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humans (38) 38
oncology (35) 35
egfr (33) 33
index medicus (31) 31
mutation (27) 27
gefitinib (25) 25
receptor, epidermal growth factor - genetics (25) 25
lung cancer (19) 19
lung neoplasms - genetics (19) 19
lung neoplasms - pathology (19) 19
lung neoplasms - drug therapy (18) 18
carcinoma, non-small-cell lung - genetics (17) 17
erlotinib (17) 17
lung cancer, non-small cell (17) 17
cell line, tumor (16) 16
female (16) 16
carcinoma, non-small-cell lung - drug therapy (15) 15
receptor, epidermal growth factor - antagonists & inhibitors (15) 15
carcinoma, non-small-cell lung - pathology (14) 14
quinazolines - pharmacology (14) 14
antineoplastic agents - pharmacology (13) 13
cell biology (12) 12
cell lung-cancer (12) 12
receptor, epidermal growth factor - metabolism (12) 12
acquired-resistance (11) 11
growth-factor-receptor (11) 11
male (11) 11
respiratory tract diseases (11) 11
tyrosine kinase inhibitors (11) 11
cancer (10) 10
egfr mutation (10) 10
egfr mutations (10) 10
genetic aspects (10) 10
aged (9) 9
animals (9) 9
drug resistance, neoplasm (9) 9
epidermal growth factor (9) 9
mutations (9) 9
protein kinase inhibitors - pharmacology (9) 9
chemotherapy (8) 8
growth-factor receptor (8) 8
lung neoplasms - metabolism (8) 8
middle aged (8) 8
non-small cell lung cancer (8) 8
nsclc (8) 8
resistance (8) 8
tumors (8) 8
tyrosine kinase inhibitor (8) 8
1st-line treatment (7) 7
adult (7) 7
analysis (7) 7
apoptosis (7) 7
phosphorylation (7) 7
quinazolines - therapeutic use (7) 7
sensitivity (7) 7
targeted therapy (7) 7
tyrosine kinase (7) 7
antineoplastic agents - therapeutic use (6) 6
blotting, western (6) 6
carcinoma, non-small-cell lung - enzymology (6) 6
cell survival - drug effects (6) 6
drug resistance (6) 6
epidermal growth factor receptor (6) 6
expression (6) 6
gene-mutations (6) 6
health aspects (6) 6
open-label (6) 6
pathology (6) 6
respiratory system (6) 6
therapy (6) 6
activating mutations (5) 5
adenocarcinoma - drug therapy (5) 5
adenocarcinoma - genetics (5) 5
afatinib (5) 5
carcinoma, non-small-cell lung - metabolism (5) 5
care and treatment (5) 5
drug-resistance (5) 5
epidermal-growth-factor (5) 5
erlotinib hydrochloride (5) 5
exons - genetics (5) 5
inhibitors (5) 5
kinases (5) 5
lung neoplasms - enzymology (5) 5
mutation - genetics (5) 5
pharmacology & pharmacy (5) 5
prognosis (5) 5
protein kinase inhibitors - therapeutic use (5) 5
research paper (5) 5
tyrosine (5) 5
adenocarcinoma (4) 4
aged, 80 and over (4) 4
apoptosis - drug effects (4) 4
biochemistry & molecular biology (4) 4
breast-cancer (4) 4
combination (4) 4
gene mutations (4) 4
growth (4) 4
hematology, oncology and palliative medicine (4) 4
inhibitor (4) 4
kinase inhibitors (4) 4
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1. Full Text Application of a Highly Sensitive Detection System for Epidermal Growth Factor Receptor Mutations in Plasma DNA
by Nakamura, Tomomi and Sueoka-Aragane, Naoko and Iwanaga, Kentaro and Sato, Akemi and Komiya, Kazutoshi and Kobayashi, Naomi and Hayashi, Shinichiro and Hosomi, Toshiya and Hirai, Mitsuharu and Sueoka, Eisaburo and Kimura, Shinya
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
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2. Full Text A phase II trial of gefitinib monotherapy in pretreated patients with advanced non-small cell lung cancer not harboring activating EGFR mutations: implications of sensitive EGFR mutation test
by Choi, Moon Ki and Hong, Jung Yong and Chang, Won Jin and Kim, Moon Jin and Kim, Sung Min and Jung, Hyun Ae and Do, In-Gu and Choi, Yoon-la and Sun, Jong-Mu and Ahn, Jin Seok and Park, Keunchil and Ahn, Myung-Ju
Cancer Chemotherapy and Pharmacology, ISSN 0344-5704, 6/2015, Volume 75, Issue 6, pp. 1229 - 1236
Efficacy of gefitinib therapy strongly depends on epidermal growth factor receptor (EGFR) mutation status in patients with non-small cell lung cancer (NSCLC).... 
EGFR mutation | Medicine & Public Health | Non-small cell lung cancer | Oncology | Cancer Research | Sensitive method | Pharmacology/Toxicology | Gefitinib | Wild type | 1ST-LINE ERLOTINIB | WILD-TYPE EGFR | MULTICENTER | OPEN-LABEL | DOCETAXEL | CHEMOTHERAPY | Nonsmall cell lung cancer | GROWTH-FACTOR RECEPTOR | RANDOMIZED PHASE-3 | ONCOLOGY | 2ND-LINE TREATMENT | PHARMACOLOGY & PHARMACY | INHIBITORS | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Prospective Studies | Carcinoma, Non-Small-Cell Lung - genetics | Humans | Middle Aged | Neoplasm Recurrence, Local - drug therapy | Male | Antineoplastic Agents - therapeutic use | Mutation - genetics | Adenocarcinoma - drug therapy | Disease-Free Survival | Quinazolines - therapeutic use | Aged, 80 and over | Adult | Female | Neoplasm Recurrence, Local - genetics | Adenocarcinoma - genetics | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Chemotherapy | Peptides | Clinical trials | Lung cancer, Small cell | Product development | Lung cancer, Non-small cell | Cancer | Index Medicus
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3. Full Text Distinctive activation patterns in constitutively active and gefitinib-sensitive EGFR mutants
by Chen, Y.-R and Fu, Y.-N and Lin, C.-H and Yang, S.-T and Hu, S.-F and Chen, Y.-T and Tsai, S.-F and Huang, S.-F
Oncogene, ISSN 0950-9232, 02/2006, Volume 25, Issue 8, pp. 1205 - 1215
Mutations in the kinase domain of epidermal growth factor receptor ( EGFR) are associated with clinical responsiveness to gefitinib in patients with... 
Mutation | NSCLC | Gefitinib | Tyrosine phosphorylation | EGFR | SURVIVAL | GROWTH-FACTOR-RECEPTOR | TYROSINE KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | gefitinib | ENDOCYTOSIS | TUMORS | CELL BIOLOGY | CELL LUNG-CANCER | TRIAL | mutation | GENE | ONCOLOGY | GENETICS & HEREDITY | tyrosine phosphorylation | MUTATIONS | INHIBITOR | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Immunoprecipitation | Lung Neoplasms - metabolism | Carcinoma, Non-Small-Cell Lung - metabolism | Ubiquitin - metabolism | Cercopithecus aethiops | Lung Neoplasms - pathology | Antineoplastic Agents - therapeutic use | Mutation - genetics | Receptor, Epidermal Growth Factor - metabolism | Tyrosine - metabolism | Animals | Quinazolines - therapeutic use | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - drug therapy | Epidermal Growth Factor - pharmacology | Phosphorylation - drug effects | Tumor Cells, Cultured | COS Cells
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4. Full Text EGF-independent activation of cell-surface EGF receptors harboring mutations found in gefitinib-sensitive lung cancer
by Choi, S.H and Mendrola, J.M and Lemmon, M.A
Oncogene, ISSN 0950-9232, 03/2007, Volume 26, Issue 11, pp. 1567 - 1576
Several somatic mutations within the tyrosine kinase domain of epidermal growth factor receptor (EGFR) have been identified that predict clinical response of... 
Autoinhibition | Constitutive activation | Somatic mutations | ErbB | Internalization | EGFR | TRANSFORMATION | TYROSINE KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | constitutive activation | autoinhibition | KINASE DOMAIN | CELL BIOLOGY | somatic mutations | BREAST-CANCER | ONCOGENE | MUTANTS | ONCOLOGY | EPIDERMAL-GROWTH-FACTOR | GENETICS & HEREDITY | internalization | INHIBITOR | EXPRESSION | PROGRESSION | Phosphorylation | Cell Proliferation | Humans | Lung Neoplasms - metabolism | Models, Molecular | Epidermal Growth Factor - metabolism | Lung Neoplasms - pathology | Interleukin-3 - pharmacology | Receptor, Epidermal Growth Factor - chemistry | Receptor, Epidermal Growth Factor - metabolism | Cell Line, Tumor | Protein Binding | Antineoplastic Agents - pharmacology | Cell Membrane - metabolism | Mutation | Quinazolines - pharmacology | Causes of | Genetic aspects | Research | Gene mutations | Lung cancer, Non-small cell | Health aspects | Hypothesis testing | Signal transduction | Oncology | Lung cancer | Genes
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5. Full Text Identification of non-small-cell lung cancer with activating EGFR mutations in malignant effusion and cerebrospinal fluid: Rapid and sensitive detection of exon 19 deletion E746-A750 and exon 21 L858R mutation by immunocytochemistry
by Kawahara, Akihiko and Azuma, Koichi and Sumi, Akiko and Taira, Tomoki and Nakashima, Kazutaka and Aikawa, Emiko and Abe, Hideyuki and Yamaguchi, Tomohiko and Takamori, Shinzo and Akiba, Jun and Kage, Masayoshi
Lung Cancer, ISSN 0169-5002, 2011, Volume 74, Issue 1, pp. 35 - 40
Abstract Background Recently, we have reported that EGFR mutation-specific antibodies performed well in immunohistochemical analysis, with good sensitivity. We... 
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | Non-small-cell lung cancer | Activating EGFR mutations | Immunocytochemistry | Effusion cytology | Mutation-specific antibody | ANTIBODIES | DIAGNOSIS | GEFITINIB | ADENOCARCINOMA | TREATED PATIENTS | P53 | ONCOLOGY | RESPIRATORY SYSTEM | EPIDERMAL-GROWTH-FACTOR | Receptor, Epidermal Growth Factor - genetics | Recurrence | Humans | Middle Aged | Antibodies, Monoclonal - therapeutic use | Lung Neoplasms - pathology | Male | Carcinoma, Non-Small-Cell Lung - diagnosis | Lung Neoplasms - physiopathology | Carcinoma, Non-Small-Cell Lung - physiopathology | Polymerase Chain Reaction - methods | Receptor, Epidermal Growth Factor - metabolism | DNA - cerebrospinal fluid | DNA - analysis | Sensitivity and Specificity | Pleural Effusion, Malignant | Adult | Female | Biomarkers, Pharmacological - cerebrospinal fluid | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Receptor, Epidermal Growth Factor - immunology | Biomarkers, Pharmacological - analysis | Carcinoma, Non-Small-Cell Lung - genetics | Exons - genetics | Lung Neoplasms - therapy | Immunohistochemistry - methods | Carcinoma, Non-Small-Cell Lung - therapy | Quinazolines - therapeutic use | Aged | Lung Neoplasms - diagnosis | Sequence Deletion - genetics | Viral antibodies | Medical colleges | Peptides | Analysis | Antibodies | Genetic aspects | Nucleic acids | Lung cancer, Non-small cell
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6. Full Text Synergistic cytotoxicity of afatinib and cetuximab against EGFR T790M involves Rab11-dependent EGFR recycling
by Watanuki, Zenta and Kosai, Hitomi and Osanai, Nanae and Ogama, Naoko and Mochizuki, Mai and Tamai, Keiichi and Yamaguchi, Kazunori and Satoh, Kennichi and Fukuhara, Tatsuro and Maemondo, Makoto and Ichinose, Masakazu and Nukiwa, Toshihiro and Tanaka, Nobuyuki
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 12/2014, Volume 455, Issue 3-4, pp. 269 - 276
EGFR is an important therapeutic target for non-small cell lung cancers (NSCLCs). Tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, are... 
Cytotoxicity | EGFR | EGFR-TKI | GEFITINIB | ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRAFFICKING | SENSITIVITY | TUMORS | CHEMOTHERAPY | CELL LUNG-CANCER | TRIAL | BIOPHYSICS | FACTOR RECEPTOR MUTATIONS | ERLOTINIB | Receptor, Epidermal Growth Factor - genetics | Humans | Cercopithecus aethiops | Drug Resistance, Neoplasm | Dose-Response Relationship, Drug | Receptor, Epidermal Growth Factor - metabolism | Bcl-2-Like Protein 11 | Antibodies, Monoclonal, Humanized - pharmacology | Antineoplastic Agents - pharmacology | Cell Membrane - metabolism | Membrane Proteins - metabolism | Cetuximab | Antibodies, Monoclonal - chemistry | Proto-Oncogene Proteins - metabolism | rab GTP-Binding Proteins - metabolism | Apoptosis Regulatory Proteins - metabolism | Microscopy, Confocal | Animals | K562 Cells | HeLa Cells | Mutation | Quinazolines - pharmacology | COS Cells | Microscopy, Fluorescence | Apoptosis | Antimitotic agents | Antineoplastic agents | Recycling (Waste, etc.)
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7. Full Text The anti-proliferative effect of heat shock protein 90 inhibitor, 17-DMAG, on non-small-cell lung cancers being resistant to EGFR tyrosine kinase inhibitor
by Kobayashi, Naruyuki and Toyooka, Shinichi and Soh, Junichi and Yamamoto, Hiromasa and Dote, Hideaki and Kawasaki, Kensuke and Otani, Hiroki and Kubo, Takafumi and Jida, Masaru and Ueno, Tsuyoshi and Ando, Midori and Ogino, Atsuko and Kiura, Katsuyuki and Miyoshi, Shinichiro
Lung Cancer, ISSN 0169-5002, 2011, Volume 75, Issue 2, pp. 161 - 166
Abstract Acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), gefitinib and erlotinib, is frequently observed after... 
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | Hsp90 | 17-DMAG | EGFR mutation | Hsp90 inhibitor | Acquired resistance | EGFR-TKI | Gefitinib | HEAT-SHOCK-PROTEIN-90 | ACQUIRED-RESISTANCE | SENSITIVITY | T790M MUTATION | RECEPTOR | DOMAIN MUTATIONS | COMBINATION | GELDANAMYCINS | HSP90 INHIBITORS | ONCOLOGY | RESPIRATORY SYSTEM | Erlotinib Hydrochloride | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Apoptosis - drug effects | Humans | Drug Resistance, Neoplasm | Lactams, Macrocyclic - pharmacology | Benzoquinones - pharmacology | Xenograft Model Antitumor Assays | Animals | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Mice | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Quinazolines - pharmacology | Tyrosine | Heat shock proteins | Epidermal growth factor | Lung cancer, Non-small cell | Health aspects | Analysis
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8. Full Text Patients with NSCLC may display a low ratio of p.T790M vs. activating EGFR mutations in plasma at disease progression: Implications for personalised treatment
by Del Re, Marzia and Bordi, P and Petrini, I and Rofi, E and Mazzoni, F and Belluomini, L and Vasile, E and Restante, G and Di Costanzo, F.D and Falcone, Alfredo and Frassoldati, A and Schaik, Ron and Steendam, C.M.J and Chella, A and Tiseo, M and Morganti, R and Danesi, Romano
Oncotarget, ISSN 1949-2553, 10/2017, Volume 8, Issue 49, pp. 86056 - 86065
textabstractIntroduction: NSCLC harboring activating mutations of EGFR is highly sensitive to first-line EGFR-tyrosine kinase inhibitors (TKIs), but drug... 
Personalized medicine | Predictive biomarkers | Circulating tumor DNA | EGFR | predictive biomarkers | GEFITINIB | ACQUIRED-RESISTANCE | EPMA POSITION PAPER | T790M MUTATION | MECHANISMS | personalized medicine | TKI RESISTANCE | CELL BIOLOGY | CELL LUNG-CANCER | TYROSINE KINASE INHIBITORS | GENETIC-HETEROGENEITY | circulating tumor DNA
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9. Full Text Fighting cancer drug resistance: Opportunities and challenges for mutation-specific EGFR inhibitors
by Juchum, Michael and Günther, Marcel and Laufer, Stefan A
Drug Resistance Updates, ISSN 1368-7646, 2015, Volume 20, pp. 12 - 28
Abstract Multiple mutations in the EGFR gene are a major cause for the failure of Erlotinib and Gefitinib in the treatment of patients harboring non-small-cell... 
Infectious Disease | Hematology, Oncology and Palliative Medicine | Resistance | Inhibitors | Mutation | NSCLC | EGFR | GENE-MUTATIONS | IRREVERSIBLE INHIBITORS | GROWTH-FACTOR-RECEPTOR | ACQUIRED-RESISTANCE | ATP-BINDING-SITE | CELL LUNG-CANCER | PHASE-II TRIAL | TYROSINE KINASE INHIBITOR | PHARMACOLOGY & PHARMACY | PATIENTS PTS | PREVIOUSLY TREATED PATIENTS | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | ErbB Receptors - antagonists & inhibitors | Adenocarcinoma of Lung | Carcinoma, Non-Small-Cell Lung - genetics | Humans | ErbB Receptors - genetics | Mutant Proteins - genetics | Adenocarcinoma - drug therapy | Drug Resistance, Neoplasm - genetics | Protein Kinase Inhibitors - therapeutic use | Adenocarcinoma - genetics | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutant Proteins - antagonists & inhibitors | Molecular Targeted Therapy - methods | Antimitotic agents | Genomics | Drug resistance | Drug therapy | Lung cancer, Non-small cell | Antineoplastic agents | Cells
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10. Full Text Anti-EGFR monoclonal antibodies and EGFR tyrosine kinase inhibitors as combination therapy for triple-negative breast cancer
by Guerrab, Abderrahim El and Bamdad, Mahchid and Kwiatkowski, Fabrice and Bignon, Yves-Jean and Penault-Llorca, Frédérique and Aubel, Corinne
Oncotarget, ISSN 1949-2553, 2016, Volume 7, Issue 45, pp. 73618 - 73637
Triple-negative breast cancer (TNBC) is characterized by overexpression of epidermal growth factor receptor (EGFR) and activation of its downstream signaling... 
Cytotoxicity | Epidermal growth factor receptor | Cell cycle | Anti-EGFR targeted therapy | Triple-negative breast cancer | 1ST-LINE TREATMENT | triple-negative breast cancer | cell cycle | epidermal growth factor receptor | anti-EGFR targeted therapy | BRCA1 MUTATIONS | DRUG-RESISTANCE | METASTATIC COLORECTAL-CANCER | CELL BIOLOGY | CELL LUNG-CANCER | GROWTH-FACTOR RECEPTOR | TARGETED THERAPIES | RANDOMIZED PHASE-II | CETUXIMAB PLUS IRINOTECAN | GENE COPY NUMBER | cytotoxicity | Phosphorylation | Apoptosis - drug effects | Humans | Cyclins - genetics | ras Proteins - metabolism | Molecular Targeted Therapy | Triple Negative Breast Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - metabolism | Triple Negative Breast Neoplasms - pathology | Inhibitory Concentration 50 | Female | Gene Expression Regulation, Neoplastic - drug effects | Cell Survival - drug effects | Antibodies, Monoclonal - pharmacology | Protein Kinase Inhibitors - administration & dosage | Triple Negative Breast Neoplasms - genetics | Signal Transduction - drug effects | Antibodies, Monoclonal - administration & dosage | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Triple Negative Breast Neoplasms - metabolism | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | G1 Phase Cell Cycle Checkpoints - drug effects | Mitogen-Activated Protein Kinases - metabolism | Life Sciences | Biomolecules | Molecular biology | Biochemistry, Molecular Biology | Genomics | Cancer
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11. Full Text ErbB-3 Mediates Phosphoinositide 3-Kinase Activity in Gefitinib-Sensitive Non-Small Cell Lung Cancer Cell Lines
by Jeffrey A. Engelman and Pasi A. Jänne and Craig Mermel and Joseph Pearlberg and Toru Mukohara and Christina Fleet and Karen Cichowski and Bruce E. Johnson and Lewis C. Cantley
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2005, Volume 102, Issue 10, pp. 3788 - 3793
Therapies that target the EGF receptor (EGFR), such as gefitinib (IRESSA), are effective in a subset of patients with advanced non-small cell lung cancer... 
Tumor cell line | Biological Sciences | Receptors | Cell growth | Phosphorylation | NIH 3T3 cells | Cell lines | Antibodies | CHO cells | Medical schools | Lung neoplasms | EGF receptor | Akt | FACTOR-RECEPTOR | PATHWAYS | PHOSPHATIDYLINOSITOL 3-KINASE | MULTIDISCIPLINARY SCIENCES | WIDE PREDICTION | EGFR MUTATIONS | TUMOR-CELLS | TRIAL | EPIDERMAL-GROWTH-FACTOR | ZD1839 IRESSA | TYROSINE KINASE INHIBITOR | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - drug therapy | Proto-Oncogene Proteins - antagonists & inhibitors | Cricetinae | Protein-Serine-Threonine Kinases - physiology | Humans | Lung Neoplasms - pathology | Proto-Oncogene Proteins c-akt | Receptor, ErbB-3 - physiology | Animals | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Cell Line, Tumor | Phosphatidylinositol 3-Kinases - physiology | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Quinazolines - pharmacology | Receptor, Epidermal Growth Factor - physiology | CHO Cells | Phosphoinositides | Care and treatment | Research | Lung cancer | Cancer
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12. Epidermal growth factor receptor exon 20 p.S768i mutation in non-small cell lung carcinoma: A case report combined with a review of the literature and investigation of clinical significance
by Improta, Giuseppina and Pettinato, Angela and Gieri, Stefania and Scandurra, Giuseppa and Skovrider-Ruminski, Wojciech and Høgdall, Estrid and Fraggetta, Filippo
Oncology Letters, ISSN 1792-1074, 01/2016, Volume 11, Issue 1, pp. 393 - 398
Epidermal growth factor receptor (EGFR) plays a significant role in non-small cell lung cancer (NSCLC), the most preyalent form of lung cancer worldwide.... 
Lung adenocarcinoma | Gefitinib | P.S768I mutation | Epidermal growth factor receptor | Tyrosine kinase inhibitors | p.S768I mutation | CANCER PATIENTS | GENE-MUTATIONS | TARGETED THERAPY | RESPONSIVENESS | epidermal growth factor receptor | lung adenocarcinoma | SENSITIVITY | PATTERNS | gefitinib | EGFR MUTATIONS | GEFITINIB TREATMENT | tyrosine kinase inhibitors | ONCOLOGY | ERLOTINIB
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13. Full Text Efficacy of EGFR tyrosine kinase inhibitors in patients with EGFR-mutated nonsmall-cell lung cancer: A meta-analysis of 13 randomized trials
by Petrelli, Fausto and Borgonovo, Karen and Cabiddu, Mary and Barni, Sandro
Clinical Lung Cancer, ISSN 1525-7304, 03/2012, Volume 13, Issue 2, pp. 107 - 114
Advanced nonsmall-cell lung cancer (NSCLC) harboring activating mutations of epidermal growth factor receptor (EGFR) are particularly sensitive to tyrosine... 
Erlotinib | Nonsmall-cell lung cancer | Mutation | Gefitinib | EGFR
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14. Full Text Long-term survival with erlotinib in advanced lung adenocarcinoma harboring synchronous EGFR G719S and KRAS G12C mutations
by Ricciuti, Biagio and Baglivo, Sara and Ludovini, Vienna and Sidoni, Angelo and Metro, Giulio and Brambilla, Marta and Siggillino, Annamaria and Reda, Maria Sole and Rebonato, Alberto and Maiettini, Daniele and Chiari, Rita
Lung Cancer, ISSN 0169-5002, 06/2018, Volume 120, pp. 70 - 74
Although epidermal growth factor receptor ( ) and v-Ki-ras2 Kirsten rat sarcoma viral oncogene ( ) mutations were thought to be mutually exclusive in patients... 
KRAS | NGS | NSCLC | Erlotinib | EGFR | ONCOLOGY | RESPIRATORY SYSTEM | AFATINIB | CANCER | Tyrosine | Medical colleges | Epidermal growth factor | Sarcoma | Analysis | Genetic research | Genetic aspects | Lung cancer, Non-small cell
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15. Full Text Efficacy of EGFR Tyrosine Kinase Inhibitors in Patients With EGFR-Mutated Non–Small-Cell Lung Cancer: A Meta-Analysis of 13 Randomized Trials
by Petrelli, Fausto and Borgonovo, Karen and Cabiddu, Mary and Barni, Sandro
Clinical Lung Cancer, ISSN 1525-7304, 2012, Volume 13, Issue 2, pp. 107 - 114
Abstract Advanced non–small-cell lung cancer (NSCLC) harboring activating mutations of epidermal growth factor receptor (EGFR) are particularly sensitive to... 
Hematology, Oncology and Palliative Medicine | Pulmonary/Respiratory | Non–small-cell lung cancer | Mutation | Erlotinib | Gefitinib | EGFR | GENE-MUTATIONS | SURVIVAL | MULTICENTER | GROWTH-FACTOR-RECEPTOR | Non-small-cell lung cancer | GEFITINIB SENSITIVITY | CHEMOTHERAPY | THERAPY | ONCOLOGY | PROSPECTIVE PHASE-II | ACTIVATING MUTATIONS | Lung Neoplasms - drug therapy | Meta-Analysis as Topic | Protein Kinase Inhibitors - therapeutic use | Humans | Lung Neoplasms - metabolism | Carcinoma, Non-Small-Cell Lung - metabolism | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Carcinoma, Non-Small-Cell Lung - drug therapy | Randomized Controlled Trials as Topic
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