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1. Full Text The Thought of Death and the Memory of War
by Marc Crépon
10/2013, ISBN 081668006X, 184
War lays bare death and our relation to it. And in the wars-or more precisely the memories of war-of the twentieth century, images of the deaths of countless... 
Death | War | Sociology | Philosophy
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2. Full Text Targeting of colony-stimulating factor 1 receptor (CSF1R) in the CLL microenvironment yields antineoplastic activity in primary patient samples
by Edwards V, David K and Sweeney, David Tyler and Ho, Hibery and Eide, Christopher A and Rofelty, Angela and Agarwal, Anupriya and Liu, Selina Qiuying and Danilov, Alexey V and Lee, Patrice and Chantry, David and McWeeney, Shannon K and Druker, Brian J and Tyner, Jeffrey W and Spurgeon, Stephen E and Loriaux, Marc M
Oncotarget, ISSN 1949-2553, 05/2018, Volume 9, Issue 37, pp. 24576 - 24589
In many malignancies, the tumor microenvironment includes CSF1R-expressing supportive monocyte/macrophages that promote tumor cell survival. For chronic... 
Chronic lymphocytic leukemia | Tumor microenvironment | Small-molecule inhibitors | Colony-stimulating factor 1 receptor | Tumor-associated macrophages
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3. Full Text Oncogenic CSF3R Mutations in Chronic Neutrophilic Leukemia and Atypical CML
by Maxson, Julia E and Gotlib, Jason and Pollyea, Daniel A and Fleischman, Angela G and Agarwal, Anupriya and Eide, Christopher A and Bottomly, Daniel and Wilmot, Beth and McWeeney, Shannon K and Tognon, Cristina E and Pond, J. Blake and Collins, Robert H and Goueli, Basem and Oh, Stephen T and Deininger, Michael W and Chang, Bill H and Loriaux, Marc M and Druker, Brian J and Tyner, Jeffrey W
The New England Journal of Medicine, ISSN 0028-4793, 05/2013, Volume 368, Issue 19, pp. 1781 - 1790
Nearly 60% of patients with chronic neutrophilic leukemia (CNL) or atypical chronic myeloid leukemia (i.e., lacking the BCR-ABL1 translocation) have mutations... 
COLONY-STIMULATING-FACTOR | FACTOR-RECEPTOR | MEDICINE, GENERAL & INTERNAL | ACTIVATING MUTATION | POLYCYTHEMIA-VERA | MYELOPROLIFERATIVE-DISORDERS | SEVERE CONGENITAL NEUTROPENIA | TYROSINE KINASE JAK2 | C-KIT | MICE | ACUTE MYELOID-LEUKEMIA | Leukemia, Neutrophilic, Chronic - diagnosis | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - diagnosis | Humans | Janus Kinases - antagonists & inhibitors | Animals | Receptors, Colony-Stimulating Factor - genetics | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - genetics | Signal Transduction - physiology | Mice | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Leukemia, Neutrophilic, Chronic - genetics | Mutation | Leukemia, Lymphoid - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | Dasatinib | Care and treatment | Gene mutations | Causes of | Genetic aspects | Dosage and administration | Chronic myeloid leukemia | Diagnosis | Research | Drug therapy | Health aspects | Oncogenes | Tyrosine | BCR protein | Transformation | Myeloid leukemia | Colonies | Leukemia | Colleges & universities | Leukocytes (neutrophilic) | Patients | Lymphoma | Bone marrow | Janus kinase | Colony-stimulating factor | Protein-tyrosine kinase | Adapter proteins | Tumors
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4. Full Text Crosstalk between ROR1 and the Pre-B Cell Receptor Promotes Survival of t(1;19) Acute Lymphoblastic Leukemia
by Bicocca, Vincent T and Chang, Bill H and Masouleh, Behzad Kharabi and Muschen, Markus and Loriaux, Marc M and Druker, Brian J and Tyner, Jeffrey W
Cancer Cell, ISSN 1535-6108, 11/2012, Volume 22, Issue 5, pp. 656 - 667
We report that t(1;19) ALL cells universally exhibit expression of and dependence on the cell surface receptor ROR1. We further identify t(1;19) ALL cell... 
ONCOLOGY | TYROSINE KINASE | GLUT4 TRANSLOCATION | CYTOPLASMIC DOMAINS | IG-BETA | CHRONIC LYMPHOCYTIC-LEUKEMIA | ACUTE MYELOID-LEUKEMIA | ANTIGEN RECEPTOR | TRANSCRIPTION FACTOR | T-CELLS | TRANSGENIC MICE | CELL BIOLOGY | Dasatinib | Translocation, Genetic | Phosphorylation | Signal Transduction | Humans | Gene Expression Regulation, Neoplastic | Gene Silencing | Pyrimidines - pharmacology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Receptor Tyrosine Kinase-like Orphan Receptors - physiology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism | Chromosomes, Human, Pair 19 | Chromosomes, Human, Pair 1 | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Pre-B Cell Receptors - metabolism | Developmental biology | Lymphomas
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5. Full Text CAL-101, a p110δ selective phosphatidylinositol-3-kinase inhibitor for the treatment of B-cell malignancies, inhibits PI3K signaling and cellular viability
by Lannutti, Brian J and Meadows, Sarah A and Herman, Sarah E. M and Kashishian, Adam and Steiner, Bart and Johnson, Amy J and Byrd, John C and Tyner, Jeffrey W and Loriaux, Marc M and Deininger, Mike and Druker, Brian J and Puri, Kamal D and Ulrich, Roger G and Giese, Neill A
Blood, ISSN 0006-4971, 01/2011, Volume 117, Issue 2, pp. 591 - 594
Phosphatidylinositol-3-kinase p110 delta serves as a central integration point for signaling from cell surface receptors known to promote malignant B-cell... 
PHOSPHOINOSITIDE 3-KINASE P110-DELTA | HEMATOLOGY | ANTIGEN RECEPTOR | Lymphoid Neoplasia | Brief Report
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6. Full Text AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based Resistance
by O'Hare, Thomas and Shakespeare, William C and Zhu, Xiaotian and Eide, Christopher A and Rivera, Victor M and Wang, Yihan and Wang, Frank and Adrian, Lauren T and Zhou, Tianjun and Zhou, Dong and Huang, Wei-Sheng and Xu, Qihong and Metcalf, Chester A and Tyner, Jeffrey W and Loriaux, Marc M and Corbin, Amie S and Wardwell, Scott and Ning, Yaoyu and Keats, Jeffrey A and Sundaramoorthi, Raji and Thomas, Mathew and Snodgrass, Joseph and Commodore, Lois and Sawyer, Tomi K and Dalgarno, David C and Deininger, Michael W.N and Druker, Brian J and Clackson, Tim
Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 5, pp. 401 - 412
Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain... 
CHEMBIO | HUMDISEASE | CHRONIC MYELOGENOUS LEUKEMIA | DASATINIB BMS-354825 | MESYLATE | CML | ONCOLOGY | KINASE DOMAIN MUTATIONS | AMN107 | IMATINIB RESISTANCE | NILOTINIB | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Pyridazines - pharmacology | Protein Kinase Inhibitors - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Antineoplastic Agents - pharmacology | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Proto-Oncogene Proteins c-abl - genetics | Cell Growth Processes - drug effects | Proto-Oncogene Proteins c-abl - chemistry | Models, Molecular | Imidazoles - pharmacology | Antineoplastic Agents - chemistry | Mice, SCID | Pyridazines - chemistry | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-abl - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism | Chronic myeloid leukemia | BCR protein | Imatinib | Mutagenesis | Abl protein | Mutation | Fusion protein | Tumors | Index Medicus | imatinib resistance | dasatinib | nilotinib | compound mutation
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7. Full Text Functional genomic landscape of acute myeloid leukaemia
by Tyner, Jeffrey W and Tognon, Cristina E and Bottomly, Daniel and Wilmot, Beth and Kurtz, Stephen E and Savage, Samantha L and Long, Nicola and Schultz, Anna Reister and Traer, Elie and Abel, Melissa and Agarwal, Anupriya and Blucher, Aurora and Borate, Uma and Bryant, Jade and Burke, Russell and Carlos, Amy and Carpenter, Richie and Carroll, Joseph and Chang, Bill H and Coblentz, Cody and d’Almeida, Amanda and Cook, Rachel and Danilov, Alexey and Dao, Kim-Hien T and Degnin, Michie and Devine, Deirdre and Dibb, James and Edwards, David K and Eide, Christopher A and English, Isabel and Glover, Jason and Henson, Rachel and Ho, Hibery and Jemal, Abdusebur and Johnson, Kara and Johnson, Ryan and Junio, Brian and Kaempf, Andy and Leonard, Jessica and Lin, Chenwei and Liu, Selina Qiuying and Lo, Pierrette and Loriaux, Marc M and Luty, Samuel and Macey, Tara and MacManiman, Jason and Martinez, Jacqueline and Mori, Motomi and Nelson, Dylan and Nichols, Ceilidh and Peters, Jill and Ramsdill, Justin and Rofelty, Angela and Schuff, Robert and Searles, Robert and Segerdell, Erik and Smith, Rebecca L and Spurgeon, Stephen E and Sweeney, Tyler and Thapa, Aashis and Visser, Corinne and Wagner, Jake and Watanabe-Smith, Kevin and Werth, Kristen and Wolf, Joelle and White, Libbey and Yates, Amy and Zhang, Haijiao and Cogle, Christopher R and Collins, Robert H and Connolly, Denise C and Deininger, Michael W and Drusbosky, Leylah and Hourigan, Christopher S and Jordan, Craig T and Kropf, Patricia and Lin, Tara L and Martinez, Micaela E and Medeiros, Bruno C and Pallapati, Rachel R and Pollyea, Daniel A and Swords, Ronan T and Watts, Justin M and Weir, Scott J and Wiest, David L and Winters, Ryan M and McWeeney, Shannon K and Druker, Brian J
Nature, ISSN 0028-0836, 10/2018, Volume 562, Issue 7728, pp. 526 - 531
The implementation of targeted therapies for acute myeloid leukaemia (AML) has been challenging because of the complex mutational patterns within and across... 
AML | INTERNAL TANDEM DUPLICATION | PHARMACOKINETICS | TET2 MUTATIONS | CLONAL HEMATOPOIESIS | FLT3 INHIBITOR | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | TRANS-RETINOIC ACID | MYELODYSPLASTIC SYNDROME | CANCER | Datasets as Topic | Genomics | Humans | Leukemia, Myeloid, Acute - metabolism | Repressor Proteins - genetics | Male | Proto-Oncogene Proteins - genetics | Molecular Targeted Therapy | Serine-Arginine Splicing Factors - genetics | Genome, Human - genetics | DNA (Cytosine-5-)-Methyltransferases - genetics | Exome - genetics | Sequence Analysis, RNA | Leukemia, Myeloid, Acute - drug therapy | Female | Nuclear Proteins - genetics | Core Binding Factor Alpha 2 Subunit - genetics | Gene Expression Regulation, Neoplastic - genetics | Leukemia, Myeloid, Acute - genetics | RNA sequencing | Medical research | Usage | Gene mutations | Myelocytic leukemia | Medicine, Experimental | Genetic aspects | Nonlymphoid leukemia | Research | Discriminant analysis | Sensitivity analysis | Leukemia | Principal components analysis | Pharmacology | Genomes | Gene expression | Kinases | Ribonucleic acid--RNA | Patients | Generalized linear models | Gene sequencing | Sensitivity | Mutation | Bioinformatics | Combinatorial analysis | Cancer | Tumors
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8. Full Text Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening
by Tyner, Jeffrey and Yang, Wayne and Bankhead III, Armand and Fan, Guang and Fletcher, Luke and Bryant, Jade and Glover, Jason and Chang, Bill and Spurgeon, Stephen and Fleming, William and Kovacsovics, T and Gotlib, Jason and Oh, Stephen and Deininger, Michael W and Zwaan, Christian Michel and Boer, Monique and Heuvel-Eibrink, Marry and O'Hare, Thomas and ker, Brian and Loriaux, Marc
Cancer Research, ISSN 0008-5472, 01/2013, Volume 73, Issue 1, pp. 285 - 296
textabstractKinases are dysregulated in most cancers, but the frequency of specific kinase mutations is low, indicating a complex etiology in kinase... 
ACTIVATING MUTATION | POLYCYTHEMIA-VERA | MYELOPROLIFERATIVE DISORDERS | ONCOLOGY | TYROSINE KINASE | ACUTE LYMPHOBLASTIC-LEUKEMIA | CHRONIC LYMPHOCYTIC-LEUKEMIA | FOLLOW-UP | ACUTE MYELOID-LEUKEMIA | MYELODYSPLASTIC SYNDROME | CHRONIC MYELOMONOCYTIC LEUKEMIA | Drug Resistance, Neoplasm - genetics | Protein-Tyrosine Kinases - genetics | Algorithms | Humans | Leukemia - enzymology | Gene Expression Profiling - methods | Signal Transduction - genetics | Leukemia - genetics | Cluster Analysis | AML | ALL | CLL | CML | CMML | MPN | molecular diagnosis | personalized medicine
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9. Full Text CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasms
by Tyner, Jeffrey W and Bumm, Thomas G and Deininger, Jutta and Wood, Lisa and Aichberger, Karl J and Loriaux, Marc M and Druker, Brian J and Burns, Christopher J and Fantino, Emmanuelle and Deininger, Michael W
Blood, ISSN 0006-4971, 06/2010, Volume 115, Issue 25, pp. 5232 - 5240
Activating alleles of Janus kinase 2 (JAK2) such as JAK2V617F are central to the pathogenesis of myeloproliferative neoplasms (MPN), suggesting that small... 
MYELOFIBROSIS | POLYCYTHEMIA-VERA | ACTIVATING MUTATION | TYROSINE KINASE JAK2 | RESISTANCE | METAPLASIA | DISORDERS | ACUTE MYELOID-LEUKEMIA | ESSENTIAL THROMBOCYTHEMIA | HEMATOLOGY | EXPRESSION | Myeloproliferative Disorders - enzymology | Apoptosis - drug effects | Apoptosis - genetics | Myeloproliferative Disorders - immunology | Hematologic Neoplasms - enzymology | Mutation, Missense | Myeloproliferative Disorders - genetics | Hematopoiesis - drug effects | Janus Kinase 1 - metabolism | Janus Kinase 1 - genetics | Janus Kinase 2 - metabolism | Benzamides - pharmacology | Cytokines - genetics | Janus Kinase 2 - antagonists & inhibitors | Cytokines - immunology | Disease Models, Animal | Janus Kinase 2 - immunology | Cytokines - metabolism | Janus Kinase 2 - genetics | Hematopoiesis - genetics | Myeloproliferative Disorders - drug therapy | Pyrimidines - pharmacology | Janus Kinase 1 - antagonists & inhibitors | Janus Kinase 1 - immunology | Hematopoiesis - immunology | Animals | Apoptosis - immunology | Cell Line, Tumor | Hematologic Neoplasms - drug therapy | Hematologic Neoplasms - genetics | Mice | Mice, Inbred BALB C | Protein Kinase Inhibitors - pharmacology | Hematologic Neoplasms - immunology | Drug Screening Assays, Antitumor | Myeloid Neoplasia
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10. Full Text Potent activity of ponatinib (AP24534) in models of FLT3-driven acute myeloid leukemia and other hematologic malignancies
by Gozgit, Joseph M and Wong, Matthew J and Wardwell, Scott and Tyner, Jeffrey W and Loriaux, Marc M and Mohemmad, Qurish K and Narasimhan, Narayana I and Shakespeare, William C and Wang, Frank and Druker, Brian J and Clackson, Tim and Rivera, Victor M
Molecular Cancer Therapeutics, ISSN 1535-7163, 06/2011, Volume 10, Issue 6, pp. 1028 - 1035
Ponatinib (AP24534) is a novel multitargeted kinase inhibitor that potently inhibits native and mutant BCR-ABL at clinically achievable drug levels. Ponatinib... 
MUTANT | ACTIVATION | ONCOLOGY | FLT3 | RESISTANCE | TYROSINE KINASES | MUTATIONS | BCR-ABL INHIBITOR | CELL-LINE | DISCOVERY | FGFR1 | Apoptosis - drug effects | Humans | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Hematologic Neoplasms - enzymology | Hematologic Neoplasms - pathology | Pyridazines - pharmacology | Proto-Oncogene Proteins c-kit - metabolism | Leukemia, Myeloid, Acute - enzymology | Leukemia, Myeloid, Acute - drug therapy | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Female | Phosphorylation - drug effects | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Leukemia, Myeloid, Acute - pathology | Imidazoles - pharmacology | Mice, SCID | Receptor Protein-Tyrosine Kinases - metabolism | fms-Like Tyrosine Kinase 3 - metabolism | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Cell Line, Tumor | Hematologic Neoplasms - drug therapy | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology
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11. Full Text TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms
by Fleischman, Angela G and Aichberger, Karl J and Luty, Samuel B and Bumm, Thomas G and Petersen, Curtis L and Doratotaj, Shirin and Vasudevan, Kavin B and LaTocha, Dorian H and Yang, Fei and Press, Richard D and Loriaux, Marc M and Pahl, Heike L and Silver, Richard T and Agarwal, Anupriya and O'Hare, Thomas and Druker, Brian J and Bagby, Grover C and Deininger, Michael W
Blood, ISSN 0006-4971, 12/2011, Volume 118, Issue 24, pp. 6392 - 6398
Proinflammatory cytokines such as TNFα are elevated in patients with myeloproliferative neoplasms (MPN), but their contribution to disease pathogenesis is... 
Tumor Necrosis Factor-alpha - metabolism | Leukocytes, Mononuclear - metabolism | Humans | Tumor Necrosis Factor-alpha - genetics | Fanconi Anemia Complementation Group C Protein - genetics | RNA, Messenger - metabolism | Myeloproliferative Disorders - genetics | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - drug therapy | Myeloproliferative Disorders - blood | Janus Kinase 2 - metabolism | Myeloproliferative Disorders - metabolism | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - genetics | Bone Marrow Cells - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Janus Kinase 2 - antagonists & inhibitors | Recombinant Proteins - metabolism | Myeloid Progenitor Cells - metabolism | Leukocytes, Mononuclear - drug effects | Cells, Cultured | Janus Kinase 2 - genetics | Mutant Proteins - metabolism | Myeloproliferative Disorders - drug therapy | Cell Transformation, Neoplastic - metabolism | Mice, Knockout | Fanconi Anemia Complementation Group C Protein - metabolism | Point Mutation | Animals | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - blood | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Bone Marrow Cells - metabolism | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - metabolism | Amino Acid Substitution | Myeloid Neoplasia
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12. Full Text The CSF3R T618I mutation causes a lethal neutrophilic neoplasia in Mice that is responsive to therapeutic JAK inhibition
by Fleischman, Angela G and Maxson, Julia E and Luty, Samuel B and Agarwal, Anupriya and Royer, Lacey R and Abel, Melissa L and Macmaniman, Jason D and Loriaux, Marc M and Druker, Brian J and Tyner, Jeffrey W
Blood, ISSN 0006-4971, 11/2013, Volume 122, Issue 22, pp. 3628 - 3631
We have recently identified targetable mutations in CSF3R (GCSFR) in 60% of chronic neutrophilic leukemia (CNL) and atypical (BCR-ABL-negative) chronic myeloid... 
MYELOFIBROSIS | ACUTE MYELOID-LEUKEMIA | HEMATOLOGY | STIMULATING-FACTOR-RECEPTOR | SEVERE CONGENITAL NEUTROPENIA | RUXOLITINIB | Pyrazoles - therapeutic use | Humans | Mice, Transgenic | Myeloproliferative Disorders - drug therapy | Myeloproliferative Disorders - pathology | Myeloproliferative Disorders - genetics | Janus Kinases - antagonists & inhibitors | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - drug therapy | Point Mutation | Animals | Receptors, Colony-Stimulating Factor - genetics | Leukemia, Neutrophilic, Chronic - drug therapy | Protein Kinase Inhibitors - therapeutic use | Bone Marrow Transplantation | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - genetics | Granulocytes - pathology | Mice | Mice, Inbred BALB C | Leukemia, Neutrophilic, Chronic - genetics | Disease Models, Animal | Neutrophils - pathology | Brief Report | Myeloid Neoplasia
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13. Full Text Small molecule inhibitor screen identifies synergistic activity of the bromodomain inhibitor CPI203 and bortezomib in drug resistant myeloma
by Siegel, Matthew B and Liu, Selina Qiuying and Davare, Monika A and Spurgeon, Stephen E and Loriaux, Marc M and Druker, Brian J and Scott, Emma C and Tyner, Jeffrey W
Oncotarget, ISSN 1949-2553, 2015, Volume 6, Issue 22, pp. 18921 - 18932
Despite significant therapeutic progress in multiple myeloma, drug resistance is uniformly inevitable and new treatments are needed. Our aim was to identify... 
BET | Resistance | Bortezomib | Bromodomain | Myeloma | Small Molecule Libraries - pharmacology | Antineoplastic Combined Chemotherapy Protocols - administration & dosage | Apoptosis - drug effects | Humans | Acetamides - pharmacology | Drug Resistance, Neoplasm | Bortezomib - pharmacology | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Azepines - pharmacology | Drug Synergism | Multiple Myeloma - drug therapy | Multiple Myeloma - pathology | Bortezomib - administration & dosage | Cell Line, Tumor | Cell Proliferation - drug effects | Azepines - administration & dosage | Acetamides - administration & dosage
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14. Full Text The colony-Stimulating factor 3 receptor T640N mutation is oncogenic, sensitive toJAKInhibition, and mimics T618i
by Maxson, Julia E and Luty, Samuel B and MacManiman, Jason D and Paik, Jason C and Gotlib, Jason and Greenberg, Peter and Bahamadi, Swaleh and Savage, Samantha L and Abel, Melissa L and Eide, Christopher A and Loriaux, Marc M and Stevens, Emily A and Tyner, Jeffrey W
Clinical Cancer Research, ISSN 1078-0432, 02/2016, Volume 22, Issue 3, pp. 757 - 764
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15. Full Text RNAi screen for rapid therapeutic target identification in leukemia patients
by Jeffrey W. Tyner and Michael W. Deininger and Marc M. Loriaux and Bill H. Chang and Jason R. Gotlib and Stephanie G. Willis and Heidi Erickson and Tibor Kovacsovics and Thomas O'Hare and Michael C. Heinrich and Brian J. Druker
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 05/2009, Volume 106, Issue 21, pp. 8695 - 8700
Targeted therapy has vastly improved outcomes in certain types of cancer. Extension of this paradigm across a broad spectrum of malignancies will require an... 
Molecular diagnosis | Acute lymphoblastic leukemia | Personalized medicine | Acute myeloid leukemia | Chronic myelomonocytic leukemia | Humans | Gene Expression Regulation, Neoplastic | Janus Kinase 2 - genetics | Leukemia - therapy | Treatment Outcome | Gene Expression Profiling | Leukemia - metabolism | Mutation - genetics | Receptors, Thrombopoietin - genetics | RNA Interference | Time Factors | Janus Kinase 2 - metabolism | Alleles | Cell Line, Tumor | Leukemia - genetics | Care and treatment | Leukemia | Drug targeting | Genetic aspects | Research | Diagnosis | Methods | Cancer | Biological Sciences | acute myeloid leukemia | acute lymphoblastic leukemia | chronic myelomonocytic leukemia | molecular diagnosis | personalized medicine
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