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1. Full Text Fulminant Myocarditis with Combination Immune Checkpoint Blockade
by Johnson, Douglas B and Balko, Justin M and Compton, Margaret L and Chalkias, Spyridon and Gorham, Joshua and Xu, Yaomin and Hicks, Mellissa and Puzanov, Igor and Alexander, Matthew R and Bloomer, Tyler L and Becker, Jason R and Slosky, David A and Phillips, Elizabeth J and Pilkinton, Mark A and Craig-Owens, Laura and Kola, Nina and Plautz, Gregory and Reshef, Daniel S and Deutsch, Jonathan S and Deering, Raquel P and Olenchock, Benjamin A and Lichtman, Andrew H and Roden, Dan M and Seidman, Jonathan G and Seidman, Christine E and Koralnik, Igor J and Hoffman, Robert D and Taube, Janis M and Diaz, Luis A and Anders, Robert A and Sosman, Jeffrey A and Moslehi, Javid J
The New England Journal of Medicine, ISSN 0028-4793, 11/2016, Volume 375, Issue 18, pp. 1749 - 1755
Fatal autoimmune myocarditis with rhabdomyolysis and refractory arrhythmias developed in two patients treated with a combination of anti–CTLA-4 and anti–PD-1... 
UNTREATED MELANOMA | HEART | MEDICINE, GENERAL & INTERNAL | AUTOPSY | PEMBROLIZUMAB | PD-1 BLOCKADE | INFLAMMATION | RISK | DILATED CARDIOMYOPATHY | NIVOLUMAB | IPILIMUMAB | Melanoma - complications | Glucocorticoids - therapeutic use | Arrhythmias, Cardiac - chemically induced | Myocarditis - etiology | Humans | Ipilimumab | Middle Aged | Myocarditis - drug therapy | Antibodies, Monoclonal - adverse effects | Antibodies, Monoclonal - therapeutic use | Electrocardiography - drug effects | Male | Myocardium - pathology | Myositis - chemically induced | Heart Block - diagnosis | Immunotherapy - adverse effects | Melanoma - drug therapy | Fatal Outcome | Female | Aged | Heart Block - etiology | Myocarditis - pathology | Care and treatment | Research | Rhabdomyolysis | Immune complexes | Cancer | Heart | Antigens | Melanoma | T cell receptors | Lymphocytes T | Metastasis | Grants | Kinases | Macrophages | Patients | Cancer therapies | Skeletal muscle | Myocarditis | Musculoskeletal system | Immune checkpoint | Lymphocytes | Immunotherapy | Myocardium | Myositis | Heart diseases | Tumors | nivolumab | myositis | ipilimumab | PD-L1 | CTLA-4 | PD-1 | cardiac
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2. Rationale for targeting the Ras/MAPK pathway in triple-negative breast cancer
by Giltnane, Jennifer M and Giltnane, Jennifer M and Balko, Justin M and Balko, Justin M
Discovery medicine, ISSN 1539-6509, 2014, Volume 17, Issue 95, pp. 275 - 283
"Triple negative" breast cancer (TNBC) is the most aggressive and least common clinical subtype of breast cancer. As its nomenclature implies, TNBC lacks... 
EPITHELIAL-MESENCHYMAL TRANSITION | MEDICINE, RESEARCH & EXPERIMENTAL | STEM-CELLS | ACTIVATED PROTEIN-KINASE | ADVANCED SOLID TUMORS | MOLECULAR PORTRAITS | NEOADJUVANT CHEMOTHERAPY | MEK INHIBITION | LONG-TERM SURVIVAL | ONCOGENIC MUTATIONS | PHASE-I | Humans | Gene Expression Regulation, Neoplastic | Neoplasm Recurrence, Local | ras Proteins - metabolism | Treatment Outcome | MAP Kinase Kinase Kinases - metabolism | Enzyme Inhibitors - therapeutic use | Triple Negative Breast Neoplasms - therapy | MAP Kinase Signaling System | Animals | Triple Negative Breast Neoplasms - genetics | Triple Negative Breast Neoplasms - metabolism | Mice | Mutation | Genome, Human
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3. Full Text RAS/MAPK activation is associated with reduced tumor-infiltrating lymphocytes in triple-negative breast cancer: Therapeutic cooperation between MEK and PD-1/PD-L1 immune checkpoint inhibitors
by Loi, Sherene and Dushyanthen, Sathana and Beavis, Paul A and Salgado, Roberto and Denkert, Carsten and Savas, Peter and Combs, Susan and Rimm, David L and Giltnane, Jennifer M and Estrada, Monica V and Sánchez, Violeta and Sanders, Melinda E and Cook, Rebecca S and Pilkinton, Mark A and Mallal, Simon A and Wang, Kai and Miller, Vincent A and Stephens, Phil J and Yelensky, Roman and Doimi, Franco D and Gómez, Henry and Ryzhov, Sergey V and Darcy, Phillip K and Arteaga, Carlos L and Balko, Justin M
Clinical Cancer Research, ISSN 1078-0432, 03/2016, Volume 22, Issue 6, pp. 1499 - 1509
Purpose: Tumor-infiltrating lymphocytes (TIL) in the residual disease (RD) of triple-negative breast cancers (TNBC) after neoadjuvant chemotherapy (NAC) are... 
NEOADJUVANT CHEMOTHERAPY | ONCOLOGY | SAFETY | PD-L1 EXPRESSION | POOR-PROGNOSIS | RESIDUAL DISEASE | ANTIBODY | CARCINOMA | IPILIMUMAB | Immunomodulation - drug effects | Humans | Transcriptome | ras Proteins - metabolism | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Gene Expression Profiling | Triple Negative Breast Neoplasms - drug therapy | Triple Negative Breast Neoplasms - immunology | Triple Negative Breast Neoplasms - pathology | Female | Lymphocytes, Tumor-Infiltrating - metabolism | Disease Models, Animal | Signal Transduction | Mortality | Immunophenotyping | Disease Progression | Phenotype | Animals | B7-H1 Antigen - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Triple Negative Breast Neoplasms - metabolism | Biomarkers | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Lymphocytes, Tumor-Infiltrating - immunology | Mitogen-Activated Protein Kinases - metabolism | neoadjuvant chemotherapy | MEK | immunotherapy
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4. Full Text Melanoma-specific MHC-II expression represents a tumour-autonomous phenotype and predicts response to anti-PD-1/PD-L1 therapy
by Johnson, Douglas B and Estrada, Monica V and Salgado, Roberto and Sanchez, Violeta and Doxie, Deon B and Opalenik, Susan R and Vilgelm, Anna E and Feld, Emily and Johnson, Adam S and Greenplate, Allison R and Sanders, Melinda E and Lovly, Christine M and Frederick, Dennie T and Kelley, Mark C and Richmond, Ann and Irish, Jonathan M and Shyr, Yu and Sullivan, Ryan J and Puzanov, Igor and Sosman, Jeffrey A and Balko, Justin M
Nature Communications, ISSN 2041-1723, 01/2016, Volume 7, Issue 1, p. 10582
Anti-PD-1 therapy yields objective clinical responses in 30-40% of advanced melanoma patients. Since most patients do not respond, predictive biomarkers to... 
GENE | SAFETY | PD-1 BLOCKADE | MULTIDISCIPLINARY SCIENCES | ANTIBODY | NRAS MUTATIONS | NIVOLUMAB | CLINICAL-RESPONSE | CANCER | T-CELLS | IPILIMUMAB | Genes, MHC Class II - genetics | Melanoma - metabolism | Antibodies, Monoclonal, Humanized | Melanoma - genetics | Antibodies, Monoclonal - pharmacology | Humans | RNA, Messenger - genetics | Cell Line, Tumor | Genotype | Programmed Cell Death 1 Receptor - antagonists & inhibitors | RNA, Messenger - metabolism | Gene Expression Regulation, Neoplastic - physiology
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5. Full Text Triple-negative breast cancer: Challenges and opportunities of a heterogeneous disease
by Bianchini, Giampaolo and Balko, Justin M and Mayer, Ingrid A and Sanders, Melinda E and Gianni, Luca
Nature Reviews Clinical Oncology, ISSN 1759-4774, 11/2016, Volume 13, Issue 11, pp. 674 - 690
Chemotherapy is the primary established systemic treatment for patients with triple-negative breast cancer (TNBC) in both the early and advanced-stages of the... 
TUMOR-INFILTRATING LYMPHOCYTES | EPITHELIAL-MESENCHYMAL TRANSITION | BASAL-LIKE | DNA-REPAIR DEFECT | NEOADJUVANT CHEMOTHERAPY | ONCOLOGY | RANDOMIZED PHASE-II | GENE-EXPRESSION | POLY(ADP-RIBOSE) POLYMERASE-1 | RESIDUAL DISEASE | PATHOLOGICAL COMPLETE RESPONSE | Immunotherapy - methods | Prognosis | Neoplastic Stem Cells - drug effects | Humans | Clinical Trials as Topic | Mutation - genetics | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use | Triple Negative Breast Neoplasms - therapy | Triple Negative Breast Neoplasms - classification | Triple Negative Breast Neoplasms - genetics | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Androgen Antagonists - therapeutic use | Biomarkers, Tumor - metabolism | Immune System - immunology | Female | Ubiquitin-Protein Ligases - genetics | BRCA2 Protein - genetics | Molecular Targeted Therapy - methods | Molecular targeted therapy | Care and treatment | Gene mutations | Innovations | Development and progression | Breast cancer | Genetic aspects | Health aspects
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6. Full Text Cardiovascular toxicities associated with immune checkpoint inhibitors: an observational, retrospective, pharmacovigilance study
by Salem, Joe-Elie and Manouchehri, Ali and Moey, Melissa and Lebrun-Vignes, Bénédicte and Bastarache, Lisa and Pariente, Antoine and Gobert, Aurélien and Spano, Jean-Philippe and Balko, Justin M and Bonaca, Marc P and Roden, Dan M and Johnson, Douglas B and Moslehi, Javid J
The Lancet Oncology, ISSN 1470-2045, 12/2018, Volume 19, Issue 12, pp. 1579 - 1589
Immune checkpoint inhibitors (ICIs) have substantially improved clinical outcomes in multiple cancer types and are increasingly being used in early disease... 
ONCOLOGY | RISK | FULMINANT MYOCARDITIS | Complications and side effects | Lung cancer | Analysis | Immunotherapy
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7. Full Text Molecular profiling of the residual disease of triple-negative breast cancers after neoadjuvant chemotherapy identifies actionable therapeutic targets
by Balko, Justin M and Giltnane, Jennifer M and Wang, Kai and Schwarz, Luis J and Young, Christian D and Cook, Rebecca S and Owens, Phillip and Sanders, Melinda E and Kuba, Maria G and Sánchez, Violeta and Kurupi, Richard and Moore, Preston D and Pinto, Joseph A and Doimi, Franco D and Gómez, Henry and Horiuchi, Dai and Goga, Andrei and Lehmann, Brian D and Bauer, Joshua A and Pietenpol, Jennifer A and Ross, Jeffrey S and Palmer, Gary A and Yelensky, Roman and Cronin, Maureen and Miller, Vincent A and Stephens, Phillip J and Arteaga, Carlos L
Cancer Discovery, ISSN 2159-8274, 02/2014, Volume 4, Issue 2, pp. 232 - 245
Neoadjuvant chemotherapy (NAC) induces a pathologic complete response (pCR) in approximately 30% of patients with triple-negative breast cancers (TNBC). In... 
CELL LUNG-CANCER | BASAL-LIKE | ACTIVATION | INHIBITION | ONCOLOGY | MYC | DOWN-REGULATION | TUMORS | EXPRESSION | AMERICAN-SOCIETY | PATHOLOGISTS GUIDELINE RECOMMENDATIONS | Prognosis | Humans | Ki-67 Antigen - metabolism | Treatment Outcome | Gene Expression Profiling | Triple Negative Breast Neoplasms - mortality | Genes, myc | Triple Negative Breast Neoplasms - drug therapy | Myeloid Cell Leukemia Sequence 1 Protein - genetics | DNA Copy Number Variations | Neoplasm, Residual | Drug Resistance, Neoplasm - genetics | Gene Amplification | Triple Negative Breast Neoplasms - genetics | Ki-67 Antigen - genetics | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Triple Negative Breast Neoplasms - pathology | Cell Line, Tumor | Female | Neoadjuvant Therapy | Cluster Analysis | neoadjuvant chemotherapy | next-generation sequencing | breast cancer
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8. Full Text PIK3CA mutations in androgen receptor-positive triple negative breast cancer confer sensitivity to the combination of PI3K and androgen receptor inhibitors
by Lehmann, Brian D and Lehmann, Brian D and Bauer, Joshua A and Bauer, Joshua A and Schafer, Johanna M and Schafer, Johanna M and Pendleton, Christopher S and Pendleton, Christopher S and Tang, Luojia and Tang, Luojia and Johnson, Kimberly C and Johnson, Kimberly C and Chen, Xi and Chen, Xi and Balko, Justin M and Balko, Justin M and Gómez, Henry and Gómez, Henry and Arteaga, Carlos L and Arteaga, Carlos L and Mills, Gordon B and Mills, Gordon B and Sanders, Melinda E and Sanders, Melinda E and Pietenpol, Jennifer A and Pietenpol, Jennifer A
Breast cancer research : BCR, ISSN 1465-5411, 2014, Volume 16, Issue 4, p. 406
Introduction: Triple negative breast cancer (TNBC) is a heterogeneous collection of biologically diverse cancers, which contributes to variable clinical... 
CLINICAL-ONCOLOGY/COLLEGE | ONCOLOGY | PROSTATE-CANCER | PATTERNS | RECURRENCE | IDENTIFICATION | CARCINOMA | AMERICAN-SOCIETY | CHEMOTHERAPY | PATHOLOGISTS GUIDELINE RECOMMENDATIONS | FEATURES | TOR Serine-Threonine Kinases - metabolism | Humans | Receptors, Androgen - metabolism | Gene Expression Regulation, Neoplastic | Antineoplastic Agents - therapeutic use | Gene Expression Profiling | Androgen Receptor Antagonists - pharmacology | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Triple Negative Breast Neoplasms - drug therapy | Triple Negative Breast Neoplasms - pathology | Dihydrotestosterone - pharmacology | Female | Antineoplastic Agents - pharmacology | Disease Models, Animal | Cell Survival - drug effects | Phosphatidylinositol 3-Kinases - genetics | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Class I Phosphatidylinositol 3-Kinases | Receptors, Androgen - genetics | Triple Negative Breast Neoplasms - genetics | Signal Transduction - drug effects | Triple Negative Breast Neoplasms - metabolism | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Mutation | Cluster Analysis | Medical research | Androgens | Chemotherapy | Analysis | Medicine, Experimental | Breast cancer | Genetic aspects | Cancer
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9. Full Text Phosphatidylinositol 3-Kinase and Antiestrogen Resistance in Breast Cancer
by Todd W. Miller and Justin M. Balko and Carlos L. Arteaga
Journal of Clinical Oncology, ISSN 0732-183X, 11/2011, Volume 29, Issue 33, pp. 4452 - 4461
Although antiestrogen therapies targeting estrogen receptor (ER) alpha signaling prevent disease recurrence in the majority of patients with hormone-dependent... 
GROWTH-FACTOR RECEPTOR | INDUCED ACTIVATION | PIK3CA MUTATIONS | ONCOLOGY | PROTEIN-KINASE | ESTROGEN-RECEPTOR-ALPHA | TAMOXIFEN RESISTANCE | GENE-EXPRESSION | ENDOCRINE THERAPY | PHASE-II | TUMOR-SUPPRESSOR | Breast Neoplasms - chemistry | Estrogen Receptor Modulators - therapeutic use | Signal Transduction - drug effects | Humans | Phosphatidylinositol 3-Kinases - physiology | Drug Resistance, Neoplasm | Female | Clinical Trials as Topic | Receptors, Estrogen - analysis | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Breast Neoplasms - drug therapy | Receptors, Estrogen - physiology | Bon | Biology of Neoplasia | Bc8 | To2 | Bc7 | To4 | To5 | To8 | To11 | To10
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10. Full Text MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation
by Lee, Kyung-min and Lee, Taekyu and Giltnane, Jennifer M and Balko, Justin M and Schwarz, Luis J and Guerrero-Zotano, Angel L and Hutchinson, Katherine E and Nixon, Mellissa J and Estrada, Mónica V and Sánchez, Violeta and Sanders, Melinda E and Gómez, Henry and Lluch, Ana and Pérez-Fidalgo, J. Alejandro and Wolf, Melissa Magdalene and Andrejeva, Gabriela and Rathmell, Jeffrey C and Fesik, Stephen W and Arteaga, Carlos L
Cell Metabolism, ISSN 1550-4131, 10/2017, Volume 26, Issue 4, pp. 633 - 647.e7
Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. and are frequently co-amplified in drug-resistant TNBC after... 
chemotherapy resistance | triple negative breast cancer | cancer stem cell | MYC | MCL1 | mitochondrial respiration | MAINTENANCE | INHIBITION | METASTASIS | METABOLISM | RESPIRATION | TRANSCRIPTION | ENDOCRINOLOGY & METABOLISM | SENSITIVITY | THERAPEUTIC TARGETS | IDENTIFICATION | EXPRESSION | CELL BIOLOGY | Reactive Oxygen Species - metabolism | Neoplastic Stem Cells - drug effects | Humans | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Drug Resistance, Neoplasm | Mitochondria - metabolism | Mitochondria - drug effects | Mitochondria - pathology | Triple Negative Breast Neoplasms - drug therapy | Proto-Oncogene Proteins c-myc - metabolism | Oxidative Phosphorylation - drug effects | Animals | Neoplastic Stem Cells - metabolism | Mice, Nude | Triple Negative Breast Neoplasms - metabolism | Triple Negative Breast Neoplasms - pathology | Cell Line, Tumor | Neoplastic Stem Cells - pathology | Female | Chemotherapy | Breast cancer | Drug resistance | Pharmaceutical industry | Stem cells | Cancer | Development and progression | Adjuvant treatment
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11. Full Text Biomarkers for Immunotherapy Toxicity: Are Cytokines the Answer?
by Johnson, DB and Balko, JM
CLINICAL CANCER RESEARCH, ISSN 1078-0432, 03/2019, Volume 25, Issue 5, pp. 1452 - 1454
Immune checkpoint inhibitors induce durable responses in some patients with advanced cancer but may simultaneously trigger autoinflammatory immune-related... 
ONCOLOGY
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12. Full Text TGF-β inhibition enhances chemotherapy action against triple-negative breast cancer
by Bhola, Neil E and Balko, Justin M and Dugger, Teresa C and Kuba, María Gabriela and Sánchez, Violeta and Sanders, Melinda and Stanford, Jamie and Cook, Rebecca S and Arteaga, Carlos L
Journal of Clinical Investigation, ISSN 0021-9738, 03/2013, Volume 123, Issue 3, pp. 1348 - 1358
After an initial response to chemotherapy, many patients with triple-negative breast cancer (TNBC) have recurrence of drug-resistant metastatic disease.... 
MEDICINE, RESEARCH & EXPERIMENTAL | STEM-CELLS | METASTASIS | THERAPY | PATHWAY | GENE-EXPRESSION | SMAD | MESENCHYMAL TRANSITION | TUMOR-GROWTH | INTERLEUKIN-8 | PACLITAXEL | Interleukin-8 - genetics | RNA, Small Interfering - genetics | Receptor, Transforming Growth Factor-beta Type I | Receptors, Estrogen - metabolism | Paclitaxel - pharmacology | Gene Expression - drug effects | Neoplastic Stem Cells - drug effects | Humans | Receptor, ErbB-2 - metabolism | Drug Resistance, Neoplasm | Quinolines - pharmacology | Breast Neoplasms - metabolism | Gene Knockdown Techniques | Receptors, Progesterone - metabolism | Neoplastic Stem Cells - metabolism | Smad4 Protein - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Female | Interleukin-8 - metabolism | Pyrazoles - pharmacology | Signal Transduction | Spheroids, Cellular - metabolism | Transforming Growth Factor beta - physiology | Breast Neoplasms - drug therapy | Smad4 Protein - metabolism | Xenograft Model Antitumor Assays | Transforming Growth Factor beta - pharmacology | Animals | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Mice | Antineoplastic Agents, Phytogenic - pharmacology
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13. Full Text EPHA2 blockade overcomes acquired resistance to EGFR kinase inhibitors in lung cancer
by Amato, Katherine R and Wang, Shan and Tan, Li and Hastings, Andrew K and Song, Wenqiang and Lovly, Christine M and Meador, Catherine B and Ye, Fei and Lu, Pengcheng and Balko, Justin M and Colvin, Daniel C and Cates, Justin M and Pao, William and Gray, Nathanael S and Chen, Jin
Cancer Research, ISSN 0008-5472, 01/2016, Volume 76, Issue 2, pp. 305 - 318
Despite the success of treating EGFR-mutant lung cancer patients with EGFR tyrosine kinase inhibitors (TKI), all patients eventually acquire resistance to... 
TARGETED THERAPY | GENE-MUTATIONS | GEFITINIB | ACTIVATION | MECHANISM | ONCOLOGY | CELL-MIGRATION | ADENOCARCINOMAS | SENSITIVITY | TUMOR ANGIOGENESIS | RECEPTOR TYROSINE KINASE | Niacinamide - analogs & derivatives | Lung Neoplasms - drug therapy | Apoptosis - drug effects | Humans | Receptor, EphA2 - metabolism | Drug Resistance, Neoplasm | Lung Neoplasms - pathology | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Benzamides - administration & dosage | Receptor, Epidermal Growth Factor - metabolism | Benzamides - pharmacology | Receptor, Epidermal Growth Factor - administration & dosage | Lung Neoplasms - genetics | Lung Neoplasms - enzymology | Signal Transduction | Erlotinib Hydrochloride - administration & dosage | Niacinamide - administration & dosage | Drug Synergism | Xenograft Model Antitumor Assays | Animals | Mice, Nude | Erlotinib Hydrochloride - pharmacology | Receptor, EphA2 - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Niacinamide - pharmacology | Receptor, EphA2 - antagonists & inhibitors | non-small cell lung cancer | acquired resistance | EPHA2
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