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1. Full Text Rational, biologically based treatment of EGFR -mutant non-small-cell lung cancer
by Chmielecki, Juliann and Pao, William
Nature Reviews Cancer, ISSN 1474-175X, 11/2010, Volume 10, Issue 11, pp. 760 - 774
Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) was first recognized in 2004 as a distinct, clinically relevant molecular... 
PHASE-III TRIAL | GROWTH-FACTOR-RECEPTOR | NONSMALL-CELL | ONCOLOGY | BCR-ABL | INCREASED SENSITIVITY | ACQUIRED-RESISTANCE | TYROSINE KINASE INHIBITOR | T790M MUTATION | GENE COPY NUMBER | PREVIOUSLY TREATED PATIENTS | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Protein Kinase Inhibitors - therapeutic use | Humans | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Protein-Tyrosine Kinases - antagonists & inhibitors | Care and treatment | Epidermal growth factor | Physiological aspects | Genetic aspects | Metastasis | Research | Lung cancer, Non-small cell | Risk factors
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2. Full Text Whole-exome sequencing identifies a recurrent NAB2-STAT6 fusion in solitary fibrous tumors
by Chmielecki, Juliann and Crago, Aimee M and Rosenberg, Mara and O'Connor, Rachael and Walker, Sarah R and Ambrogio, Lauren and Auclair, Daniel and McKenna, Aaron and Heinrich, Michael C and Frank, David A and Meyerson, Matthew
Nature Genetics, ISSN 1061-4036, 02/2013, Volume 45, Issue 2, pp. 131 - 132
Solitary fibrous tumors (SFTs) are rare mesenchymal tumors. Here, we describe the identification of a NAB2-STAT6 fusion from whole-exome sequencing of 17 SFTs.... 
ACTIVATION | COREPRESSOR | NAB2 | GROWTH | GENETICS & HEREDITY | STAT6 | MUTATIONS | EXPRESSION | CANCER | Usage | Identification and classification | Health aspects | Gene fusion | Exome sequencing | Medical research | Genomics | Genomes | Mutation | Gene expression | Deoxyribonucleic acid--DNA | Tumors
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3. Full Text How Data Exchange Can Help Advance the Promise of Precision Medicine
by Chmielecki, Juliann
Oncology Times, ISSN 0276-2234, 08/2016, Volume 38, Issue 16, p. 21
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4. Full Text Analysis of 100,000 human cancer genomes reveals the landscape of tumor mutational burden
by Chalmers, Zachary R and Connelly, Caitlin F and Fabrizio, David and Gay, Laurie and Ali, Siraj M and Ennis, Riley and Schrock, Alexa and Campbell, Brittany and Shlien, Adam and Chmielecki, Juliann and Huang, Franklin and He, Yuting and Sun, James and Tabori, Uri and Kennedy, Mark and Lieber, Daniel S and Roels, Steven and White, Jared and Otto, Geoffrey A and Ross, Jeffrey S and Garraway, Levi and Miller, Vincent A and Stephens, Phillip J and Frampton, Garrett M
Genome Medicine, ISSN 1756-994X, 04/2017, Volume 9, Issue 1, pp. 1 - 14
Background: High tumor mutational burden (TMB) is an emerging biomarker of sensitivity to immune checkpoint inhibitors and has been shown to be more... 
Tumor mutational burden | PMS2 | Mismatch repair | Cancer genomics | CTLA-4 BLOCKADE | GERMLINE | MICROSATELLITE INSTABILITY | PD-1 BLOCKADE | SOMATIC MUTATIONS | P53 | POLYMERASE-EPSILON | DNA MISMATCH REPAIR | GENETICS & HEREDITY | ANTITUMOR IMMUNITY | EXPRESSION | DNA damage | Gene regulation | Melanoma | Genomes | Gene expression | Patients | Cancer therapies | DNA repair | Promoters | Defects | Proteins | Immune checkpoint | Immunotherapy | Tumorigenesis | Mutation | Bioinformatics | Deoxyribonucleic acid--DNA | Tumors
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5. Full Text New strategies in overcoming acquired resistance to epidermal growth factor receptor tyrosinekinase inhibitors in lung cancer
by Oxnard, Geoffrey R and Arcila, Maria E and Chmielecki, Juliann and Ladanyi, Marc and Miller, Vincent A and Pao, William
Clinical Cancer Research, ISSN 1078-0432, 09/2011, Volume 17, Issue 17, pp. 5530 - 5537
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6. DNA Sequencing of Cancer: What Have We Learned?
by Juliann Chmielecki and Matthew Meyerson
Annual Review of Medicine, ISSN 0066-4219, 01/2014, Volume 65, p. 63
  DNA sequencing has taught us much about the structure of cancer genomes and enabled the discovery of novel genes that drive and maintain tumorigenesis. With... 
Signal transduction | Genomics | Cell cycle | Genomes | Metabolism | Deoxyribonucleic acid--DNA | Cancer
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7. Full Text Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1
by Kadoaki Ohashi and Lecia V. Sequist and Maria E. Arcila and Teresa Moran and Juliann Chmielecki and Ya-Lun Lin and Yumei Pan and Lu Wang and Elisa de Stanchina and Kazuhiko Shien and Keisuke Aoe and Shinichi Toyooka and Katsuyuki Kiura and Lynnette Fernandez-Cuesta and Panos Fidias and James Chih-Hsin Yang and Vincent A. Miller and Gregory J. Riely and Mark G. Kris and Jeffrey A. Engelman and Cindy L. Vnencak-Jones and Dora Dias-Santagata and Marc Ladanyi and William Pao
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 07/2012, Volume 109, Issue 31, pp. E2127 - E2133
Acquired resistance to EGF receptor (EGFR) tyrosine kinase inhibitors (TKIs) is inevitable in metastatic EGFR -mutant lung cancers. Here, we modeled disease... 
Nras mutation | Erlotinib | Gefitinib | PLATFORM | GROWTH-FACTOR-RECEPTOR | SIGNALING PATHWAY GENES | MET AMPLIFICATION | erlotinib | MULTIDISCIPLINARY SCIENCES | ADENOCARCINOMAS | NRAS mutation | T790M MUTATION | gefitinib | TUMORS | FEATURES | Proto-Oncogene Proteins - metabolism | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Lung Neoplasms - enzymology | Humans | ras Proteins - metabolism | Drug Resistance, Neoplasm | MAP Kinase Kinase 1 - metabolism | Male | Proto-Oncogene Proteins - genetics | Clinical Trials as Topic | Mutation, Missense | MAP Kinase Kinase 1 - genetics | Receptor, Epidermal Growth Factor - metabolism | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Female | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins B-raf - metabolism | Amino Acid Substitution | Biological Sciences | PNAS Plus
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8. Full Text The distribution of BRAF gene fusions in solid tumors and response to targeted therapy
by Ross, Jeffrey S and Wang, Kai and Chmielecki, Juliann and Gay, Laurie and Johnson, Adrienne and Chudnovsky, Jacob and Yelensky, Roman and Lipson, Doron and Ali, Siraj M and Elvin, Julia A and Vergilio, Jo‐Anne and Roels, Steven and Miller, Vincent A and Nakamura, Brooke N and Gray, Adam and Wong, Michael K and Stephens, Philip J
International Journal of Cancer, ISSN 0020-7136, 02/2016, Volume 138, Issue 4, pp. 881 - 890
Although the BRAF V600E base substitution is an approved target for the BRAF inhibitors in melanoma, BRAF gene fusions have not been investigated as anticancer... 
targeted therapy | pilocytic astrocytoma | Sptizoid melanoma | pancreatic acinar carcinoma | comprehensive genomic profiling | cancer | NGS | BRAF fusions | solid tumors | CANCER-THERAPY | ERDHEIM-CHESTER DISEASE | MELANOMA | ONCOLOGY | RECURRENT | THYROID-CANCER | B-RAF | MUTATIONS | MAPK PATHWAY | VEMURAFENIB | Niacinamide - analogs & derivatives | Humans | Middle Aged | Transcriptome | Child, Preschool | Infant | Male | Antineoplastic Agents - therapeutic use | Gene Expression Profiling | Young Adult | Neoplasms - genetics | Aged, 80 and over | Adult | Female | Child | Molecular Targeted Therapy - methods | Pyrimidinones - therapeutic use | Niacinamide - therapeutic use | Phenylurea Compounds - therapeutic use | Treatment Outcome | Neoplasms - drug therapy | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Adolescent | Aged | Pyridones - therapeutic use | Thyroid cancer | Gliomas | Pancreatic cancer | Genes | Colorectal cancer | Melanoma | Genetic research | Lung cancer, Non-small cell | Kinases | Tumors | Cancer Genetics and Epigenetics
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9. Full Text Induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors in mutant EGFR-dependent lung adenocarcinomas
by Gong, Yixuan and Somwar, Romel and Politi, Katerina and Balak, Marissa and Chmielecki, Juliann and Jiang, Xuejun and Pao, William
PLoS Medicine, ISSN 1549-1277, 10/2007, Volume 4, Issue 10, pp. 1655 - 1668
Background Mutations in the epidermal growth factor receptor ( EGFR) gene are associated with increased sensitivity of lung cancers to kinase inhibitors like... 
SURVIVAL | MEDICINE, GENERAL & INTERNAL | GEFITINIB | CANCER CELLS | TYROSINE KINASE | BH3-ONLY PROTEIN | DOWN-REGULATION | BAX | FACTOR-RECEPTOR MUTATIONS | BCL-2 FAMILY | CELL-DEATH | Erlotinib Hydrochloride | Lung Neoplasms - genetics | bcl-Associated Death Protein - genetics | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Apoptosis - drug effects | Humans | Cells, Cultured | Apoptosis - genetics | Drug Resistance, Neoplasm | Cell Line, Tumor - drug effects | Adenocarcinoma - drug therapy | Cell Differentiation - genetics | Animals | Flow Cytometry | Cell Differentiation - drug effects | Sensitivity and Specificity | Fluorescent Antibody Technique | bcl-Associated Death Protein - drug effects | Adenocarcinoma - genetics | Mice | Mutation | Quinazolines - pharmacology | Disease Models, Animal | Genetic aspects | Research | Lung cancer | Risk factors | Mutation (Biology) | Oncology | Genetics | Pharmacology and Toxicology | Lung | Cancer
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10. Full Text DNA Sequencing of Cancer: What Have We Learned?
by Chmielecki, Juliann and Meyerson, Matthew
Annual Review of Medicine, ISSN 0066-4219, 1/2014, Volume 65, Issue 1, pp. 63 - 79
DNA sequencing has taught us much about the structure of cancer genomes and enabled the discovery of novel genes that drive and maintain tumorigenesis. With... 
genomics | pathways | cancer | mutations | rearrangements | Mutations | Pathways | Genomics | Rearrangements | Cancer | MEDICINE, RESEARCH & EXPERIMENTAL | TERT PROMOTER MUTATIONS | COMPREHENSIVE GENOMIC CHARACTERIZATION | METASTATIC COLORECTAL-CANCER | CHRONIC MYELOID-LEUKEMIA | LINEAGE-SURVIVAL ONCOGENE | CELL LUNG-CANCER | BREAST-CANCER | CHRONIC LYMPHOCYTIC-LEUKEMIA | TRANSCRIPTION FACTOR GENES | GASTROINTESTINAL STROMAL TUMORS | Neoplasms - metabolism | Cell Cycle - genetics | Epigenesis, Genetic | Humans | Signal Transduction - genetics | Transcription Factors - genetics | Neoplasms - genetics | DNA Mutational Analysis | Oncogene Fusion | Gene Rearrangement | Oncogene Protein v-akt - genetics | Mitogen-Activated Protein Kinases - genetics | Transcription, Genetic | Oncogene Protein v-akt - metabolism | Mitogen-Activated Protein Kinases - metabolism | RNA - metabolism | Genetic aspects | Research | Nucleotide sequencing | DNA sequencing
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