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1. Full Text Driven by Mutations: The Predictive Value of Mutation Subtype in EGFR-Mutated Non–Small Cell Lung Cancer
by Castellanos, Emily and Feld, Emily and Horn, Leora
Journal of Thoracic Oncology, ISSN 1556-0864, 04/2017, Volume 12, Issue 4, pp. 612 - 623
-mutated NSCLC is a genetically heterogeneous disease that includes more than 200 distinct mutations. The implications of mutational subtype for both... 
Targeted therapy | Lung cancer | EGFR | Mutation subtype | 1ST-LINE TREATMENT | T790M MUTATION | OPEN-LABEL | DRUG-RESISTANCE | EXON 20 INSERTIONS | TYROSINE KINASE INHIBITORS | GROWTH-FACTOR RECEPTOR | RANDOMIZED PHASE-3 TRIAL | CLINICOPATHOLOGICAL CHARACTERISTICS | ONCOLOGY | RESPIRATORY SYSTEM | ACTIVATING MUTATIONS | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Prognosis | Carcinoma, Non-Small-Cell Lung - genetics | Humans | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Lung Neoplasms - pathology | Antineoplastic Agents - therapeutic use | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation - genetics
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2. Full Text Genotyping of an Italian papillary thyroid carcinoma cohort revealed high prevalence of BRAF mutations, absence of RAS mutations and allowed the detection of a new mutation of BRAF oncoprotein (BRAFV599Ins)
by Carta, Claudio and Moretti, Sonia and Passeri, Lucia and Barbi, Flavia and Avenia, Nicola and Cavaliere, Antonio and Monacelli, Massimo and Macchiarulo, Antonio and Santeusanio, Fausto and Tartaglia, Marco and Puxeddu, Efisio
Clinical Endocrinology, ISSN 0300-0664, 01/2006, Volume 64, Issue 1, pp. 105 - 109
Summary Objectives  The genes RET and RAS, and more recently BRAF, have been shown to be frequently mutated in human papillary thyroid carcinomas (PTC). The... 
ONCOGENES | RET | ACTIVATION | PATHWAY | FREQUENCY | ENDOCRINOLOGY & METABOLISM | CANCER | TUMORIGENESIS | TUMORS | EVENT | ras Proteins - genetics | Carcinoma, Papillary - genetics | Gene Frequency | Humans | Middle Aged | Genotype | Genetic Markers | Thyroid Neoplasms - genetics | DNA Mutational Analysis | Proto-Oncogene Proteins B-raf - genetics | Gene Rearrangement | Adult | Aged | Mutation | Cohort Studies | Proto-Oncogene Proteins c-ret - genetics | Genetic aspects | Thyroid diseases
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3. Full Text Insulin mutation screening in 1,044 patients with diabetes mutations in the INS gene are a common cause of neonatal diabetes but a rare cause of diabetes diagnosed in childhood or adulthood
by Edghill, Emma L and Flanagan, Sarah E and Patch, Ann-Marie and Boustred, Chris and Parrish, Andrew and Shields, Beverley and Shepherd, Maggie H and Hussain, Khalid and Kapoor, Ritika R and Malecki, Maciej and MacDonald, Michael J and Støy, Julie and Steiner, Donald F and Philipson, Louis H and Bell, Graeme I and Hattersley, Andrew T and Ellard, Sian and Neonatal Diabet Int Collaborative and Neonatal Diabetes International Collaborative Group and the Neonatal Diabetes International Collaborative Group
Diabetes, ISSN 0012-1797, 04/2008, Volume 57, Issue 4, pp. 1034 - 1042
OBJECTIVE-Insulin gene (INS) mutations have recently been described as a cause of permanent neonatal diabetes (PND). We aimed to determine the prevalence,... 
KIR6.2 | YOUNG | KCNJ11 | SULFONYLUREA THERAPY | ENDOCRINOLOGY & METABOLISM | DOMINANT | PROINSULIN | MELLITUS | STRESS | ACTIVATING MUTATIONS | LIFE | DNA Mutational Analysis | Humans | Diabetes Mellitus, Type 1 - genetics | Adult | Infant | Mutation | Insulin - genetics | Child | Infant, Newborn | Amino Acid Substitution | Genetic aspects | Diabetes | Gene mutations | Insulin | Health aspects
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4. Full Text Allele-Specific p53 Mutant Reactivation
by Yu, Xin and Vazquez, Alexei and Levine, Arnold J and Carpizo, Darren R
Cancer Cell, ISSN 1535-6108, 05/2012, Volume 21, Issue 5, pp. 614 - 625
Rescuing the function of mutant p53 protein is an attractive cancer therapeutic strategy. Using the National Cancer Institute's anticancer drug screen data, we... 
WILD-TYPE CONFORMATION | DNA-BINDING DOMAIN | RESCUE | ONCOLOGY | IRON CHELATORS | MUTATION | REDOX ACTIVITY | TUMOR-SUPPRESSOR | CANCER MUTANTS | RESTORATION | ANTITUMOR-ACTIVITY | CELL BIOLOGY | Neoplasms - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Zinc - metabolism | Humans | Transcriptional Activation - drug effects | Structure-Activity Relationship | Mutation, Missense | Tumor Suppressor Protein p53 - genetics | Dose-Response Relationship, Drug | Transfection | Neoplasms - genetics | RNA Interference | Time Factors | Antineoplastic Agents - pharmacology | Thiosemicarbazones - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Cell Line | Cell Survival - drug effects | Oxidation-Reduction | Mice, Inbred C57BL | Tumor Suppressor Protein p53 - metabolism | Mice, Transgenic | Chelating Agents - pharmacology | DNA - metabolism | Tumor Suppressor Protein p53 - drug effects | Gene Knock-In Techniques | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | Tumor Burden - drug effects | Mice, Nude | Alleles | Protein Conformation | Mice | Mice, Inbred BALB C | Tumor Suppressor Protein p53 - chemistry | Oxidative Stress - drug effects | Neoplasms - pathology | Care and treatment | Nuclear radiation | Oncology, Experimental | Research | Tumor proteins | Health aspects | Cancer | Antitumor agents | Lymphocytes B | Xenografts | Data processing | Drug development | Zinc | p53 protein | Apoptosis | Structure-function relationships | Tumors
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5. Full Text Pooled Analysis of the Prognostic and Predictive Effects of KRAS Mutation Status and KRAS Mutation Subtype in Early-Stage Resected Non–Small-Cell Lung Cancer in Four Trials of Adjuvant Chemotherapy
by Frances A. Shepherd and Caroline Domerg and Pierre Hainaut and Pasi A. Jänne and Jean-Pierre Pignon and Stephen Graziano and Jean-Yves Douillard and Elizabeth Brambilla and Thierry Le Chevalier and Lesley Seymour and Abderrahmane Bourredjem and Gwénaël Le Teuff and Robert Pirker and Martin Filipits and Rafael Rosell and Robert Kratzke and Bizhan Bandarchi and Xiaoli Ma and Marzia Capelletti and Jean-Charles Soria and Ming-Sound Tsao
Journal of Clinical Oncology, ISSN 0732-183X, 06/2013, Volume 31, Issue 17, pp. 2173 - 2181
Purpose We undertook this analysis of KRAS mutation in four trials of adjuvant chemotherapy (ACT) versus observation (OBS) to clarify the prognostic/predictive... 
GROWTH-FACTOR RECEPTOR | ACTIVATION | K-RAS ONCOGENE | VINORELBINE PLUS CISPLATIN | ONCOLOGY | MARKER | COLORECTAL-CANCER | ADENOCARCINOMA | PHASE-III | MOLECULAR BIOMARKERS | EGFR | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Prognosis | Carcinoma, Non-Small-Cell Lung - genetics | Gene Pool | Humans | Middle Aged | Lung Neoplasms - pathology | Male | Proto-Oncogene Proteins - genetics | Treatment Outcome | Randomized Controlled Trials as Topic | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Survival Analysis | Female | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Chemotherapy, Adjuvant | Mutation | Genes, ras | Neoplasm Staging | Thor3 | Thor12 | ORIGINAL REPORTS | To2 | Thor5 | To20
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6. Full Text A novel variant glanzmann thrombasthenia due to co-inheritance of a loss-and a gain-of-function mutation of ITGB3: Evidence of a dominant effect of gain-of-function mutations
by Bury, Loredana and Zetterberg, Eva and Leinøe, Eva B and Falcinelli, Emanuela and Marturano, Alessandro and Manni, Giorgia and Nurden, Alan T and Gresele, Paolo
Haematologica, ISSN 0390-6078, 06/2018, Volume 103, Issue 6, pp. e259 - e263
PLATELET DYSFUNCTION | ACTIVATION | DOMAIN | INTEGRIN | MACROTHROMBOCYTOPENIA | PHENOTYPE | HEMATOLOGY | Loss of Function Mutation | Genetic Association Studies | Humans | Erythrocyte Indices | Phenotype | Thrombasthenia - diagnosis | Genes, Dominant | Blood Platelets - metabolism | DNA Mutational Analysis | Pedigree | Thrombasthenia - genetics | Blood Platelets - ultrastructure | Alleles | Platelet Function Tests | Biomarkers | Adult | Female | Integrin beta3 - genetics | Gain of Function Mutation | Amino Acid Substitution | Online Only | Clinical Medicine | Hematologi | Medical and Health Sciences | Hematology | Klinisk medicin | Medicin och hälsovetenskap
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7. Full Text TAS-121, A Selective Mutant EGFR Inhibitor, Shows Activity Against Tumors Expressing Various EGFR Mutations Including T790M and Uncommon Mutations G719X
by Ito, K and Nishio, M and Kato, M and Murakami, H and Aoyagi, Y and Ohe, Y and Okayama, T and Hashimoto, A and Ohsawa, H and Tanaka, G and Nonoshita, K and Ito, S and Matsuo, K and Miyadera, K
MOLECULAR CANCER THERAPEUTICS, ISSN 1535-7163, 05/2019, Volume 18, Issue 5, pp. 920 - 928
TAS-121 is a novel orally active selective covalent inhibitor of the mutant EGFR. We performed preclinical characterization of TAS-121 and compared its... 
CELL LUNG-CANCER | GEFITINIB | MULTICENTER | AMPLIFICATION | OSIMERTINIB | ONCOLOGY | EML4-ALK FUSION | ACQUIRED-RESISTANCE | CLINICAL ACTIVITY | ACTIVATING MUTATIONS | AZD9291
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8. Full Text Mutant p53: One name, many proteins
by Freed-Pastor, William A and Prives, Carol
Genes and Development, ISSN 0890-9369, 06/2012, Volume 26, Issue 12, pp. 1268 - 1286
There is now strong evidence that mutation not only abrogates p53 tumor-suppressive functions, but in some instances can also endow mutant proteins with novel... 
Oncogenic | Gain of function | Mutant p53 | Tumor suppression | Transcriptome | P53 | WILD-TYPE P53 | TRANSCRIPTIONAL ACTIVATION | oncogenic | transcriptome | CELL-CYCLE ARREST | DEVELOPMENTAL BIOLOGY | p53 | CELL BIOLOGY | tumor suppression | BREAST-CANCER | mutant p53 | DNA-DAMAGING AGENTS | GAIN-OF-FUNCTION | TUMOR-SUPPRESSOR FUNCTION | IN-VIVO ANALYSIS | gain of function | GENETICS & HEREDITY | GENE-EXPRESSION | BINDING-SITE | Proto-Oncogene Proteins - metabolism | Neoplasms - genetics | Models, Biological | Humans | Tumor Suppressor Protein p53 - metabolism | Mutant Proteins - metabolism | Transcription, Genetic | Tumor Suppressor Protein p53 - genetics | Neoplasms - drug therapy | Control | Research | Suppression, Genetic | Tumors | Review
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9. Full Text Mutant BRAF Melanomas—Dependence and Resistance
by Poulikakos, Poulikos I and Rosen, Neal
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 11 - 15
RAF inhibitors have the unique property of transactivating RAS-dependent RAF dimers in most cells but inhibit RAF/MEK/ERK signaling in cells expressing mutant... 
CELLS | ACTIVATION | AMPLIFICATION | GENE | ONCOLOGY | PATHWAY | RAF | ACQUIRED-RESISTANCE | AKT | MEK INHIBITORS | CANCER | CELL BIOLOGY | Drug Resistance, Neoplasm - genetics | Signal Transduction - drug effects | Melanoma - genetics | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Humans | Melanoma - drug therapy | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects
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10. Full Text Mutant p53 partners in crime
by Kim, Michael P and Lozano, Guillermina
Cell Death and Differentiation, ISSN 1350-9047, 2018, Volume 25, Issue 1, pp. 161 - 168
Mutant p53 proteins impart changes in cellular behavior and function through interactions with proteins that alter gene expression. The milieu of intracellular... 
WILD-TYPE P53 | COMPLEX | LI-FRAUMENI-SYNDROME | DRIVE CANCER | METASTASIS | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | P63 | BINDING | MOUSE MODELS | GAIN | CELL BIOLOGY | Proteins | Therapy | Missense mutation | Mathematical analysis | p53 Protein | Transcription activation | Crime | Mutation | Gene expression | Protein interaction | Environmental conditions | Review
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11. Full Text Not all pycnodysostosis‐related mutants of human cathepsin K are inactive – crystal structure and biochemical studies of an active mutant I249T
by Roy, Sumana and Das Chakraborty, Sudeshna and Biswas, Sampa
The FEBS Journal, ISSN 1742-464X, 11/2018, Volume 285, Issue 22, pp. 4265 - 4280
Human lysosomal cathepsin K (CTSK) protease plays an important role in bone remodelling and is responsible for the bone disorder, pycnodysostosis. Here, we... 
cysteine protease | collagenase | X‐ray structure | cathepsin K | pycnodysostosis | X-ray structure | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DISEASE | MUTATIONS | PRO | EXPRESSION | OSTEOPOROSIS | Amino Acid Sequence | Humans | Models, Molecular | Pycnodysostosis - genetics | Crystallography, X-Ray | Sequence Homology | Cathepsin K - genetics | Cathepsin K - metabolism | DNA Mutational Analysis | Cathepsin K - chemistry | Protein Conformation | Catalysis | Mutation | Cathepsins | Cysteine | Structure | Analysis | Crystals | Data banks | Cathepsin K | Crystallization | Cysteine proteinase | Fluorescence | Bone turnover | Mutants | Hereditary diseases | Proenzymes | Proteins | Missense mutation | E coli | Proteolysis | Collagen | Reaction kinetics | Kinetics | Bone | Pycnodysostosis | Crystal structure | Recombinant
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12. Full Text Next-Generation Sequencing Reveals a Novel NSCLC ALK F1174V Mutation and Confirms ALK G1202R Mutation Confers High-Level Resistance to Alectinib (CH5424802/RO5424802) in ALK-Rearranged NSCLC Patients Who Progressed on Crizotinib
by Ou, Sai-Hong Ignatius and Azada, Michele and Hsiang, David J and Herman, June M and Kain, Tatiana S and Siwak-Tapp, Christina and Casey, Cameron and He, Jie and Ali, Siraj M and Klempner, Samuel J and Miller, Vincent A
Journal of Thoracic Oncology, ISSN 1556-0864, 04/2014, Volume 9, Issue 4, pp. 549 - 553
Acquired secondary mutations in the anaplastic lymphoma kinase ( ) gene have been identified in -rearranged ( ) non–small-cell lung cancer (NSCLC) patients who... 
ALK F1174V | ALK G1202R | Alectinib | Next-generation sequencing | ALK-rearranged NSCLC | Crizotinib resistance | ONCOLOGY | CELL LUNG CANCERS | RESPIRATORY SYSTEM | KINASE | INHIBITOR | ACTIVATING MUTATIONS | Lung Neoplasms - drug therapy | Pyrazoles - therapeutic use | Adenocarcinoma - pathology | Prognosis | Humans | Middle Aged | Lung Neoplasms - pathology | Male | Female | Adenocarcinoma - genetics | Pyridines - therapeutic use | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Mutation - genetics | Adenocarcinoma - drug therapy | Drug Resistance, Neoplasm - genetics | Receptor Protein-Tyrosine Kinases - genetics | Piperidines - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Carbazoles - therapeutic use | High-Throughput Nucleotide Sequencing | Carcinoma, Non-Small-Cell Lung - drug therapy | Gene Rearrangement - genetics | Neoplasm Staging
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13. Full Text Analysis of IDH1-R132 mutation, BRAF V600 mutation and KIAA1549–BRAF fusion transcript status in central nervous system tumors supports pediatric tumor classification
by Gierke, Midea and Sperveslage, Jan and Schwab, David and Beschorner, Rudi and Ebinger, Martin and Schuhmann, Martin U and Schittenhelm, Jens
Journal of Cancer Research and Clinical Oncology, ISSN 0171-5216, 1/2016, Volume 142, Issue 1, pp. 89 - 100
Gliomas are the leading cause of cancer-related morbidity in children and comprise a clinical, histological and molecular heterogenous group of CNS tumors.... 
BRAF V600E | Medicine & Public Health | Hematology | Glioma | IDH1 | Classification | KIAA1549 – BRAF | Oncology | Cancer Research | Internal Medicine | KIAA1549–BRAF | KIAA1549-BRAF | ACTIVATION | DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMORS | CHRONIC EPILEPSY | IDH1 MUTATIONS | ADULTS | LOW-GRADE GLIOMAS | DIFFUSE GLIOMAS | BRAF(V600E) MUTATION | PILOCYTIC ASTROCYTOMAS | GENE | ONCOLOGY | Oncogene Proteins, Fusion - metabolism | Prognosis | Follow-Up Studies | Tissue Array Analysis | Humans | Middle Aged | Child, Preschool | Infant | Male | Immunoenzyme Techniques | Young Adult | Polymerase Chain Reaction | Aged, 80 and over | Biomarkers, Tumor - metabolism | Adult | Female | Child | Infant, Newborn | Proto-Oncogene Proteins B-raf - metabolism | Central Nervous System Neoplasms - classification | Central Nervous System Neoplasms - genetics | Isocitrate Dehydrogenase - genetics | Mutation - genetics | Central Nervous System Neoplasms - pathology | Oncogene Proteins, Fusion - genetics | Proto-Oncogene Proteins B-raf - genetics | Adolescent | Isocitrate Dehydrogenase - metabolism | Aged | Biomarkers, Tumor - genetics | Neoplasm Staging | Immunohistochemistry | Pediatrics | Genetic aspects | Gene mutations | Gliomas | Analysis
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14. Full Text Targeting mutant p53 for efficient cancer therapy
by Bykov, Vladimir J. N and Eriksson, Sofi E and Bianchi, Julie and Wiman, Klas G
Nature Reviews Cancer, ISSN 1474-175X, 01/2018, Volume 18, Issue 2, pp. 89 - 102
The tumour suppressor gene TP53 is the most frequently mutated gene in cancer. Wild-type p53 can suppress tumour development by multiple pathways. However,... 
OXIDATIVE STRESS | TUMOR-SUPPRESSOR FUNCTION | ONCOLOGY | SMALL-MOLECULE | TEMPERATURE-SENSITIVE MUTANT | MUTATIONAL LANDSCAPE | DNA-BINDING FUNCTION | CORE DOMAIN | TERMINATION CODON READTHROUGH | ZINC METALLOCHAPERONES | GLUTAMINE-METABOLISM | Neoplasms - metabolism | Tumor Suppressor Protein p53 - antagonists & inhibitors | Humans | Mutant Proteins - genetics | Tumor Suppressor Protein p53 - metabolism | Mutant Proteins - metabolism | Antineoplastic Agents - administration & dosage | Tumor Suppressor Protein p53 - genetics | Neoplasms - drug therapy | Animals | Neoplasms - genetics | Cell Death - drug effects | Mutation | Mutant Proteins - antagonists & inhibitors | Molecular targeted therapy | Care and treatment | Gene mutations | Innovations | Tumor suppressor genes | Health aspects | Cancer | Medical research | Deactivation | p53 Protein | Clinical trials | Recovery of function | Activation | Pharmacology | Inactivation | Cell death | Tumors | Apoptosis
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