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International Journal of Hematology, ISSN 0925-5710, 9/2017, Volume 106, Issue 3, pp. 326 - 327
To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s12185-017-2301-6 Byline:... 
Medicine & Public Health | Hematology | Oncology | HEMATOLOGY | College teachers | DNA repair | DNA damage | DNA | Immunology | Deoxyribonucleic acid--DNA
Journal Article
Journal Article
[Rinshō ketsueki] The Japanese journal of clinical hematology, ISSN 0485-1439, 10/2014, Volume 55, Issue 10, pp. 2233 - 2241
Journal Article
Journal Article
International Journal of Hematology, ISSN 0925-5710, 1/2013, Volume 97, Issue 1, pp. 1 - 2
Byline: Shuki Mizutani (1) Author Affiliation: (1) Department of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, 1-5-45 Yushima,... 
Medicine & Public Health | Hematology | Oncology | HEMATOLOGY | Humans | Adolescent | Child, Preschool | Infant | Hematologic Neoplasms - genetics | Child | Infant, Newborn | Developmental biology | Genetic aspects
Journal Article
Journal Article
Journal Article
Immunity, ISSN 1074-7613, 2006, Volume 25, Issue 5, pp. 745 - 755
Journal Article
International Journal of Hematology, ISSN 0925-5710, 9/2014, Volume 100, Issue 3, pp. 260 - 265
Myeloid cell differentiation is the process by which stem cells develop into mature monocytes or granulocytes. This process is achieved by the sequential... 
XAB2 | Oncology | Nucleotide excision repair | Medicine & Public Health | Hematology | Myeloid differentiation | PROTEIN | HETEROCHROMATIN | GENE-EXPRESSION | DNA-REPAIR | HEMATOLOGY | TRANSCRIPTION-COUPLED REPAIR | ACUTE PROMYELOCYTIC LEUKEMIA | Granulocytes - cytology | Leukemia, Promyelocytic, Acute - pathology | Luciferases - metabolism | Apoptosis - drug effects | Monocytes - cytology | Humans | Leukemia, Myeloid, Acute - metabolism | Monocytes - metabolism | DNA Repair - genetics | Luciferases - genetics | Leukemia, Promyelocytic, Acute - metabolism | Granulocytes - drug effects | Transcription, Genetic | Antineoplastic Agents - pharmacology | Cell Differentiation | Granulocytes - metabolism | Genes, Reporter | Tretinoin - pharmacology | Hematopoietic Stem Cells - drug effects | DNA Repair - drug effects | Signal Transduction | Leukemia, Myeloid, Acute - pathology | Transcription Factors - antagonists & inhibitors | Hematopoietic Stem Cells - metabolism | Cisplatin - pharmacology | Gene Expression Regulation, Leukemic | Transcription Factors - genetics | Monocytes - drug effects | Transcription Factors - metabolism | Hematopoietic Stem Cells - cytology | Cell Line, Tumor | Leukemia, Promyelocytic, Acute - genetics | Leukemia, Myeloid, Acute - genetics | Anthracyclines | Crosslinked polymers | Developmental biology | Leukemia | Stem cells | Cell differentiation | DNA repair | Tretinoin
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2015, Volume 10, Issue 12, p. e0144540
Etoposide, a topoisomerase 2 (TOP2) inhibitor, is associated with the development of KMT2A (MLL)-rearranged infant leukemia. An epidemiological study suggested... 
MLL GENE | INFANT-LEUKEMIA | IN-VITRO | ETOPOSIDE | THERAPY | MECHANISM | MULTIDISCIPLINARY SCIENCES | ATM | CLEAVAGE | ATAXIA-TELANGIECTASIA | EXPRESSION | Gene Rearrangement - drug effects | Leukemia - pathology | Liver - embryology | Maternal Exposure | DNA Breaks, Double-Stranded - drug effects | Liver - drug effects | Chromosome Breakage - drug effects | Female | Leukemia - genetics | Hematopoietic Stem Cells - drug effects | Histone-Lysine N-Methyltransferase - genetics | Mice, Inbred C57BL | Injections, Intraperitoneal | Etoposide - pharmacology | Etoposide - administration & dosage | Hematopoietic Stem Cells - metabolism | Mice, Knockout | Carcinogenesis - pathology | Fetus - cytology | Animals | Bone Marrow Cells | Myeloid-Lymphoid Leukemia Protein - genetics | DNA Damage | Histones - metabolism | Cell Cycle - drug effects | Complications and side effects | DNA damage | Leukemia | Physiological aspects | Etoposide | Genetic aspects | Dosage and administration | Research | Hematopoietic stem cells | Risk factors | Pediatrics | Chromatin | Immunoprecipitation | Liver | Science | Stem cell transplantation | Leukocytes (mononuclear) | mRNA | Epidemiology | Gene sequencing | Cell cycle | Bone marrow | Ataxia | Deoxyribonucleic acid--DNA | Translocation | Developmental biology | Fetuses | Exposure | Gene expression | Ribonucleic acid--RNA | Intrauterine exposure | Studies | Herbal medicine | Babies | Chemotherapy | Flavonoids | Inhibitors | Damage detection | Hepatocytes | Breakage | Stem cells | Mice | Mutation | Laboratory animals | Cancer | RNA | Deoxyribonucleic acid | Ribonucleic acid | DNA
Journal Article
Cancer Science, ISSN 1347-9032, 12/2016, Volume 107, Issue 12, pp. 1745 - 1754
The Ewing sarcoma breakpoint region 1 (EWSR1) gene is known to fuse with various partner genes to promote the development of the Ewing sarcoma family of tumors... 
senescence | Acute myelogenous leukemia | EWSR1 | TP53 | ELF5 | EWS GENE | RNA-BINDING PROTEIN | FAMILY | CHROMOSOME-TRANSLOCATION | ONCOLOGY | EWS-FLI1 | ACUTE LYMPHOBLASTIC-LEUKEMIA | EWINGS-SARCOMA TRANSLOCATION | ERG | GENE FUSION | TRANSCRIPTION FACTOR | NIH 3T3 Cells | RNA-Binding Proteins - genetics | Oncogene Proteins, Fusion - metabolism | Proto-Oncogene Proteins c-ets - genetics | Humans | Leukemia, Myeloid, Acute - metabolism | Transcriptome | Child, Preschool | Male | Gene Expression Profiling | Cell Transformation, Neoplastic - genetics | Female | Proto-Oncogene Proteins p21(ras) - agonists | Disease Models, Animal | Proto-Oncogene Proteins p21(ras) - metabolism | Calmodulin-Binding Proteins - genetics | Gene Expression | Chromosome Banding | Signal Transduction | Tumor Suppressor Protein p53 - metabolism | In Situ Hybridization, Fluorescence | Cell Transformation, Neoplastic - metabolism | Animals | Leukemia, Myeloid, Acute - diagnosis | Oncogene Proteins, Fusion - genetics | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Cell Line, Tumor | Mice | Mutation | Cell Line, Transformed | Leukemia, Myeloid, Acute - genetics | RNA-Binding Protein EWS | Chemotherapy | Sarcoma | RNA | Development and progression | Transplantation | Genetic transcription | Tumor proteins | Chromosomes | Hematopoietic stem cells | Cancer | Original
Journal Article
Cancer Letters, ISSN 0304-3835, 2016, Volume 386, pp. 131 - 140
Abstract Poly (ADP-ribose) polymerase (PARP) is an indispensable component of the DNA repair machinery. PARP inhibitors are used as cutting-edge treatments for... 
Hematology, Oncology and Palliative Medicine | Homologous recombination repair | TCF3-HLF | Acute lymphoblastic leukemia | PARP inhibitor | POLY(ADP-RIBOSE) POLYMERASE | ADVANCED SOLID TUMORS | ACUTE-LYMPHOBLASTIC-LEUKEMIA | DNA-DAMAGE RESPONSE | ONCOGENIC TRANSCRIPTION FACTORS | ONCOLOGY | E2A-HLF FUSION PROTEINS | MYELOID-LEUKEMIA | HOMOLOGOUS RECOMBINATION | B-LINEAGE LEUKEMIA | PHASE-I | Oncogene Proteins, Fusion - metabolism | Leukemia - pathology | Humans | Drug Resistance, Neoplasm | RNA, Messenger - metabolism | DNA Breaks, Double-Stranded | Dose-Response Relationship, Drug | Transfection | Time Factors | U937 Cells | BRCA1 Protein - metabolism | Female | Leukemia - genetics | Recombinational DNA Repair | Jurkat Cells | Leukemia - enzymology | RNA, Messenger - genetics | Leukemia - drug therapy | Gene Expression Regulation, Leukemic | Nerve Tissue Proteins - genetics | Piperazines - pharmacology | Nerve Tissue Proteins - metabolism | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Cell Lineage | Phthalazines - pharmacology | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Poly(ADP-ribose) Polymerases - metabolism | Oncogene Proteins, Fusion - genetics | K562 Cells | Medical colleges | Developmental biology | Analysis | Leukemia | B cells | Sugars | Monosaccharides | Immunoglobulins | Hematology | Cytotoxicity | Breast cancer | DNA repair | Proteins | Rodents | Medical prognosis | Fibroblasts | Lymphomas | Mutation | Deoxyribonucleic acid--DNA | Tumors | Apoptosis
Journal Article