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51. MODL-05. ELUCIDATING THE EPIGENETIC DRIVEN TRANSCRIPTIONAL PROGRAM UNDERLYING THE INVASIVE PHENOTYPE OF THE NOVEL EGFRA289VARIANT OF GBM

Author

Lin, Benjamin, primary, Ziebro, Julia, additional, Shelton, Abigail, additional, Skinner, Kasey, additional, Bash, Ryan, additional, Osuka, Satoru, additional, Sudarshan, Sunil, additional, Binder, Zev, additional, O'Rourke, Donald M, additional, Nathanson, David, additional, Furnari, Frank, additional, and Miller, Christopher, additional

Published
2023
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57. CSIG-04. INTEGRATED MOLECULAR AND FUNCTIONAL CHARACTERIZATION OF THE INTRINSIC APOPTOTIC MACHINERY IDENTIFIES A DIAGNOSTICALLY INFORMED THERAPEUTIC APPROACH FOR MALIGNANT GLIOMA

Author

Fernandez, Elizabeth, primary, Mai, Wilson, additional, Song, Kai, additional, Bayley, Nicholas, additional, Kim, Jiyoon, additional, Zhu, Henan, additional, Liau, Linda, additional, Li, Gang, additional, Yong, William, additional, Souers, Andrew, additional, Li, Jingyi Jessica, additional, Graeber, Thomas, additional, Cloughesy, Timothy, additional, and Nathanson, David, additional

Published
2023
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59. 2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling.

Author

Fu, Xudong, Chin, Randall M, Vergnes, Laurent, Hwang, Heejun, Deng, Gang, Xing, Yanpeng, Pai, Melody Y, Li, Sichen, Ta, Lisa, Fazlollahi, Farbod, Chen, Chuo, Prins, Robert M, Teitell, Michael A, Nathanson, David A, Lai, Albert, Faull, Kym F, Jiang, Meisheng, Clarke, Steven G, Cloughesy, Timothy F, Graeber, Thomas G, Braas, Daniel, Christofk, Heather R, Jung, Michael E, Reue, Karen, and Huang, Jing

Subjects
Animals, Humans, Caenorhabditis elegans, Glioblastoma, Glutarates, Isocitrate Dehydrogenase, Signal Transduction, Cell Proliferation, Longevity, Mutation, Adenosine Triphosphatases, TOR Serine-Threonine Kinases, Brain Disorders, Aging, Cancer, Brain Cancer, Rare Diseases, Biochemistry and Cell Biology, Medical Biochemistry and Metabolomics, Endocrinology & Metabolism
Abstract

We discovered recently that the central metabolite α-ketoglutarate (α-KG) extends the lifespan of C. elegans through inhibition of ATP synthase and TOR signaling. Here we find, unexpectedly, that (R)-2-hydroxyglutarate ((R)-2HG), an oncometabolite that interferes with various α-KG-mediated processes, similarly extends worm lifespan. (R)-2HG accumulates in human cancers carrying neomorphic mutations in the isocitrate dehydrogenase (IDH) 1 and 2 genes. We show that, like α-KG, both (R)-2HG and (S)-2HG bind and inhibit ATP synthase and inhibit mTOR signaling. These effects are mirrored in IDH1 mutant cells, suggesting a growth-suppressive function of (R)-2HG. Consistently, inhibition of ATP synthase by 2-HG or α-KG in glioblastoma cells is sufficient for growth arrest and tumor cell killing under conditions of glucose limitation, e.g., when ketone bodies (instead of glucose) are supplied for energy. These findings inform therapeutic strategies and open avenues for investigating the roles of 2-HG and metabolites in biology and disease.

Published
2015

60. Chemical Methods for the Simultaneous Quantitation of Metabolites and Proteins from Single Cells

Author

Xue, Min, Wei, Wei, Su, Yapeng, Kim, Jungwoo, Shin, Young Shik, Mai, Wilson X, Nathanson, David A, and Heath, James R

Subjects
Engineering, Chemical Sciences, Biotechnology, Brain Disorders, Cancer, 1.1 Normal biological development and functioning, Underpinning research, Antineoplastic Agents, Cell Line, Tumor, Drug Screening Assays, Antitumor, Equipment Design, ErbB Receptors, Erlotinib Hydrochloride, Fluorescent Antibody Technique, Glioblastoma, Humans, Metabolomics, Microarray Analysis, Proteomics, General Chemistry, Chemical sciences
Abstract

We describe chemical approaches for integrated metabolic and proteomic assays from single cells. Quantitative assays for intracellular metabolites, including glucose uptake and three other species, are designed as surface-competitive binding assays with fluorescence readouts. This enables integration into a microarray format with functional protein immunoassays, all of which are incorporated into the microchambers of a single-cell barcode chip (SCBC). By using the SCBC, we interrogate the response of human-derived glioblastoma cancer cells to epidermal growth factor receptor inhibition. We report, for the first time, on both the intercellular metabolic heterogeneity as well as the baseline and drug-induced changes in the metabolite-phosphoprotein correlation network.

Published
2015

64. Fully Automated Production of Diverse 18F-Labeled PET Tracers on the ELIXYS Multireactor Radiosynthesizer Without Hardware Modification

Author

Lazari, Mark, Collins, Jeffrey, Shen, Bin, Farhoud, Mohammed, Yeh, Daniel, Maraglia, Brandon, Chin, Frederick T, Nathanson, David A, Moore, Melissa, and van Dam, R Michael

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Biomedical Imaging, Animals, Chemistry Techniques, Synthetic, Chromatography, High Pressure Liquid, Female, Fluorodeoxyglucose F18, Mice, Mice, Inbred BALB C, Positron-Emission Tomography, Quality Control, Radiopharmaceuticals, Software, Whole Body Imaging, automated radiosynthesis, radiochemistry kits, F-18-FAC, F-18-FEAU, F-18-FMAU, 18F-FAC, 18F-FEAU, 18F-FMAU, Nuclear Medicine & Medical Imaging, Clinical sciences
Abstract

UnlabelledFully automated radiosynthesizers are continuing to be developed to meet the growing need for the reliable production of PET tracers made under current good manufacturing practice guidelines. There is a current trend toward supporting kitlike disposable cassettes that come preconfigured for particular tracers, thus eliminating the need for cleaning protocols between syntheses and enabling quick transitions to synthesizing other tracers. Though ideal for production, these systems are often limited for the development of novel tracers because of pressure, temperature, and chemical compatibility considerations. This study demonstrated the versatile use of the ELIXYS fully automated radiosynthesizer to adapt and produce 8 different (18)F-labeled PET tracers of varying complexity.MethodsThree-reactor syntheses of 2-deoxy-2-(18)F-fluoro-β-d-arabinofuranosylcytosine (d-(18)F-FAC), 2-deoxy-2-(18)F-fluoro-5-methyl-β-l-arabinofuranosyluracil (l-(18)F-FMAU), and 2-deoxy-2-(18)F-fluoro-5-ethyl-β-d-arabinofuranosyluracil (d-(18)F-FEAU) along with the 1-reactor syntheses of d-(18)F-FEAU, (18)F-FDG, 3-deoxy-3-(18)F-fluoro-l-thymidine ((18)F-FLT), (18)F-fallypride, 9-(4-(18)F-fluoro-3-hydroxymethylbutyl)-guanine ((18)F-FHBG), and N-succinimidyl-4-(18)F-fluorobenzoate ((18)F-SFB), were all produced using ELIXYS without the need for any hardware modifications or reconfiguration. Synthesis protocols were adapted and slightly modified from those in the literature but were not fully optimized. Furthermore, (18)F-FLT, (18)F-FDG, and (18)F-fallypride were produced sequentially on the same day and used for preclinical imaging of A431 tumor-bearing severe combined immunodeficient mice and wild-type BALB/c mice. To assess future translation to the clinical setting, several batches of tracers were subjected to a full set of quality control tests.ResultsAll tracers were produced with radiochemical yields comparable to those in the literature. (18)F-FLT, (18)F-FDG, and (18)F-fallypride were successfully used to image the mice, with results consistent with those reported in the literature. All tracers that were subjected to clinical quality control tests passed.ConclusionThe ELIXYS radiosynthesizer facilitates rapid tracer development and is capable of producing multiple (18)F-labeled PET tracers suitable for clinical applications using the same hardware setup.

Published
2014

65. Co-targeting of convergent nucleotide biosynthetic pathways for leukemia eradication

Author

Nathanson, David A, Armijo, Amanda L, Tom, Michelle, Li, Zheng, Dimitrova, Elizabeth, Austin, Wayne R, Nomme, Julian, Campbell, Dean O, Ta, Lisa, Le, Thuc M, Lee, Jason T, Darvish, Ryan, Gordin, Ari, Wei, Liu, Liao, Hsiang-I, Wilks, Moses, Martin, Colette, Sadeghi, Saman, Murphy, Jennifer M, Boulos, Nidal, Phelps, Michael E, Faull, Kym F, Herschman, Harvey R, Jung, Michael E, Czernin, Johannes, Lavie, Arnon, and Radu, Caius G

Subjects
Biomedical and Clinical Sciences, Health Sciences, Pediatric Cancer, Hematology, Genetics, Orphan Drug, Pediatric, Biomedical Imaging, Childhood Leukemia, Rare Diseases, Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Biosynthetic Pathways, Deoxycytidine Kinase, Deoxycytosine Nucleotides, Disease Eradication, Mice, Positron-Emission Tomography, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Thymidine, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Pharmacological targeting of metabolic processes in cancer must overcome redundancy in biosynthetic pathways. Deoxycytidine (dC) triphosphate (dCTP) can be produced both by the de novo pathway (DNP) and by the nucleoside salvage pathway (NSP). However, the role of the NSP in dCTP production and DNA synthesis in cancer cells is currently not well understood. We show that acute lymphoblastic leukemia (ALL) cells avoid lethal replication stress after thymidine (dT)-induced inhibition of DNP dCTP synthesis by switching to NSP-mediated dCTP production. The metabolic switch in dCTP production triggered by DNP inhibition is accompanied by NSP up-regulation and can be prevented using DI-39, a new high-affinity small-molecule inhibitor of the NSP rate-limiting enzyme dC kinase (dCK). Positron emission tomography (PET) imaging was useful for following both the duration and degree of dCK inhibition by DI-39 treatment in vivo, thus providing a companion pharmacodynamic biomarker. Pharmacological co-targeting of the DNP with dT and the NSP with DI-39 was efficacious against ALL models in mice, without detectable host toxicity. These findings advance our understanding of nucleotide metabolism in leukemic cells, and identify dCTP biosynthesis as a potential new therapeutic target for metabolic interventions in ALL and possibly other hematological malignancies.

Published
2014

66. Targeted Therapy Resistance Mediated by Dynamic Regulation of Extrachromosomal Mutant EGFR DNA

Author

Nathanson, David A, Gini, Beatrice, Mottahedeh, Jack, Visnyei, Koppany, Koga, Tomoyuki, Gomez, German, Eskin, Ascia, Hwang, Kiwook, Wang, Jun, Masui, Kenta, Paucar, Andres, Yang, Huijun, Ohashi, Minori, Zhu, Shaojun, Wykosky, Jill, Reed, Rachel, Nelson, Stanley F, Cloughesy, Timothy F, James, C David, Rao, P Nagesh, Kornblum, Harley I, Heath, James R, Cavenee, Webster K, Furnari, Frank B, and Mischel, Paul S

Subjects
Cancer, Genetics, Rare Diseases, Brain Disorders, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Antineoplastic Agents, Central Nervous System Neoplasms, DNA, Drug Resistance, Neoplasm, ErbB Receptors, Erlotinib Hydrochloride, Glioblastoma, Humans, Mice, Molecular Targeted Therapy, Mutation, Neoplasm Transplantation, Protein Kinase Inhibitors, Quinazolines, Single-Cell Analysis, Tumor Cells, Cultured, Withholding Treatment, General Science & Technology
Abstract

Intratumoral heterogeneity contributes to cancer drug resistance, but the underlying mechanisms are not understood. Single-cell analyses of patient-derived models and clinical samples from glioblastoma patients treated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) demonstrate that tumor cells reversibly up-regulate or suppress mutant EGFR expression, conferring distinct cellular phenotypes to reach an optimal equilibrium for growth. Resistance to EGFR TKIs is shown to occur by elimination of mutant EGFR from extrachromosomal DNA. After drug withdrawal, reemergence of clonal EGFR mutations on extrachromosomal DNA follows. These results indicate a highly specific, dynamic, and adaptive route by which cancers can evade therapies that target oncogenes maintained on extrachromosomal DNA.

Published
2014

67. Supplementary Data 1 from Depth of Radiographic Response and Time to Tumor Regrowth Predicts Overall Survival Following Anti-VEGF Therapy in Recurrent Glioblastoma

Author

Ellingson, Benjamin M., primary, Hagiwara, Akifumi, primary, Morris, Connor J., primary, Cho, Nicholas S., primary, Oshima, Sonoko, primary, Sanvito, Francesco, primary, Oughourlian, Talia C., primary, Telesca, Donatello, primary, Raymond, Catalina, primary, Abrey, Lauren E., primary, Garcia, Josep, primary, Aftab, Dana T., primary, Hessel, Colin, primary, Rachmilewitz Minei, Tamar, primary, Harats, Dror, primary, Nathanson, David A., primary, Wen, Patrick Y., primary, and Cloughesy, Timothy F., primary

Published
2023
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68. Data from Depth of Radiographic Response and Time to Tumor Regrowth Predicts Overall Survival Following Anti-VEGF Therapy in Recurrent Glioblastoma

Author

Ellingson, Benjamin M., primary, Hagiwara, Akifumi, primary, Morris, Connor J., primary, Cho, Nicholas S., primary, Oshima, Sonoko, primary, Sanvito, Francesco, primary, Oughourlian, Talia C., primary, Telesca, Donatello, primary, Raymond, Catalina, primary, Abrey, Lauren E., primary, Garcia, Josep, primary, Aftab, Dana T., primary, Hessel, Colin, primary, Rachmilewitz Minei, Tamar, primary, Harats, Dror, primary, Nathanson, David A., primary, Wen, Patrick Y., primary, and Cloughesy, Timothy F., primary

Published
2023
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69. Supplemental Figure S1 from Depth of Radiographic Response and Time to Tumor Regrowth Predicts Overall Survival Following Anti-VEGF Therapy in Recurrent Glioblastoma

Author

Ellingson, Benjamin M., primary, Hagiwara, Akifumi, primary, Morris, Connor J., primary, Cho, Nicholas S., primary, Oshima, Sonoko, primary, Sanvito, Francesco, primary, Oughourlian, Talia C., primary, Telesca, Donatello, primary, Raymond, Catalina, primary, Abrey, Lauren E., primary, Garcia, Josep, primary, Aftab, Dana T., primary, Hessel, Colin, primary, Rachmilewitz Minei, Tamar, primary, Harats, Dror, primary, Nathanson, David A., primary, Wen, Patrick Y., primary, and Cloughesy, Timothy F., primary

Published
2023
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72. Fast Metabolic Response to Drug Intervention Through Analysis on a Miniaturized, Highly Integrated Molecular Imaging System

Author

Wang, Jun, Hwang, Kiwook, Braas, Daniel, Dooraghi, Alex, Nathanson, David, Campbell, Dean O, Gu, Yuchao, Sandberg, Troy, Mischel, Paul, Radu, Caius, Chatziioannou, Arion F, Phelps, Michael E, Christofk, Heather, and Heath, James R

Subjects
Cancer, Rare Diseases, Bioengineering, Biomedical Imaging, HIV/AIDS, Biological Transport, Cell Line, Tumor, Drug Evaluation, Preclinical, Fluorodeoxyglucose F18, Glycolysis, Humans, Kinetics, Miniaturization, Molecular Imaging, Systems Integration, microfluidics, molecular imaging, radiopharmaceuticals, radioassay, Clinical Sciences, Nuclear Medicine & Medical Imaging
Abstract

UnlabelledWe report on a radiopharmaceutical imaging platform designed to capture the kinetics of cellular responses to drugs.MethodsA portable in vitro molecular imaging system comprising a microchip and a β-particle imaging camera permitted routine cell-based radioassays of small numbers of either suspended or adherent cells. We investigated the kinetics of responses of model lymphoma and glioblastoma cancer cell lines to (18)F-FDG uptake after drug exposure. Those responses were correlated with kinetic changes in the cell cycle or with changes in receptor tyrosine kinase signaling.ResultsThe platform enabled direct radioassays of multiple cell types and yielded results comparable to those from conventional approaches; however, the platform used smaller sample sizes, permitted a higher level of quantitation, and did not require cell lysis.ConclusionThe kinetic analysis enabled by the platform provided a rapid (≈ 1 h) drug screening assay.

Published
2013

73. Development of New Deoxycytidine Kinase Inhibitors and Noninvasive in Vivo Evaluation Using Positron Emission Tomography

Author

Murphy, Jennifer M, Armijo, Amanda L, Nomme, Julian, Lee, Chi Hang, Smith, Quentin A, Li, Zheng, Campbell, Dean O, Liao, Hsiang-I, Nathanson, David A, Austin, Wayne R, Lee, Jason T, Darvish, Ryan, Wei, Liu, Wang, Jue, Su, Ying, Damoiseaux, Robert, Sadeghi, Saman, Phelps, Michael E, Herschman, Harvey R, Czernin, Johannes, Alexandrova, Anastassia N, Jung, Michael E, Lavie, Arnon, and Radu, Caius G

Subjects
Medicinal and Biomolecular Chemistry, Chemical Sciences, Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Cell Line, Tumor, Crystallography, X-Ray, Deoxycytidine Kinase, Enzyme Inhibitors, Humans, Inhibitory Concentration 50, Kinetics, Magnetic Resonance Spectroscopy, Models, Molecular, Monte Carlo Method, Positron-Emission Tomography, Spectrometry, Mass, Electrospray Ionization, Organic Chemistry, Pharmacology and Pharmaceutical Sciences, Medicinal & Biomolecular Chemistry, Pharmacology and pharmaceutical sciences, Medicinal and biomolecular chemistry, Organic chemistry
Abstract

Combined inhibition of ribonucleotide reductase and deoxycytidine kinase (dCK) in multiple cancer cell lines depletes deoxycytidine triphosphate pools leading to DNA replication stress, cell cycle arrest, and apoptosis. Evidence implicating dCK in cancer cell proliferation and survival stimulated our interest in developing small molecule dCK inhibitors. Following a high throughput screen of a diverse chemical library, a structure-activity relationship study was carried out. Positron Emission Tomography (PET) using (18)F-L-1-(2'-deoxy-2'-FluoroArabinofuranosyl) Cytosine ((18)F-L-FAC), a dCK-specific substrate, was used to rapidly rank lead compounds based on their ability to inhibit dCK activity in vivo. Evaluation of a subset of the most potent compounds in cell culture (IC50 = ∼1-12 nM) using the (18)F-L-FAC PET pharmacodynamic assay identified compounds demonstrating superior in vivo efficacy.

Published
2013

74. PET/CT in Oncology: Current Status and Perspectives

Author

Czernin, Johannes, Allen-Auerbach, Martin, Nathanson, David, and Herrmann, Ken

Subjects
Physical Sciences, Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Bioengineering, Biomedical Imaging, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Initial treatment strategies, Molecular imaging, Oncology, PET/CT, Subsequent treatment strategies
Abstract

The discovery of the Warburg effect in the early twentieth century followed by the development of the fluorinated glucose analogue 18F-fluorodeoxyglucose (18F-FDG) and the invention of positron emission tomographs laid the foundation of clinical PET/CT. This review discusses the challenges and obstacles in clinical adoption of this technique. We then discuss advances in instrumentation, including the critically important introduction of PET/CT and current PET/CT protocols. Moreover, we provide evidence for the clinical utility of PET/CT for patient management and its potential impact on patient outcome, and address its cost and cost-effectiveness. Although this review largely focuses on 18F-FDG imaging, we also discuss a variety of additional molecular imaging approaches that can be used for cancer phenotyping with PET. Throughout this review we emphasize the critical contributions of CT to the strength of PET/CT.

Published
2013

75. Nucleoside salvage pathway kinases regulate hematopoiesis by linking nucleotide metabolism with replication stress

Author

Austin, Wayne R, Armijo, Amanda L, Campbell, Dean O, Singh, Arun S, Hsieh, Terry, Nathanson, David, Herschman, Harvey R, Phelps, Michael E, Witte, Owen N, Czernin, Johannes, and Radu, Caius G

Subjects
Biomedical and Clinical Sciences, Hematology, Underpinning research, 2.1 Biological and endogenous factors, Aetiology, 1.1 Normal biological development and functioning, Animals, Blotting, Western, Bromodeoxyuridine, DNA Replication, Deoxycytidine Kinase, Deoxycytosine Nucleotides, Flow Cytometry, Hematopoiesis, Immunophenotyping, Metabolic Networks and Pathways, Mice, Mice, Knockout, Models, Biological, Nucleosides, Nucleotides, Stress, Physiological, Thymidine Kinase, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Nucleotide deficiency causes replication stress (RS) and DNA damage in dividing cells. How nucleotide metabolism is regulated in vivo to prevent these deleterious effects remains unknown. In this study, we investigate a functional link between nucleotide deficiency, RS, and the nucleoside salvage pathway (NSP) enzymes deoxycytidine kinase (dCK) and thymidine kinase (TK1). We show that inactivation of dCK in mice depletes deoxycytidine triphosphate (dCTP) pools and induces RS, early S-phase arrest, and DNA damage in erythroid, B lymphoid, and T lymphoid lineages. TK1(-/-) erythroid and B lymphoid lineages also experience nucleotide deficiency but, unlike their dCK(-/-) counterparts, they still sustain DNA replication. Intriguingly, dCTP pool depletion, RS, and hematopoietic defects induced by dCK inactivation are almost completely reversed in a newly generated dCK/TK1 double-knockout (DKO) mouse model. Using NSP-deficient DKO hematopoietic cells, we identify a previously unrecognized biological activity of endogenous thymidine as a strong inducer of RS in vivo through TK1-mediated dCTP pool depletion. We propose a model that explains how TK1 and dCK "tune" dCTP pools to both trigger and resolve RS in vivo. This new model may be exploited therapeutically to induce synthetic sickness/lethality in hematological malignancies, and possibly in other cancers.

Published
2012

79. Cover Image, Volume 36, Issue 6

Author

Cho, Nicholas S., primary, Hagiwara, Akifumi, additional, Yao, Jingwen, additional, Nathanson, David A., additional, Prins, Robert M., additional, Wang, Chencai, additional, Raymond, Catalina, additional, Desousa, Brandon R., additional, Divakaruni, Ajit, additional, Morrow, Danielle H., additional, Nghiemphu, Phioanh L., additional, Lai, Albert, additional, Liau, Linda M., additional, Everson, Richard G., additional, Salamon, Noriko, additional, Pope, Whitney B., additional, Cloughesy, Timothy F., additional, and Ellingson, Benjamin M., additional

Published
2023
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80. Cardiovascular mortality and morbidity in patients with type 2 diabetes following initiation of sodium-glucose co-transporter-2 inhibitors versus other glucose-lowering drugs (CVD-REAL Nordic): a multinational observational analysis

Author

Birkeland, Kåre I, Jørgensen, Marit E, Carstensen, Bendix, Persson, Frederik, Gulseth, Hanne L, Thuresson, Marcus, Fenici, Peter, Nathanson, David, Nyström, Thomas, Eriksson, Jan W, Bodegård, Johan, and Norhammar, Anna

Published
2017
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84. Table S2 from Pathway-based Approach Reveals Differential Sensitivity to E2F1 Inhibition in Glioblastoma

Author

Alvarado, Alvaro G., primary, Tessema, Kaleab, primary, Muthukrishnan, Sree Deepthi, primary, Sober, Mackenzie, primary, Kawaguchi, Riki, primary, Laks, Dan R., primary, Bhaduri, Aparna, primary, Swarup, Vivek, primary, Nathanson, David A., primary, Geschwind, Daniel H., primary, Goldman, Steven A., primary, and Kornblum, Harley I., primary

Published
2023
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86. Figure S4 from Pathway-based Approach Reveals Differential Sensitivity to E2F1 Inhibition in Glioblastoma

Author

Alvarado, Alvaro G., primary, Tessema, Kaleab, primary, Muthukrishnan, Sree Deepthi, primary, Sober, Mackenzie, primary, Kawaguchi, Riki, primary, Laks, Dan R., primary, Bhaduri, Aparna, primary, Swarup, Vivek, primary, Nathanson, David A., primary, Geschwind, Daniel H., primary, Goldman, Steven A., primary, and Kornblum, Harley I., primary

Published
2023
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87. Data from African Ancestry–Associated Gene Expression Profiles in Triple-Negative Breast Cancer Underlie Altered Tumor Biology and Clinical Outcome in Women of African Descent

Author

Martini, Rachel, primary, Delpe, Princesca, primary, Chu, Timothy R., primary, Arora, Kanika, primary, Lord, Brittany, primary, Verma, Akanksha, primary, Bedi, Deepa, primary, Karanam, Balasubramanyam, primary, Elhussin, Isra, primary, Chen, Yalei, primary, Gebregzabher, Endale, primary, Oppong, Joseph K., primary, Adjei, Ernest K., primary, Jibril Suleiman, Aisha, primary, Awuah, Baffour, primary, Muleta, Mahteme Bekele, primary, Abebe, Engida, primary, Kyei, Ishmael, primary, Aitpillah, Frances S., primary, Adinku, Michael O., primary, Ankomah, Kwasi, primary, Osei-Bonsu, Ernest Baawuah, primary, Chitale, Dhananjay A., primary, Bensenhaver, Jessica M., primary, Nathanson, David S., primary, Jackson, LaToya, primary, Petersen, Lindsay F., primary, Proctor, Erica, primary, Stonaker, Brian, primary, Gyan, Kofi K., primary, Gibbs, Lee D., primary, Monojlovic, Zarko, primary, Kittles, Rick A., primary, White, Jason, primary, Yates, Clayton C., primary, Manne, Upender, primary, Gardner, Kevin, primary, Mongan, Nigel, primary, Cheng, Esther, primary, Ginter, Paula, primary, Hoda, Syed, primary, Elemento, Olivier, primary, Robine, Nicolas, primary, Sboner, Andrea, primary, Carpten, John D., primary, Newman, Lisa, primary, and Davis, Melissa B., primary

Published
2023
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88. Supplementary Table from African Ancestry–Associated Gene Expression Profiles in Triple-Negative Breast Cancer Underlie Altered Tumor Biology and Clinical Outcome in Women of African Descent

Author

Martini, Rachel, primary, Delpe, Princesca, primary, Chu, Timothy R., primary, Arora, Kanika, primary, Lord, Brittany, primary, Verma, Akanksha, primary, Bedi, Deepa, primary, Karanam, Balasubramanyam, primary, Elhussin, Isra, primary, Chen, Yalei, primary, Gebregzabher, Endale, primary, Oppong, Joseph K., primary, Adjei, Ernest K., primary, Jibril Suleiman, Aisha, primary, Awuah, Baffour, primary, Muleta, Mahteme Bekele, primary, Abebe, Engida, primary, Kyei, Ishmael, primary, Aitpillah, Frances S., primary, Adinku, Michael O., primary, Ankomah, Kwasi, primary, Osei-Bonsu, Ernest Baawuah, primary, Chitale, Dhananjay A., primary, Bensenhaver, Jessica M., primary, Nathanson, David S., primary, Jackson, LaToya, primary, Petersen, Lindsay F., primary, Proctor, Erica, primary, Stonaker, Brian, primary, Gyan, Kofi K., primary, Gibbs, Lee D., primary, Monojlovic, Zarko, primary, Kittles, Rick A., primary, White, Jason, primary, Yates, Clayton C., primary, Manne, Upender, primary, Gardner, Kevin, primary, Mongan, Nigel, primary, Cheng, Esther, primary, Ginter, Paula, primary, Hoda, Syed, primary, Elemento, Olivier, primary, Robine, Nicolas, primary, Sboner, Andrea, primary, Carpten, John D., primary, Newman, Lisa, primary, and Davis, Melissa B., primary

Published
2023
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89. Supplementary Data from African Ancestry–Associated Gene Expression Profiles in Triple-Negative Breast Cancer Underlie Altered Tumor Biology and Clinical Outcome in Women of African Descent

Author

Martini, Rachel, primary, Delpe, Princesca, primary, Chu, Timothy R., primary, Arora, Kanika, primary, Lord, Brittany, primary, Verma, Akanksha, primary, Bedi, Deepa, primary, Karanam, Balasubramanyam, primary, Elhussin, Isra, primary, Chen, Yalei, primary, Gebregzabher, Endale, primary, Oppong, Joseph K., primary, Adjei, Ernest K., primary, Jibril Suleiman, Aisha, primary, Awuah, Baffour, primary, Muleta, Mahteme Bekele, primary, Abebe, Engida, primary, Kyei, Ishmael, primary, Aitpillah, Frances S., primary, Adinku, Michael O., primary, Ankomah, Kwasi, primary, Osei-Bonsu, Ernest Baawuah, primary, Chitale, Dhananjay A., primary, Bensenhaver, Jessica M., primary, Nathanson, David S., primary, Jackson, LaToya, primary, Petersen, Lindsay F., primary, Proctor, Erica, primary, Stonaker, Brian, primary, Gyan, Kofi K., primary, Gibbs, Lee D., primary, Monojlovic, Zarko, primary, Kittles, Rick A., primary, White, Jason, primary, Yates, Clayton C., primary, Manne, Upender, primary, Gardner, Kevin, primary, Mongan, Nigel, primary, Cheng, Esther, primary, Ginter, Paula, primary, Hoda, Syed, primary, Elemento, Olivier, primary, Robine, Nicolas, primary, Sboner, Andrea, primary, Carpten, John D., primary, Newman, Lisa, primary, and Davis, Melissa B., primary

Published
2023
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90. Supplementary Figure from African Ancestry–Associated Gene Expression Profiles in Triple-Negative Breast Cancer Underlie Altered Tumor Biology and Clinical Outcome in Women of African Descent

Author

Martini, Rachel, primary, Delpe, Princesca, primary, Chu, Timothy R., primary, Arora, Kanika, primary, Lord, Brittany, primary, Verma, Akanksha, primary, Bedi, Deepa, primary, Karanam, Balasubramanyam, primary, Elhussin, Isra, primary, Chen, Yalei, primary, Gebregzabher, Endale, primary, Oppong, Joseph K., primary, Adjei, Ernest K., primary, Jibril Suleiman, Aisha, primary, Awuah, Baffour, primary, Muleta, Mahteme Bekele, primary, Abebe, Engida, primary, Kyei, Ishmael, primary, Aitpillah, Frances S., primary, Adinku, Michael O., primary, Ankomah, Kwasi, primary, Osei-Bonsu, Ernest Baawuah, primary, Chitale, Dhananjay A., primary, Bensenhaver, Jessica M., primary, Nathanson, David S., primary, Jackson, LaToya, primary, Petersen, Lindsay F., primary, Proctor, Erica, primary, Stonaker, Brian, primary, Gyan, Kofi K., primary, Gibbs, Lee D., primary, Monojlovic, Zarko, primary, Kittles, Rick A., primary, White, Jason, primary, Yates, Clayton C., primary, Manne, Upender, primary, Gardner, Kevin, primary, Mongan, Nigel, primary, Cheng, Esther, primary, Ginter, Paula, primary, Hoda, Syed, primary, Elemento, Olivier, primary, Robine, Nicolas, primary, Sboner, Andrea, primary, Carpten, John D., primary, Newman, Lisa, primary, and Davis, Melissa B., primary

Published
2023
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93. Data from An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway

Author

Guo, Deliang, primary, Reinitz, Felicia, primary, Youssef, Mary, primary, Hong, Cynthia, primary, Nathanson, David, primary, Akhavan, David, primary, Kuga, Daisuke, primary, Amzajerdi, Ali Nael, primary, Soto, Horacio, primary, Zhu, Shaojun, primary, Babic, Ivan, primary, Tanaka, Kazuhiro, primary, Dang, Julie, primary, Iwanami, Akio, primary, Gini, Beatrice, primary, DeJesus, Jason, primary, Lisiero, Dominique D., primary, Huang, Tiffany T., primary, Prins, Robert M., primary, Wen, Patrick Y., primary, Robins, H. Ian, primary, Prados, Michael D., primary, DeAngelis, Lisa M., primary, Mellinghoff, Ingo K., primary, Mehta, Minesh P., primary, James, C. David, primary, Chakravarti, Arnab, primary, Cloughesy, Timothy F., primary, Tontonoz, Peter, primary, and Mischel, Paul S., primary

Published
2023
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94. Supplementary Figure Legend and Methods from Metabolomics Strategy Reveals Subpopulation of Liposarcomas Sensitive to Gemcitabine Treatment

Author

Braas, Daniel, primary, Ahler, Ethan, primary, Tam, Brenna, primary, Nathanson, David, primary, Riedinger, Mirielle, primary, Benz, Matthias R., primary, Smith, Kathleen B., primary, Eilber, Fritz C., primary, Witte, Owen N., primary, Tap, William D., primary, Wu, Hong, primary, and Christofk, Heather R., primary

Published
2023
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98. Data from Oncogenic EGFR Signaling Activates an mTORC2–NF-κB Pathway That Promotes Chemotherapy Resistance

Author

Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Nathanson, David, primary, Akhavan, David, primary, Guo, Deliang, primary, Gini, Beatrice, primary, Dang, Julie, primary, Zhu, Shaojun, primary, Yang, Huijun, primary, De Jesus, Jason, primary, Amzajerdi, Ali Nael, primary, Zhang, Yinan, primary, Dibble, Christian C., primary, Dan, Hancai, primary, Rinkenbaugh, Amanda, primary, Yong, William H., primary, Vinters, Harry V., primary, Gera, Joseph F., primary, Cavenee, Webster K., primary, Cloughesy, Timothy F., primary, Manning, Brendan D., primary, Baldwin, Albert S., primary, and Mischel, Paul S., primary

Published
2023
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99. Data from De-Repression of PDGFRβ Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients

Author

Akhavan, David, primary, Pourzia, Alexandra L., primary, Nourian, Alex A., primary, Williams, Kevin J., primary, Nathanson, David, primary, Babic, Ivan, primary, Villa, Genaro R., primary, Tanaka, Kazuhiro, primary, Nael, Ali, primary, Yang, Huijun, primary, Dang, Julie, primary, Vinters, Harry V., primary, Yong, William H., primary, Flagg, Mitchell, primary, Tamanoi, Fuyuhiko, primary, Sasayama, Takashi, primary, James, C. David, primary, Kornblum, Harley I., primary, Cloughesy, Tim F., primary, Cavenee, Webster K., primary, Bensinger, Steven J., primary, and Mischel, Paul S., primary

Published
2023
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100. Supplementary Material from Oncogenic EGFR Signaling Activates an mTORC2–NF-κB Pathway That Promotes Chemotherapy Resistance

Author

Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Nathanson, David, primary, Akhavan, David, primary, Guo, Deliang, primary, Gini, Beatrice, primary, Dang, Julie, primary, Zhu, Shaojun, primary, Yang, Huijun, primary, De Jesus, Jason, primary, Amzajerdi, Ali Nael, primary, Zhang, Yinan, primary, Dibble, Christian C., primary, Dan, Hancai, primary, Rinkenbaugh, Amanda, primary, Yong, William H., primary, Vinters, Harry V., primary, Gera, Joseph F., primary, Cavenee, Webster K., primary, Cloughesy, Timothy F., primary, Manning, Brendan D., primary, Baldwin, Albert S., primary, and Mischel, Paul S., primary

Published
2023
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