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Clinical Cancer Research, ISSN 1078-0432, 12/2018, Volume 24, Issue 23, pp. 5787 - 5789
Immune checkpoint inhibition is dramatically improving patient outcomes in diverse cancers, many of which responded poorly to traditional cytotoxic agents.... 
ONCOLOGY
Journal Article
Clinical cancer research : an official journal of the American Association for Cancer Research, ISSN 1078-0432, 07/2018, Volume 24, Issue 23, pp. 5787 - 5789
Immune check-point inhibition is dramatically improving patient outcomes in diverse cancers, many of which responded poorly to traditional cytotoxic agents.... 
Journal Article
Cancer Research, ISSN 0008-5472, 11/2019, p. canres.1117.2019
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2016, Volume 11, Issue 7, p. e0159607
Acalabrutinib (ACP-196) is a second-generation inhibitor of Bruton agammaglobulinemia tyrosine kinase (BTK) with increased target selectivity and potency... 
SURVIVAL | CLL | ACTIVATION | BRUTON TYROSINE KINASE | ONCOLOGY | MULTIDISCIPLINARY SCIENCES | IBRUTINIB | PCI-32765 | CHRONIC LYMPHOCYTIC-LEUKEMIA | GERMINAL CENTER | ANTIGEN | Lethargy - physiopathology | Protein-Tyrosine Kinases - metabolism | Diarrhea - physiopathology | Humans | Pyrazines - administration & dosage | Male | Antineoplastic Agents - administration & dosage | Protein Kinase Inhibitors - adverse effects | Weight Loss - drug effects | Diarrhea - chemically induced | Anorexia - physiopathology | Benzamides - administration & dosage | Protein-Tyrosine Kinases - genetics | Antineoplastic Agents - adverse effects | Female | B-Lymphocytes - pathology | Drug Evaluation, Preclinical | Benzamides - adverse effects | Disease Models, Animal | Lymphoma, Large B-Cell, Diffuse - drug therapy | Drug Administration Schedule | Lymphoma, Large B-Cell, Diffuse - enzymology | Lethargy - chemically induced | Lymphoma, Large B-Cell, Diffuse - mortality | B-Lymphocytes - drug effects | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Vomiting - chemically induced | Animals | B-Lymphocytes - immunology | Agammaglobulinaemia Tyrosine Kinase | Dogs | Pyrazines - adverse effects | Cell Line, Tumor | Anorexia - chemically induced | Lymphoma, Large B-Cell, Diffuse - veterinary | Vomiting - physiopathology | Protein-Tyrosine Kinases - antagonists & inhibitors | Antimitotic agents | Care and treatment | Safety and security measures | Dosage and administration | Non-Hodgkin's lymphomas | Research | Antineoplastic agents | Cell proliferation | Cell culture | Flow cytometry | Veterinary colleges | Anorexia | Leukemia | Cytotoxicity | Malignancy | Kinases | Veterinary medicine | Vomiting | Quality | Inhibition | Protein-tyrosine kinase | Tyrosine | Internal medicine | Hematology | Agammaglobulinemia | Diarrhea | Gene expression | Lymphoma | Bruton's tyrosine kinase | Inhibitors | Lymphocytes B | Lethargy | Lymphomas | Cancer | B-cell lymphoma
Journal Article
Cancer Research, ISSN 0008-5472, 11/2017, Volume 77, Issue 22, pp. 6282 - 6298
Androgen receptor (AR) mediates the growth of prostate cancer throughout its course of development, including in abnormal splice variants (AR-SV)-driven... 
ACTIVATION | ANTIANDROGEN | ONCOLOGY | TRANSCRIPTION | TRANSACTIVATION DOMAIN | LIGAND-BINDING DOMAIN | EXPRESSION | BICALUTAMIDE | PROGRESSION | ENZALUTAMIDE | ABIRATERONE | Alternative Splicing | Humans | Receptors, Androgen - metabolism | Anilides - chemistry | Male | Androgen Receptor Antagonists - pharmacology | Prostatic Neoplasms, Castration-Resistant - genetics | Androgen Receptor Antagonists - chemistry | Indoles - pharmacology | Molecular Structure | Gene Expression Regulation, Neoplastic - drug effects | Cell Proliferation - genetics | Gene Expression Profiling - methods | Prostatic Neoplasms, Castration-Resistant - drug therapy | Mice, SCID | Prostatic Neoplasms, Castration-Resistant - metabolism | Mice, Knockout | Xenograft Model Antitumor Assays | Animals | Receptors, Androgen - genetics | Anilides - pharmacology | Cell Line, Tumor | Mice, Inbred NOD | Cell Proliferation - drug effects | Indoles - chemistry | Binding | Alternative splicing | Antagonists | Sustainable development | Degradation | Receptors | Androgens | Castration | Transcription activation | Steroid hormone receptors | Isoforms | Proteasomes | Ligands | Prostate cancer | Prostate | Cancer | Androgen Receptor (AR) | AR Splice Variants (AR-SV) | prostate cancer | AR translocation inhibitor | AF-1-binding AR antagonist | AR antagonist | Castration-Resistant Prostate Cancer (CRPC) | AR pan-antagonist | Selective Androgen Receptor Degraders (SARDs)
Journal Article
PLOS ONE, ISSN 1932-6203, 07/2017, Volume 12, Issue 7, p. e0181885
Background STAT3 is a transcription factor involved in cytokine and receptor kinase signal transduction that is aberrantly activated in a variety of sarcomas,... 
MEK INHIBITOR | ACTIVATION | THERAPY | CELL VIABILITY | CANCER CELLS | SIGNALING PATHWAY | RESEARCH-AND-DEVELOPMENT | MULTIDISCIPLINARY SCIENCES | TRANSDUCER | ANTITUMOR-ACTIVITY | DISCOVERY | Osteosarcoma - drug therapy | Humans | Aminopyridines - pharmacokinetics | Sarcoma, Ewing - pathology | Rhabdomyosarcoma - pathology | Aminopyridines - therapeutic use | Lung Neoplasms - secondary | Female | Rhabdomyosarcoma - drug therapy | Phosphorylation - drug effects | STAT3 Transcription Factor - metabolism | Cell Survival - drug effects | Treatment Outcome | Sulfonamides - pharmacology | Sulfonamides - pharmacokinetics | Sarcoma, Ewing - drug therapy | Xenograft Model Antitumor Assays | Animals | Sulfonamides - therapeutic use | Aminopyridines - pharmacology | Dogs | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | STAT3 Transcription Factor - antagonists & inhibitors | Cytokines - pharmacology | Osteosarcoma - pathology | Physiological aspects | Enzyme inhibitors | Sarcoma | Drug therapy | Pharmacokinetics | Testing | Cell proliferation | Pediatrics | Biotechnology | Animal models | Phosphorylation | Phosphotyrosine | Rhabdomyosarcoma | Colorectal cancer | Science | Oncology | Biology | Metastasis | Drug development | Assaying | Veterinary medicine | Cancer therapies | Ewing's sarcoma | Anticancer properties | Metastases | Signal transduction | Biological effects | Biomedical materials | Cell growth | Osteosarcoma | Rodents | Xenografts | Biocompatibility | Inhibition | Medical research | RNA-mediated interference | Stat3 protein | Pharmacology | Bioavailability | Tumor cell lines | Bone cancer | Chemotherapy | Inhibitors | In vivo methods and tests | Transduction | Aberration | In vitro methods and tests | Binding sites | Tumors | Pharmaceuticals
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2013, Volume 8, Issue 12, p. e83380
Receptor tyrosine kinases (RTKs), in response to their growth factor ligands, phosphorylate and activate downstream signals important for physiological... 
CELLS | GLIOBLASTOMA | MULTIDISCIPLINARY SCIENCES | MOUSE | AIR | NGF | EXPRESSION | PSORIASIS | NERVE GROWTH-FACTOR | Neoplasms - metabolism | NIH 3T3 Cells | Humans | Receptor, trkA - antagonists & inhibitors | Dermatitis, Atopic - chemically induced | Inflammation - metabolism | Neoplasms - genetics | Inflammation - drug therapy | Anti-Inflammatory Agents - therapeutic use | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Tumor Burden - genetics | Phosphorylation - drug effects | Disease Models, Animal | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Gene Expression | Anti-Inflammatory Agents - pharmacology | Rats | Proto-Oncogene Proteins - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | Dermatitis, Atopic - drug therapy | Receptor Protein-Tyrosine Kinases - genetics | Receptor, trkA - metabolism | Signal Transduction - drug effects | Tumor Burden - drug effects | Protein Kinase Inhibitors - therapeutic use | Cell Line, Tumor | Inflammation - genetics | Receptor, trkA - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Tyrosine | Nervous system diseases | Care and treatment | Oncology, Experimental | Inflammation | Research | Atopic dermatitis | Phenols | Drug therapy | Comparative analysis | Gene therapy | Health aspects | Phosphotransferases | Cancer | Phosphorylation | Physiological effects | Transformation | Transcription factors | Authorship | Lung cancer | Neuropathy | Kinases | Dermatitis | Neuroblastoma cells | Ret protein | Pain | Animal tissues | Cell cycle | Tumor necrosis factor-TNF | Inhibition | Chemical synthesis | Growth factors | Protein-tyrosine kinase | Immunoglobulins | Psoriasis | Neurodegenerative diseases | Research & development--R&D | Breast cancer | Neurological diseases | Overexpression | DNA microarrays | Volatile organic compounds--VOCs | Mutation | Research & development | VOCs | Volatile organic compounds | R&D
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 10/2018, Volume 17, Issue 10, pp. 2123 - 2135
High-grade serous ovarian cancer (HGSOC) is a lethal gynecological malignancy with a need for new therapeutics. Many of the most widely used chemotherapeutic... 
TARGET | CELLS | ASSAY | ONCOLOGY | PRODUCTS | CISPLATIN RESISTANCE | MESENCHYMAL TRANSITION | COMBINATION | ATPASE INHIBITOR | cancer therapeutics | natural products | apoptosis | autophagy | ovarian cancer
Journal Article