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1. Full Text Mitochondrial Dysfunction in Normal and Malignant Hematopoiesis
by Schimmer, Aaron
Blood, ISSN 0006-4971, 11/2018, Volume 132, Issue Supplement 1, pp. SCI-11 - SCI-11
Abstract AML (Acute Myeloid Leukemia) is an aggressive hematologic malignancy with a high rate of relapse. Therefore, it is important to identify novel... 
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2. BAD as a prototype for a novel therapeutic agent for the treatment of acute leukemia
by Schimmer, Aaron D. (Aaron David)
ISBN 0612637336, 143 leaves.
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3. Full Text Inhibitor of apoptosis proteins: Translating basic knowledge into clinical practice
by Schimmer, Aaron D
Cancer Research, ISSN 0008-5472, 10/2004, Volume 64, Issue 20, pp. 7183 - 7190
The inhibitor of apoptosis proteins (IAPs) are a family of antiapoptotic proteins that bind and inhibit caspases 3, 7, and/or 9, but not caspase 8. Growing... 
CYTOCHROME-C | BACULOVIRUS INHIBITOR | SURVIVIN EXPRESSION | X-LINKED INHIBITOR | ONCOLOGY | STRUCTURAL BASIS | IN-VIVO | ENDOTHELIAL-CELLS | SERINE-PROTEASE | LUNG-CANCER CELLS | CASPASE ACTIVATION | Proteins - physiology | Animals | Caspases - metabolism | Inhibitor of Apoptosis Proteins | Isoenzymes | Humans | Apoptosis - physiology | Enzyme Activation | Caspase Inhibitors
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4. Full Text Anoikis resistance and tumor metastasis
by Simpson, Craig D and Anyiwe, Kika and Schimmer, Aaron D
Cancer Letters, ISSN 0304-3835, 2008, Volume 272, Issue 2, pp. 177 - 185
Abstract As a barrier to metastases, cells normally undergo apoptosis after they lose contact with their extra cellular matrix or their neighbouring cells.... 
Hematology, Oncology and Palliative Medicine | Anoikis | Caspase activation | Metastasis | TRIGGERS ANOIKIS | DOWN-REGULATION | INTESTINAL EPITHELIAL-CELLS | PROSTATE-CANCER METASTASIS | LUNG-CANCER | ONCOLOGY | BCL-2 PROTEIN FAMILY | DETACHMENT-INDUCED APOPTOSIS | EXTRACELLULAR-MATRIX | MOLECULAR-MECHANISMS | Receptors, Death Domain - metabolism | Mitochondria - enzymology | Neoplasm Metastasis | Caspases - metabolism | Humans | Mitochondria - metabolism | Enzyme Activation | Proteins | Medical research | Mortality | Ligands | Kinases | Prostate cancer | Apoptosis
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5. Full Text Mitochondrial Shapeshifting Impacts AML Stemness and Differentiation
by Schimmer, Aaron D
Cell Stem Cell, ISSN 1934-5909, 07/2018, Volume 23, Issue 1, pp. 3 - 4
In this issue of , demonstrate that leukemic stem cells (LSCs) have enhanced mitochondrial fission, which is positively regulated by FIS1. FIS1 is necessary to... 
CELLS | INHIBITION | ACUTE MYELOID-LEUKEMIA | CELL & TISSUE ENGINEERING | CELL BIOLOGY
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6. Full Text Mapping the cellular response to small molecules using chemogenomic fitness signatures
by Lee, Anna Y and St.Onge, Robert P and Proctor, Michael J and Wallace, Iain M and Nile, Aaron H and Spagnuolo, Paul A and Jitkova, Yulia and Gronda, Marcela and Wu, Yan and Kim, Moshe K and Cheung-Ong, Kahlin and Torres, Nikko P and Spear, Eric D and Han, Mitchell K. L and Schlecht, Ulrich and Suresh, Sundari and Duby, Geoffrey and Heisler, Lawrence E and Surendra, Anuradha and Fung, Eula and Urbanus, Malene L and Gebbia, Marinella and Lissina, Elena and Miranda, Molly and Chiang, Jennifer H and Aparicio, Ana Maria and Zeghouf, Mahel and Davis, Ronald W and Cherfils, Jacqueline and Boutry, Marc and Kaiser, Chris A and Cummins, Carolyn L and Trimble, William S and Brown, Grant W and Schimmer, Aaron D and Bankaitis, Vytas A and Nislow, Corey and Bader, Gary D and Giaever, Guri
Science, ISSN 0036-8075, 2014, Volume 344, Issue 6180, pp. 208 - 211
Genome-wide characterization of the in vivo cellular response to perturbation is fundamental to understanding how cells survive stress. Identifying the... 
YEAST | DRUG-INDUCED PHOSPHOLIPIDOSIS | PROTEIN | PATHWAY | MULTIDISCIPLINARY SCIENCES | GENES | DISCOVERY | GENOME | Cells - drug effects | Drug Evaluation, Preclinical - methods | Drug Resistance - genetics | Small Molecule Libraries - pharmacology | Pharmacogenetics | Saccharomyces cerevisiae - genetics | Humans | Cell Line, Tumor | Saccharomyces cerevisiae - drug effects | Gene Regulatory Networks | Genome-Wide Association Study - methods | Haploinsufficiency | Proteins | Molecules | Genetics | Cellular biology | Genomics
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7. Full Text A Multicenter Phase I/II Study of Obatoclax Mesylate Administered as a 3-or 24-Hour Infusion in Older Patients with Previously Untreated Acute Myeloid Leukemia
by Schimmer, AD and Raza, A and Carter, TH and Claxton, D and Erba, H and DeAngelo, DJ and Tallman, MS and Goard, C and Borthakur, G
PLOS ONE, ISSN 1932-6203, 10/2014, Volume 9, Issue 10, pp. e108694 - e108694
Purpose: An open-label phase I/II study of single-agent obatoclax determined a maximum tolerated dose (MTD) and schedule, safety, and efficacy in older... 
BCL-2 | APOPTOSIS | INHIBITION | PAN-BCL-2 FAMILY ANTAGONIST | GX15-070 | MCL-1 | MULTIDISCIPLINARY SCIENCES | RESISTANCE | CHRONIC LYMPHOCYTIC-LEUKEMIA | NAVITOCLAX | Blast Crisis - drug therapy | Blast Crisis - pathology | Demography | Drug Administration Schedule | Leukemia, Myeloid, Acute - pathology | Humans | Male | Treatment Outcome | Leukemia, Myeloid, Acute - blood | Platelet Count | Pyrroles - administration & dosage | Aged, 80 and over | Leukemia, Myeloid, Acute - drug therapy | Pyrroles - adverse effects | Female | Aged | Pyrroles - therapeutic use | Neutrophils - pathology | Schedules | Toxicity | Myeloid leukemia | Leukemia | Lung cancer | Cancer therapies | Patients | Subgroups | Infusion | Chemotherapy | Experimental design | Safety engineering | Medical prognosis | Reagents | Ataxia | Lymphomas | Safety | Acute myeloid leukemia | Apoptosis | Index Medicus
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8. Full Text An evidence-based review of obatoclax mesylate in the treatment of hematological malignancies
by Goard, Carolyn A and Schimmer, Aaron D
Core Evidence, ISSN 1555-1741, 03/2013, Volume 8, pp. 15 - 26
Obatoclax mesylate is an intravenously-administered drug under investigation in Phase I and II clinical trials as a novel anticancer therapeutic for... 
BCL-2 | Myelofibrosis | Obatoclax | Lymphoma | Leukemia | BH3 mimetic | Antimitotic agents | Reports | Dosage and administration | Lymphomas | Research | Antineoplastic agents | Drug therapy | Hematology | Cancer | Apoptosis | obatoclax | leukemia | myelofibrosis | lymphoma | Review
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9. Full Text MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells
by Bahat, Amir and Goldman, Andres and Zaltsman, Yehudit and Khan, Dilshad H and Halperin, Coral and Amzallag, Emmanuel and Krupalnik, Vladislav and Mullokandov, Michael and Silberman, Alon and Erez, Ayelet and Schimmer, Aaron D and Hanna, Jacob H and Gross, Atan
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 5132 - 11
The role of mitochondria dynamics and its molecular regulators remains largely unknown during naive-to-primed pluripotent cell interconversion. Here we report... 
TRANSITION | TARGET | HOMEOSTASIS | ACETYL-COA | METABOLISM | PATHWAY | MULTIDISCIPLINARY SCIENCES | DYNAMICS | MUSCLE | DIFFERENTIATION | FATE | Regulators | Embryo cells | Stem cell transplantation | Metabolism | Embryos | Proteins | Mitochondria | Stem cells | Dynamin | Acetylation | Fusion protein | Pluripotency | Elongation | Glutamine
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10. Full Text A 17-gene stemness score for rapid determination of risk in acute leukaemia
by Ng, Stanley W. K and Mitchell, Amanda and Kennedy, James A and Chen, Weihsu C and McLeod, Jessica and Ibrahimova, Narmin and Arruda, Andrea and Popescu, Andreea and Gupta, Vikas and Schimmer, Aaron D and Schuh, Andre C and Yee, Karen W and Bullinger, Lars and Herold, Tobias and Görlich, Dennis and Büchner, Thomas and Hiddemann, Wolfgang and Berdel, Wolfgang E and Wörmann, Bernhard and Cheok, Meyling and Preudhomme, Claude and Dombret, Hervé and Metzeler, Klaus and Buske, Christian and Löwenberg, Bob and Valk, Peter J. M and Zandstra, Peter W and Minden, Mark D and Dick, John E and Wang, Jean C. Y
Nature, ISSN 0028-0836, 12/2016, Volume 540, Issue 7633, pp. 433 - 437
Refractoriness to induction chemotherapy and relapse after achievement of remission are the main obstacles to cure in acute myeloid leukaemia (AML)(1). After... 
AML | SURVIVAL | GENE-EXPRESSION SIGNATURE | ADULT PATIENTS | GEMTUZUMAB OZOGAMICIN | PROPORTIONAL HAZARDS MODEL | RECOMMENDATIONS | MULTIDISCIPLINARY SCIENCES | REGULARIZATION PATHS | ACUTE MYELOID-LEUKEMIA | OUTCOMES | Prognosis | Risk Assessment | Leukemia, Myeloid, Acute - pathology | Humans | Transcriptome | Treatment Outcome | Gene Expression Regulation, Leukemic | Transplantation, Homologous | Stem Cell Transplantation | Xenograft Model Antitumor Assays | Algorithms | Animals | Leukemia, Myeloid, Acute - diagnosis | Neoplastic Stem Cells - metabolism | Survival Analysis | Neoplastic Stem Cells - pathology | Female | Mice | Leukemia, Myeloid, Acute - therapy | Cohort Studies | Leukemia, Myeloid, Acute - genetics | Leukemia | Genetic aspects | Nucleotide sequencing | Gene expression | Health aspects | Methods | DNA sequencing | Survival analysis | Chemotherapy | Genes | Mutation | Health risk assessment | Patients | Clinical outcomes
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11. Full Text Targeting p53 via JNK pathway: A novel role of RITA for apoptotic signaling in multiple myeloma
by Saha, Manujendra N and Jiang, Hua and Yang, Yijun and Zhu, Xiaoyun and Wang, Xiaoming and Schimmer, Aaron D and Qiu, Lugui and Chang, Hong
PLoS ONE, ISSN 1932-6203, 01/2012, Volume 7, Issue 1, p. e30215
The low frequency of p53 alterations e.g., mutations/deletions (similar to 10%) in multiple myeloma (MM) makes this tumor type an ideal candidate for... 
EFFICIENT APOPTOSIS | IN-VITRO | ACTIVATED PROTEIN-KINASE | ANTIMYELOMA ACTIVITY | MULTIDISCIPLINARY SCIENCES | N-TERMINAL KINASE | JUN NH2-TERMINAL KINASE | DEPENDENT APOPTOSIS | C-JUN | STRESS | SMALL-MOLECULE RITA | Cell Line | Cell Survival - drug effects | Apoptosis - drug effects | Furans - pharmacology | Humans | Tumor Suppressor Protein p53 - metabolism | Immunoblotting | JNK Mitogen-Activated Protein Kinases - metabolism | Multiple Myeloma - metabolism | Chromatin Immunoprecipitation | Signal Transduction - drug effects | Cell Line, Tumor | In Vitro Techniques | Real-Time Polymerase Chain Reaction | Chromatin | RNA | Genes | Analysis | Genetic aspects | Tumor proteins | Gene expression | Protein binding | Apoptosis | Drugs | Transcription factors | Phosphorylation | Substance abuse treatment | Immunoprecipitation | Nuclear magnetic resonance--NMR | Laboratories | p53 Protein | Leukemia | Genotoxicity | Multiple myeloma | Cytotoxicity | Feedback loops | Kinases | Positive feedback | Proteins | Angiogenesis | Signal transduction | Health care networks | Transcription activation | Life sciences | Inhibition | Medical research | Dexamethasone | Hematology | Tumor cells | Activator protein 1 | c-Jun protein | siRNA | Ribonucleic acid--RNA | Medicine | Signaling | Hospitals | DNA microarrays | Molecular modelling | Inhibitors | Cellular biology | Cell lines | Mutation | Disruption | Binding sites | Cancer | Nuclear magnetic resonance | Ribonucleic acid | NMR
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12. Full Text RB1 status in triple negative breast cancer cells dictates response to radiation treatment and selective therapeutic drugs
by Robinson, Tyler J. W and Liu, Jeff C and Vizeacoumar, Frederick and Sun, Thomas and Maclean, Neil and Egan, Sean E and Schimmer, Aaron D and Datti, Alessandro and Zacksenhaus, Eldad
PLoS ONE, ISSN 1932-6203, 11/2013, Volume 8, Issue 11, p. e78641
Triple negative breast cancer (TNBC) includes basal-like and claudin-low subtypes for which only chemotherapy and radiation therapy are currently available.... 
KINASE 4/6 INHIBITOR | INITIATING CELLS | BASAL-LIKE | PATHWAY DISRUPTION | PHASE-II TRIAL | NEOADJUVANT CHEMOTHERAPY | CONSERVING SURGERY | MULTIDISCIPLINARY SCIENCES | RETINOBLASTOMA TUMOR-SUPPRESSOR | ANTITUMOR-ACTIVITY | PD 0332991 | Methotrexate - pharmacology | Doxorubicin - therapeutic use | Pharmacogenetics | Oligonucleotide Array Sequence Analysis | Neoplasm Invasiveness | Neoplastic Stem Cells - drug effects | Humans | Retinoblastoma Protein - metabolism | Gamma Rays - therapeutic use | Retinoblastoma Protein - deficiency | Treatment Outcome | Antineoplastic Agents - therapeutic use | Methotrexate - therapeutic use | Triple Negative Breast Neoplasms - drug therapy | Triple Negative Breast Neoplasms - metabolism | Triple Negative Breast Neoplasms - pathology | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Triple Negative Breast Neoplasms - radiotherapy | Doxorubicin - pharmacology | Neoplastic Stem Cells - radiation effects | Anthracyclines | Chemotherapy | Stem cells | Radiation | Breast cancer | Methotrexate | Radiotherapy | Health aspects | Drug approval | Fluorouracil | Cancer | Drugs | Biotechnology | Phosphorylation | 5-Fluorouracil | Laboratories | Kinases | Cancer therapies | Doxorubicin | Proteins | CD44 antigen | Health care networks | Cell cycle | Epirubicin | Antineoplastic drugs | Radiation therapy | Patients | Cisplatin | Sensitivity | Hospitals | Fludarabine | Cell lines | Irradiation | Tumor suppressor genes | Mutation | Retinoblastoma | Tumors
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13. Full Text Inhibition of Mitochondrial Translation as a Therapeutic Strategy for Human Acute Myeloid Leukemia
by Škrtić, Marko and Sriskanthadevan, Shrivani and Jhas, Bozhena and Gebbia, Marinella and Wang, Zezhou and Wang, Jean C.Y and Wang, Xiaoming and Hurren, Rose and Jitkova, Yulia and Gronda, Marcela and Maclean, Neil and Lai, Courteney K and Eberhard, Yanina and Bartoszko, Justyna and Spagnuolo, Paul and Rutledge, Angela C and Datti, Alessandro and Ketela, Troy and Moffat, Jason and Robinson, Brian H and Cameron, Jessie H and Wrana, Jeffery and Eaves, Connie J and Minden, Mark D and Dick, John E and Humphries, Keith and Nislow, Corey and Giaever, Guri and Schimmer, Aaron D
Cancer Cell, ISSN 1535-6108, 2011, Volume 20, Issue 5, pp. 674 - 688
To identify FDA-approved agents targeting leukemic cells, we performed a chemical screen on two human leukemic cell lines and identified the antimicrobial... 
TRANSFORMATION | APOPTOSIS | ELONGATION-FACTOR TU | STEM-CELLS | TOPOISOMERASE-II | ONCOLOGY | INITIATION | GENOMIC ASSAYS | OXAZOLIDINONES | MEMBRANE POTENTIALS | PROTEIN-SYNTHESIS | CELL BIOLOGY | Minocycline - pharmacology | Neoplastic Stem Cells - drug effects | Humans | Minocycline - analogs & derivatives | Leukemia - drug therapy | Saccharomyces cerevisiae - drug effects | Mitochondrial Proteins - genetics | Mitochondria - drug effects | Genes, Mitochondrial | Animals | Peptide Elongation Factor Tu - genetics | Cell Line, Tumor | Protein Biosynthesis - drug effects | Antineoplastic Agents - pharmacology | Mice | RNA, Small Interfering | Developmental biology | Analysis | Children's hospitals | Oncology, Experimental | Genomics | Stem cells | Biosynthesis | Research | Health aspects | Cancer
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14. Full Text Novel mitochondrial mechanisms of cytarabine resistance in primary AML cells
by Schimmer, Aaron D
Cancer Discovery, ISSN 2159-8274, 07/2017, Volume 7, Issue 7, pp. 670 - 672
Farge and colleagues describe a novel in vivo approach to identify and study primary acute myeloid leukemia (AML) cells that persist in the marrow after... 
ONCOLOGY | ACUTE MYELOID-LEUKEMIA | Oxidative Phosphorylation - drug effects | Animals | Cytarabine - therapeutic use | Leukemia, Myeloid, Acute - pathology | Humans | Leukemia, Myeloid, Acute - drug therapy | Bone Marrow Cells - drug effects | Mice | Mitochondria - drug effects | Mitochondria - pathology | Drug Resistance, Neoplasm - drug effects
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