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1. Full Text Targeting oncogenic drivers in lung cancer: Recent progress, current challenges and future opportunities
by Yoda, Satoshi and Dagogo-Jack, Ibiayi and Hata, Aaron N
Pharmacology and Therapeutics, ISSN 0163-7258, 01/2019, Volume 193, pp. 20 - 30
Targeted therapies have changed the landscape of treatments for non-small cell lung cancer (NSCLC). Specific targeted therapies have been approved for NSCLC... 
ALK | BRAF | NSCLC | Targeted therapy | ROS1 | EGFR | 1ST-LINE TREATMENT | EGFR-MUTATION | ACQUIRED-RESISTANCE | OPEN-LABEL | SINGLE-ARM | MESENCHYMAL TRANSITION | PHASE-II TRIAL | PLATINUM-BASED CHEMOTHERAPY | TYROSINE KINASE INHIBITOR | PHARMACOLOGY & PHARMACY | PREVIOUSLY TREATED PATIENTS
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2. Sequence, Treat, Repeat: Addressing Resistance in EGFR-Mutant NSCLC
by Klempner, SJ and Hata, AN
JOURNAL OF THORACIC ONCOLOGY, ISSN 1556-0864, 11/2019, Volume 14, Issue 11, pp. 1875 - 1877
ONCOLOGY | RESPIRATORY SYSTEM | MUTATION
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3. Full Text Abstract 4795: Potency of a new ALK/ROS1 inhibitor TPX-0005 to ALK G1202R mutation and ROS1 G2032R mutation
by Yoda, Satoshi and Dardaei, Leila and Prutisto-Chang, Kylie and Cui, Jean and Shaw, Alice T and Hata, Aaron N
Cancer Research, ISSN 0008-5472, 07/2018, Volume 78, Issue 13 Supplement, pp. 4795 - 4795
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4. Full Text Abstract 877: Evolution of resistance to EGFR inhibition from drug tolerant cancer cells
by Hata, Aaron N and Drier, Yotam and Gomez-Caraballo, Maria and Siddiqui, Faria and Sequist, Lecia and Bernstein, Bradley and Engelman, Jeffrey
Cancer Research, ISSN 0008-5472, 07/2016, Volume 76, Issue 14 Supplement, pp. 877 - 877
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5. Full Text Pharmacology and signaling of prostaglandin receptors: Multiple roles in inflammation and immune modulation
by Hata, Aaron N and Breyer, Richard M
Pharmacology and Therapeutics, ISSN 0163-7258, 2004, Volume 103, Issue 2, pp. 147 - 166
Prostaglandins are lipid-derived autacoids that modulate many physiological systems including the CNS, cardiovascular, gastrointestinal, genitourinary,... 
Signal transduction | Prostaglandin | Eicosanoid | G-protein-coupled receptor | Inflammation | Pharmacology | Immune modulation | PROTEIN-KINASE-C | prostaglandin | signal transduction | DP RECEPTOR | FP PROSTANOID RECEPTOR | IN-SITU HYBRIDIZATION | MICE LACKING | GROWTH-FACTOR RECEPTOR | inflammation | pharmacology | THROMBOXANE A RECEPTOR | PHARMACOLOGY & PHARMACY | ANTIGEN-PRESENTING CELLS | immune modulation | HUMAN PROSTACYCLIN RECEPTOR | AIRWAY SMOOTH-MUSCLE | Receptors, Epoprostenol - metabolism | Receptors, Thromboxane A2, Prostaglandin H2 - metabolism | Humans | Phylogeny | Receptors, Thromboxane A2, Prostaglandin H2 - genetics | Receptors, Prostaglandin - metabolism | Receptors, Prostaglandin E - genetics | Inflammation - metabolism | Prostaglandins - physiology | Receptors, Epoprostenol - genetics | Receptors, Prostaglandin - genetics | Receptors, Immunologic - genetics | Receptors, Immunologic - metabolism | Receptors, Prostaglandin E - metabolism
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6. Full Text The BCL2 family: Key mediators of the apoptotic response to targeted anticancer therapeutics
by Hata, Aaron N and Engelman, Jeffrey A and Faber, Anthony C
Cancer Discovery, ISSN 2159-8274, 05/2015, Volume 5, Issue 5, pp. 475 - 487
The ability of cancer cells to suppress apoptosis is critical for carcinogenesis. The BCL2 family proteins comprise the sentinel network that regulates the... 
CELL LUNG-CANCER | ONCOLOGY | BIM DELETION POLYMORPHISM | ABL TYROSINE KINASE | PROAPOPTOTIC GENE | ACUTE LYMPHOBLASTIC-LEUKEMIA | OBATOCLAX MESYLATE GX15-070 | BH3 MIMETIC ABT-737 | MOLECULE MCL-1 INHIBITORS | CHRONIC MYELOID-LEUKEMIA | TRANSGENIC MICE | Neoplasms - metabolism | Proto-Oncogene Proteins - metabolism | Apoptosis - drug effects | Humans | Apoptosis - genetics | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Apoptosis Regulatory Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Neoplasms - therapy | Animals | Bcl-2-Like Protein 11 | Neoplasms - genetics | Signal Transduction - drug effects | Biomarkers | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics
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7. Full Text Colon carcinoma cell growth is associated with prostaglandin E 2/EP4 receptor-evoked ERK activation
by Pozzi, Ambra and Yan, Xuexian and Macias-Perez, Ines and Wei, Shouzuo and Hata, Aaron N and Breyer, Richard M and Morrow, Jason D and Capdevila, Jorge H
Journal of Biological Chemistry, ISSN 0021-9258, 07/2004, Volume 279, Issue 28, pp. 29797 - 29804
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8. Full Text Abstract 741: Combined inhibition of MDM2 and MEK for KRAS mutant non-small cell lung cancer
by Hata, Aaron N and Archibald, Hannah L and Gomez-Caraballo, Maria D and DeBussche, Laurent R and Sidhu, Sukhvinder and Watters, James and Engelman, Jeffrey A
Cancer Research, ISSN 0008-5472, 10/2014, Volume 74, Issue 19 Supplement, pp. 741 - 741
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9. Full Text Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition
by Hata, Aaron N and Niederst, Matthew J and Archibald, Hannah L and Gomez-Caraballo, Maria and Siddiqui, Faria M and Mulvey, Hillary E and Maruvka, Yosef E and Ji, Fei and Bhang, Hyo-Eun C and Radhakrishna, Viveksagar Krishnamurthy and Siravegna, Giulia and Hu, Haichuan and Raoof, Sana and Lockerman, Elizabeth and Kalsy, Anuj and Lee, Dana and Keating, Celina L and Ruddy, David A and Damon, Leah J and Crystal, Adam S and Costa, Carlotta and Piotrowska, Zofia and Bardelli, Alberto and Iafrate, Anthony J and Sadreyev, Ruslan I and Stegmeier, Frank and Getz, Gad and Sequist, Lecia V and Faber, Anthony C and Engelman, Jeffrey A
Nature Medicine, ISSN 1078-8956, 03/2016, Volume 22, Issue 3, pp. 262 - 269
Although mechanisms of acquired resistance of epidermal growth factor receptor (EGFR)-mutant non -small -cell lung cancers to EGFR inhibitors have been... 
EGFR KINASE INHIBITORS | MEDICINE, RESEARCH & EXPERIMENTAL | GEFITINIB | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | T790M | CELL BIOLOGY | HETEROGENEITY | LUNG-CANCER | MET AMPLIFICATION | MODELS | MUTATION | AZD9291 | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Apoptosis - drug effects | Humans | Lung Neoplasms - metabolism | Apoptosis - genetics | RNA, Messenger - metabolism | Gene Expression Regulation, Neoplastic - drug effects | RNA, Messenger - drug effects | Lung Neoplasms - genetics | Cell Survival - drug effects | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Drug Resistance, Neoplasm - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Cell Cycle - drug effects | In Vitro Techniques | Quinazolines - pharmacology | Drug Resistance, Neoplasm - drug effects | Development and progression | Genetic aspects | Research | Drug resistance | Drug therapy | Risk factors | Tumors | Epidermal growth factor | Inhibitor drugs | Neurons
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10. Full Text Heterogeneity underlies the emergence of EGFR T790 wild-type clones following treatment of T790M-positive cancers with a third-generation EGFR inhibitor
by Piotrowska, Zofia and Niederst, Matthew J and Karlovich, Chris A and Wakelee, Heather A and Neal, Joel W and Mino-Kenudson, Mari and Fulton, Linnea and Hata, Aaron N and Lockerman, Elizabeth L and Kalsy, Anuj and Digumarthy, Subba and Muzikansky, Alona and Raponi, Mitch and Garcia, Angel R and Mulvey, Hillary E and Parks, Melissa K and DiCecca, Richard H and Dias-Santagata, Dora and Iafrate, A. John and Shaw, Alice T and Allen, Andrew R and Engelman, Jeffrey A and Sequist, Lecia V
Cancer Discovery, ISSN 2159-8274, 07/2015, Volume 5, Issue 7, pp. 713 - 723
Rociletinib is a third-generation EGFR inhibitor active in lung cancers with T790M, the gatekeeper mutation underlying most first-generation EGFR drug... 
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11. Full Text Synthetic Lethal Interaction of Combined BCL-XL and MEK Inhibition Promotes Tumor Regressions in KRAS Mutant Cancer Models
by Corcoran, Ryan B and Cheng, Katherine A and Hata, Aaron N and Faber, Anthony C and Ebi, Hiromichi and Coffee, Erin M and Greninger, Patricia and Brown, Ronald D and Godfrey, Jason T and Cohoon, Travis J and Song, Youngchul and Lifshits, Eugene and Hung, Kenneth E and Shioda, Toshi and Dias-Santagata, Dora and Singh, Anurag and Settleman, Jeffrey and Benes, Cyril H and Mino-Kenudson, Mari and Wong, Kwok-Kin and Engelman, Jeffrey A
Cancer Cell, ISSN 1535-6108, 01/2013, Volume 23, Issue 1, pp. 121 - 128
KRAS is the most commonly mutated oncogene, yet no effective targeted therapies exist for KRAS mutant cancers. We developed a pooled shRNA-drug screen strategy... 
PATHWAYS | GENE-EXPRESSION SIGNATURE | APOPTOSIS | CELLS | ACTIVATION | RAS ONCOGENE | K-RAS | ONCOLOGY | SENSITIVITY | RESISTANCE | INDUCTION | CELL BIOLOGY | Aniline Compounds - pharmacology | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Antineoplastic Agents - therapeutic use | Sulfonamides - pharmacology | Neoplasms - drug therapy | Animals | Neoplasms - genetics | Sulfonamides - therapeutic use | bcl-X Protein - antagonists & inhibitors | Benzimidazoles - pharmacology | Antineoplastic Agents - pharmacology | Mice | Aniline Compounds - therapeutic use | MAP Kinase Kinase Kinases - antagonists & inhibitors | Benzimidazoles - therapeutic use | Drug Screening Assays, Antitumor | Proto-Oncogene Proteins p21(ras) - metabolism | Proteins | Care and treatment | Lung cancer | Analysis | Genes | Genetically modified organisms | Cancer | Protein binding
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12. Full Text EGFR mutations and ALK rearrangements are associated with low response rates to PD-1 pathway blockade in non-small cell lung cancer: A retrospective analysis
by Gainor, Justin F and Shaw, Alice T and Sequist, Lecia V and Fu, Xiujun and Azzoli, Christopher G and Piotrowska, Zofia and Huynh, Tiffany G and Zhao, Ling and Fulton, Linnea and Schultz, Katherine R and Howe, Emily and Farago, Anna F and Sullivan, Ryan J and Stone, James R and Digumarthy, Subba and Moran, Teresa and Hata, Aaron N and Yagi, Yukako and Yeap, Beow Y and Engelman, Jeffrey A and Mino-Kenudson, Mari
Clinical Cancer Research, ISSN 1078-0432, 09/2016, Volume 22, Issue 18, pp. 4585 - 4593
Purpose: PD-1 inhibitors are established agents in the management of non-small cell lung cancer (NSCLC); however, only a subset of patients derives clinical... 
ACTIVATION | ONCOLOGY | LANDSCAPE | DEATH-LIGAND 1 | IMMUNE ESCAPE | RESISTANCE | ANTIBODY | PULMONARY ADENOCARCINOMA | NIVOLUMAB | TUMORS | EXPRESSION | Lung Neoplasms - drug therapy | Translocation, Genetic | Humans | Lung Neoplasms - metabolism | Middle Aged | ErbB Receptors - genetics | Male | Tomography, X-Ray Computed | Carcinoma, Non-Small-Cell Lung - diagnosis | Molecular Targeted Therapy | Anaplastic Lymphoma Kinase | DNA Mutational Analysis | Adult | Female | Lymphocytes, Tumor-Infiltrating - metabolism | Lung Neoplasms - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Programmed Cell Death 1 Receptor - metabolism | Genotype | Treatment Outcome | Lymphocytes, Tumor-Infiltrating - drug effects | Antineoplastic Agents, Immunological - pharmacology | B7-H1 Antigen - metabolism | Receptor Protein-Tyrosine Kinases - genetics | Signal Transduction - drug effects | Antineoplastic Agents, Immunological - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Lung Neoplasms - diagnosis | Lymphocytes, Tumor-Infiltrating - immunology | ALK | PD-1 Inhibitors | EGFR | Non-small cell lung cancer
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13. Full Text Exploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy Combination
by Ham, Jungoh and Costa, Carlotta and Sano, Renata and Lochmann, Timothy L and Sennott, Erin M and Patel, Neha U and Dastur, Anahita and Gomez-Caraballo, Maria and Krytska, Kateryna and Hata, Aaron N and Floros, Konstantinos V and Hughes, Mark T and Jakubik, Charles T and Heisey, Daniel A.R and Ferrell, Justin T and Bristol, Molly L and March, Ryan J and Yates, Craig and Hicks, Mark A and Nakajima, Wataru and Gowda, Madhu and Windle, Brad E and Dozmorov, Mikhail G and Garnett, Mathew J and McDermott, Ultan and Harada, Hisashi and Taylor, Shirley M and Morgan, Iain M and Benes, Cyril H and Engelman, Jeffrey A and Mossé, Yael P and Faber, Anthony C
Cancer Cell, ISSN 1535-6108, 02/2016, Volume 29, Issue 2, pp. 159 - 172
Fewer than half of children with high-risk neuroblastoma survive. Many of these tumors harbor high-level amplification of , which correlates with poor disease... 
CELL LUNG-CANCER | DRUG-SENSITIVITY | LIFE-SPAN | ONCOLOGY | BCL-2 INHIBITOR | N-MYC | MITOTIC ARREST | DIRECT TRANSCRIPTIONAL TARGET | AURORA KINASE | SMALL-MOLECULE INHIBITOR | TRANSLATIONAL CONTROL | CELL BIOLOGY | Sulfonamides - therapeutic use | Humans | Neuroblastoma - drug therapy | Neuroblastoma - genetics | Cell Line, Tumor | Oncogene Proteins | Apoptosis - genetics | Antineoplastic Agents - therapeutic use | N-Myc Proto-Oncogene Protein | Aniline Compounds - therapeutic use | Neuroblastoma - pathology | Nuclear Proteins | Analysis | Neuroblastoma | Apoptosis
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14. Full Text Abstract 3144: Prediction of ALK mutations associated with acquired resistance to lorlatinib
by Yoda, Satoshi and Dardaei, Leila and Singh, Manrose and Engelman, Jeffrey A and Shaw, Alice T and Hata, Aaron N
Cancer Research, ISSN 0008-5472, 07/2017, Volume 77, Issue 13 Supplement, pp. 3144 - 3144
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15. Full Text The new-generation selective ROS1/NTRK inhibitor DS-6051b overcomes crizotinib resistant ROS1-G2032R mutation in preclinical models
by Katayama, R and Gong, B and Togashi, N and Miyamoto, M and Kiga, M and Iwasaki, S and Kamai, Y and Tominaga, Y and Takeda, Y and Kagoshima, Y and Shimizu, Y and Seto, Y and Oh-hara, T and Koike, S and Nakao, N and Hanzawa, H and Watanabe, K and Yoda, S and Yanagitani, N and Hata, AN and Shaw, AT and Nishio, M and Fujita, N and Isoyama, T
NATURE COMMUNICATIONS, ISSN 2041-1723, 08/2019, Volume 10, Issue 1, pp. 3604 - 12
ROS1 gene rearrangement was observed in around 1-2 % of NSCLC patients and in several other cancers such as cholangiocarcinoma, glioblastoma, or colorectal... 
ALK | LUNG-CANCER | ENTRECTINIB | FUSION | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | EGFR MUTATIONS | REARRANGEMENTS | TRK | CLINICAL-RESPONSE | ROS1 | Refractory materials | Inhibitors | Lung cancer | Colorectal carcinoma | Glioblastoma | Gene rearrangement | Non-small cell lung carcinoma | Models | Mutation | Kinases | Cholangiocarcinoma | Cancer
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