | GENE COPY NUMBER | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Adenocarcinoma - pathology | Adenocarcinoma of Lung | Adenocarcinoma, Bronchiolo-Alveolar - pathology | Lung Neoplasms - mortality | Humans | Lung Neoplasms - metabolism | ErbB Receptors - genetics | Lung Neoplasms - pathology | Male | Adenocarcinoma, Bronchiolo-Alveolar - genetics | Adenocarcinoma - metabolism | Female | Adenocarcinoma - genetics | Lung Neoplasms - genetics | Proto-Oncogene Proteins - genetics | Gene Dosage | Proto-Oncogene Proteins c-met - genetics | Disease-Free Survival | Gene Amplification | Cell Line, Tumor | Mutation | In Situ Hybridization, Fluorescence - methods | Protein-Tyrosine Kinases - antagonists & inhibitors | Adenocarcinoma | Tyrosine | Genes | Fluorescence | Development and progression | Respiratory agents | Anopheles | Epidermal growth factor | Genetic research | Genetic aspects | Universities and colleges
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | EGFR mutation | FISH | Prognosis | BAC | MET | Lung cancer | CANCER PATIENTS | GEFITINIB | ACTIVATION | ACQUIRED-RESISTANCE | TYROSINE KINASE INHIBITORS | GROWTH-FACTOR RECEPTOR | BRONCHIOLOALVEOLAR CARCINOMA | AMPLIFICATION | ONCOLOGY | RESPIRATORY SYSTEM | C-MET | GENE COPY NUMBER | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Adenocarcinoma - pathology | Adenocarcinoma of Lung | Adenocarcinoma, Bronchiolo-Alveolar - pathology | Lung Neoplasms - mortality | Humans | Lung Neoplasms - metabolism | ErbB Receptors - genetics | Lung Neoplasms - pathology | Male | Adenocarcinoma, Bronchiolo-Alveolar - genetics | Adenocarcinoma - metabolism | Female | Adenocarcinoma - genetics | Lung Neoplasms - genetics | Proto-Oncogene Proteins - genetics | Gene Dosage | Proto-Oncogene Proteins c-met - genetics | Disease-Free Survival | Gene Amplification | Cell Line, Tumor | Mutation | In Situ Hybridization, Fluorescence - methods | Protein-Tyrosine Kinases - antagonists & inhibitors | Adenocarcinoma | Tyrosine | Genes | Fluorescence | Development and progression | Respiratory agents | Anopheles | Epidermal growth factor | Genetic research | Genetic aspects | Universities and colleges
Journal Article