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1. Full Text Comment on "DNA damage is a pervasive cause of sequencing errors, directly confounding variant identification"
by Stewart, Chip and Leshchiner, Ignaty and Hess, Julian and Getz, Gad
Science (American Association for the Advancement of Science), ISSN 0036-8075, 09/2018, Volume 361, Issue 6409, p. 1324
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Causes of | Nucleotide sequencing | Analysis | DNA damage | DNA sequencing | Deoxyribonucleic acid--DNA | Gene sequencing | Index Medicus
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2. Full Text Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F
by Shaw, Alice T and Friboulet, Luc and Leshchiner, Ignaty and Gainor, Justin F and Bergqvist, Simon and Brooun, Alexei and Burke, Benjamin J and Deng, Ya-Li and Liu, Wei and Dardaei, Leila and Frias, Rosa L and Schultz, Kate R and Logan, Jennifer and James, Leonard P and Smeal, Tod and Timofeevski, Sergei and Katayama, Ryohei and Iafrate, A. John and Le, Long and McTigue, Michele and Getz, Gad and Johnson, Ted W and Engelman, Jeffrey A and Argonne National Lab. (ANL), Argonne, IL (United States). Advanced Photon Source (APS)
The New England journal of medicine, ISSN 0028-4793, 01/2016, Volume 374, Issue 1, pp. 54 - 61
Medicine, General & Internal | Life Sciences & Biomedicine | General & Internal Medicine | Science & Technology | Liver Failure - etiology | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Sulfones - therapeutic use | Pyrazoles - therapeutic use | Carcinoma, Non-Small-Cell Lung - genetics | Humans | Middle Aged | Drug Resistance, Neoplasm - genetics | Carcinoma, Non-Small-Cell Lung - secondary | Receptor Protein-Tyrosine Kinases - genetics | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Female | Molecular Structure | Carcinoma, Non-Small-Cell Lung - drug therapy | Lactams, Macrocyclic - therapeutic use | Mutation | Liver Neoplasms - secondary | Binding Sites | Pyridines - therapeutic use | Crizotinib | Gene mutations | Analysis | Lung cancer | Dosage and administration | Research | Drug resistance | Drug therapy | Tyrosine | Inhibitor drugs | Liver diseases | Genes | Lymphoma | Cancer therapies | Metastases | Amino acid substitution | Liver cancer | Protein-tyrosine kinase | Cancer | Index Medicus | Abridged Index Medicus
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3. Full Text A mutational signature reveals alterations underlying deficient homologous recombination repair in breast cancer
by Polak, Paz and Kim, Jaegil and Braunstein, Lior Z and Karlic, Rosa and Haradhavala, Nicholas J and Tiao, Grace and Rosebrock, Daniel and Livitz, Dimitri and Kübler, Kirsten and Mouw, Kent W and Kamburov, Atanas and Maruvka, Yosef E and Leshchiner, Ignaty and Lander, Eric S and Golub, Todd R and Zick, Aviad and Orthwein, Alexandre and Lawrence, Michael S and Batra, Rajbir N and Caldas, Carlos and Haber, Daniel A and Laird, Peter W and Shen, Hui and Ellisen, Leif W and D'Andrea, Alan D and Chanock, Stephen J and Foulkes, William D and Getz, Gad
Nature genetics, ISSN 1061-4036, 10/2017, Volume 49, Issue 10, pp. 1476 - 1486
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Genetic Predisposition to Disease | Gene Regulatory Networks - genetics | Recombinational DNA Repair - genetics | Genes, Neoplasm | Humans | Gene Silencing | Transcriptome - genetics | Allelic Imbalance | DNA Methylation | Breast Neoplasms - genetics | Genes, BRCA2 | Germ-Line Mutation | Female | Genes, BRCA1 | Mutation | Neoplasm Proteins - genetics | Gene Expression Regulation, Neoplastic - genetics | Care and treatment | Gene mutations | Development and progression | Breast cancer | Genetic aspects | Genetic recombination | Health aspects | BRCA2 protein | Deactivation | BRCA1 protein | Genomics | Homologous recombination | Homology | Genomes | Gene expression | Inactivation | Ovarian cancer | Homologous recombination repair | Cell cycle | DNA methylation | Epigenetics | Methylation | Signatures | Deoxyribonucleic acid--DNA | Cancer | Tumors | Index Medicus
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4. Full Text Paired exome analysis of Barrett's esophagus and adenocarcinoma
by Stachler, Matthew D and Taylor-Weiner, Amaro and Peng, Shouyong and McKenna, Aaron and Agoston, Agoston T and Odze, Robert D and Davison, Jon M and Nason, Katie S and Loda, Massimo and Leshchiner, Ignaty and Stewart, Chip and Stojanov, Petar and Seepo, Sara and Lawrence, Michael S and Ferrer-Torres, Daysha and Lin, Jules and Chang, Andrew C and Gabriel, Stacey B and Lander, Eric S and Beer, David G and Getz, Gad and Carter, Scott L and Bass, Adam J
Nature genetics, ISSN 1061-4036, 08/2015, Volume 47, Issue 9, pp. 1047 - 1055
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Genetic Predisposition to Disease | Genome-Wide Association Study | Gene Frequency | Humans | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Tumor Suppressor Protein p53 - genetics | Exome | Phosphatidylinositol 3-Kinases - genetics | Point Mutation | Class I Phosphatidylinositol 3-Kinases | Gene Amplification | Esophageal Neoplasms - genetics | DNA Mutational Analysis | Adenocarcinoma - genetics | Barrett Esophagus - genetics | Usage | Genetic aspects | Diagnosis | Research | Barrett's esophagus | Exome sequencing | Datasets | Cloning | Genomes | Mutation | Endoscopy | Patients | Impaired risk | Cancer | Index Medicus
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5. Full Text The evolutionary landscape of chronic lymphocytic leukemia treated with ibrutinib targeted therapy
by Landau, Dan A and Sun, Clare and Rosebrock, Daniel and Herman, Sarah E. M and Fein, Joshua and Sivina, Mariela and Underbayev, Chingiz and Liu, Delong and Hoellenriegel, Julia and Ravichandran, Sarangan and Farooqui, Mohammed Z. H and Zhang, Wandi and Cibulskis, Carrie and Zviran, Asaf and Neuberg, Donna S and Livitz, Dimitri and Bozic, Ivana and Leshchiner, Ignaty and Getz, Gad and Burger, Jan A and Wiestner, Adrian and Wu, Catherine J
Nature communications, ISSN 2041-1723, 12/2017, Volume 8, Issue 1, pp. 2185 - 12
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Pyrazoles - therapeutic use | Prognosis | Humans | Middle Aged | Male | Leukemia, Lymphocytic, Chronic, B-Cell - genetics | Clonal Evolution - genetics | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Rituximab - therapeutic use | Phospholipase C gamma - genetics | Aged, 80 and over | Adult | Female | Gene Expression Regulation, Neoplastic - drug effects | Molecular Targeted Therapy - methods | Pyrazoles - pharmacology | Signal Transduction | Clonal Evolution - drug effects | Down-Regulation | Treatment Outcome | Pyrimidines - pharmacology | Disease Progression | Leukemia, Lymphocytic, Chronic, B-Cell - pathology | Whole Exome Sequencing | Rituximab - pharmacology | Drug Resistance, Neoplasm - genetics | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Pyrimidines - therapeutic use | Agammaglobulinaemia Tyrosine Kinase | Aged | Leukemia, Lymphocytic, Chronic, B-Cell - mortality | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Mutation | Longitudinal Studies | Drug Resistance, Neoplasm - drug effects | Protein-Tyrosine Kinases - antagonists & inhibitors | Lymphocyte receptors | Therapy | Energy metabolism | Chronic lymphatic leukemia | Transcription | Leukemia | Lymphatic leukemia | Metabolism | Drug resistance | Gene expression | Signaling | Lymphocytes B | Immunotherapy | Cell cycle | Evolution | Cancer | Index Medicus
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6. Full Text Summarizing polygenic risks for complex diseases in a clinical whole-genome report
by Kong, Sek Won and Lee, In-Hee and Leshchiner, Ignaty and Krier, Joel and Kraft, Peter and Rehm, Heidi L and Green, Robert C and Kohane, Isaac S and Macrae, Calum A and Bates, David W and Carere, Alexis D and Cirino, Allison and Connor, Lauren and Christensen, Kurt D and Duggan, Jake and Ho, Carolyn Y and Krier, Joel B and Lane, William J and Lautenbach, Denise M and Lehmann, Lisa and Liu, Christina and Miller, Rachel and Morton, Cynthia C and Seidman, Christine E and Sunyaev, Shamil and Vassy, Jason L and Aronson, Sandy and Ceyhan-Birsoy, Ozge and Gowrisankar, Siva and Lebo, Matthew S and Leschiner, Ignat and Machini, Kalotina and McLaughlin, Heather M and Metterville, Danielle R and Blumenthal-Barby, Jennifer and Zausmer Feuerman, Lindsay and McGuire, Amy L and Panchang, Sarita and Robinson, Jill Oliver and Slashinski, Melody J and Alexander, Stewart C and Davis, Kelly and Ubel, Peter A and Roberts, J. Scott and Garber, Judy E and Hambuch, Tina and Murray, Michael F and MedSeq Project and the MedSeq Project
Genetics in medicine, ISSN 1098-3600, 07/2015, Volume 17, Issue 7, pp. 536 - 544
risk alleles | polygenic score | clinical whole-genome sequencing | common complex disorders | Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Cardiomyopathies - genetics | Multifactorial Inheritance - genetics | Genetic Predisposition to Disease | Genome-Wide Association Study | Reproducibility of Results | Genetic Association Studies | Humans | Alleles | Genome, Human | Genetic Testing - methods | Case-Control Studies | Index Medicus
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7. Full Text Growth dynamics in naturally progressing chronic lymphocytic leukaemia
by Gruber, Michaela and Bozic, Ivana and Leshchiner, Ignaty and Livitz, Dimitri and Stevenson, Kristen and Rassenti, Laura and Rosebrock, Daniel and Taylor-Weiner, Amaro and Olive, Oriol and Goyetche, Reaha and Fernandes, Stacey M and Sun, Jing and Stewart, Chip and Wong, Alicia and Cibulskis, Carrie and Zhang, Wandi and Reiter, Johannes G and Gerold, Jeffrey M and Gribben, John G and Rai, Kanti R and Keating, Michael J and Brown, Jennifer R and Neuberg, Donna and Kipps, Thomas J and Nowak, Martin A and Getz, Gad and Wu, Catherine J
Nature (London), ISSN 0028-0836, 06/2019, Volume 570, Issue 7762, pp. 474 - 479
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Recurrence | Reproducibility of Results | Clone Cells - drug effects | Humans | Male | Leukemia, Lymphocytic, Chronic, B-Cell - genetics | Disease Progression | Leukemia, Lymphocytic, Chronic, B-Cell - pathology | Neoplasm Recurrence, Local - pathology | Clone Cells - pathology | Female | Neoplasm Recurrence, Local - genetics | Cell Proliferation - drug effects | High-Throughput Nucleotide Sequencing | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Cohort Studies | Evolution, Molecular | Development and progression | Chronic lymphocytic leukemia | Chronic lymphatic leukemia | Growth rate | Leukemia | Genomes | Patients | Blood | Next-generation sequencing | Reaction kinetics | Evolution | Mutation | Kinetics | Evolution & development | Cancer | Index Medicus | CLL | cancer genetics | Chronic lymphocytic leukaemia | clonal evolution | cancer growth rate | logistic growth | carrying capacity | cancer growth dynamics
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8. Full Text Mutations in RABL3 alter KRAS prenylation and are associated with hereditary pancreatic cancer
by Nissim, Sahar and Leshchiner, Ignaty and Mancias, Joseph D and Greenblatt, Matthew B and Maertens, Ophelia and Cassa, Christopher A and Rosenfeld, Jill A and Cox, Andrew G and Hedgepeth, John and Wucherpfennig, Julia I and Kim, Andrew J and Henderson, Jake E and Gonyo, Patrick and Brandt, Anthony and Lorimer, Ellen and Unger, Bethany and Prokop, Jeremy W and Heidel, Jerry R and Wang, Xiao-Xu and Ukaegbu, Chinedu I and Jennings, Benjamin C and Paulo, Joao A and Gableske, Sebastian and Fierke, Carol A and Getz, Gad and Sunyaev, Shamil R and Harper, J. Wade and Cichowski, Karen and Kimmelman, Alec C and Houvras, Yariv and Syngal, Sapna and Williams, Carol and Goessling, Wolfram
Nature genetics, ISSN 1061-4036, 09/2019, Volume 51, Issue 9, pp. 1308 - 1314
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Prenylation | Cell Proliferation | Pancreatic Neoplasms - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Middle Aged | Carcinoma, Pancreatic Ductal - metabolism | Male | rab GTP-Binding Proteins - genetics | Carcinoma, Pancreatic Ductal - genetics | Sequence Homology | Aged, 80 and over | Germ-Line Mutation | Adult | Female | Carcinoma - pathology | Proto-Oncogene Proteins p21(ras) - metabolism | Amino Acid Sequence | Genetic Predisposition to Disease | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Zebrafish | Carcinoma, Pancreatic Ductal - pathology | Animals | Pedigree | Carcinoma - genetics | Aged | Carcinoma - metabolism | Usage | Care and treatment | Zebra fish | Pancreatic cancer | Genetic aspects | Nucleotide sequencing | Research | Mass spectrometry | DNA sequencing | Cell proliferation | Adenocarcinoma | Nucleotide sequence | Genes | Mass spectroscopy | Genomes | Genetic screening | K-Ras protein | Proteins | Cell growth | Proteomics | Scientific imaging | Mutation | Siblings | Cancer | Tumors | Index Medicus
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9. Full Text Distinct evolutionary paths in chronic lymphocytic leukemia during resistance to the graft-versus-leukemia effect
by Bachireddy, Pavan and Ennis, Christina and Nguyen, Vinhkhang N and Gohil, Satyen H and Clement, Kendell and Shukla, Sachet A and Forman, Juliet and Barkas, Nikolaos and Freeman, Samuel and Bavli, Natalie and Elagina, Liudmila and Leshchiner, Ignaty and Mohammad, Arman W and Mathewson, Nathan D and Keskin, Derin B and Rassenti, Laura Z and Kipps, Thomas J and Brown, Jennifer R and Getz, Gad and Ho, Vincent T and Gnirke, Andreas and Neuberg, Donna and Soiffer, Robert J and Ritz, Jerome and Alyea, Edwin P and Kharchenko, Peter and Wu, Catherine J
Science translational medicine, ISSN 1946-6234, 09/2020, Volume 12, Issue 561, p. eabb7661
Life Sciences & Biomedicine | Medicine, Research & Experimental | Science & Technology | Cell Biology | Research & Experimental Medicine | Subpopulations | Chronic lymphatic leukemia | Transplants & implants | Transcription | Graft-versus-leukemia reaction | Leukemia | Stem cell transplantation | Lymphatic leukemia | Hematopoietic stem cells | Hemopoiesis | Chemotherapy | Genetic analysis | Stem cells | Epigenetics | Evolution | Histocompatibility antigen HLA | Evolution & development | Index Medicus
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