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PLoS ONE, ISSN 1932-6203, 06/2012, Volume 7, Issue 6, p. e38614
A balanced pool of hematopoietic stem cells (HSCs) in bone marrow is tightly regulated, and this regulation is disturbed in hematopoietic malignancies such as chronic myeloid leukemia (CML... 
CLONAL ORIGIN | GENE | BONE-MARROW | BIOLOGY | COMMON LYMPHOID PROGENITORS | BINDING-PROTEIN ICSBP | PTEN | CHRONIC MYELOCYTIC-LEUKEMIA | MICE | DIFFERENTIATION | CHRONIC MYELOID-LEUKEMIA | Gamma Rays | Apoptosis - drug effects | Apoptosis - radiation effects | Neoplastic Stem Cells - drug effects | Interferon Regulatory Factors - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Hematopoietic Stem Cells - pathology | Proto-Oncogene Proteins c-kit - metabolism | Cell Lineage - drug effects | Antigens, CD - metabolism | Neoplastic Stem Cells - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Time Factors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | src-Family Kinases - metabolism | Neoplastic Stem Cells - pathology | Antigens, Ly - metabolism | Membrane Proteins - metabolism | Signal Transduction - radiation effects | Hematopoietic Stem Cells - radiation effects | Neoplastic Stem Cells - radiation effects | Hematopoietic Stem Cells - drug effects | Cell Survival - drug effects | Arachidonate 5-Lipoxygenase - metabolism | Receptors, Cell Surface - metabolism | Hematopoietic Stem Cells - metabolism | Piperazines - therapeutic use | Pyrimidines - pharmacology | Cell Survival - radiation effects | Imatinib Mesylate | Piperazines - pharmacology | Cell Lineage - radiation effects | Animals | Signal Transduction - drug effects | Pyrimidines - therapeutic use | HSP90 Heat-Shock Proteins - metabolism | Fluorouracil - pharmacology | Mice | Benzamides | Fusion Proteins, bcr-abl - metabolism | BCR protein | Regulations | Hsp90 protein | 5-Fluorouracil | Leukemia | Radiation | Stem cell transplantation | Cytotoxicity | Oncology | Blood | Medical schools | Hematopoietic stem cells | Allografts | Granulocytes | Bone marrow | Population | Fusion protein | Cell survival | Hematology | Myeloid leukemia | Heat shock proteins | Abl protein | Chronic myeloid leukemia | Gene expression | Survival | c-Kit protein | Medicine | Depletion | Stem cells | Apoptosis | Heat shock
Journal Article
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 2891 - 12
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2017, Volume 12, Issue 7, p. e0180895
The X-linked inhibitor of apoptosis (XIAP) is a viable molecular target for anticancer drugs that overcome apoptosis-resistance of malignant cells... 
CANCER-CELLS | AKT ACTIVITY | PATHWAY | MULTIDISCIPLINARY SCIENCES | XIAP EXPRESSION | THERAPEUTIC TARGET | DOWN-REGULATION | RESISTANCE | RECEPTOR | PROGNOSTIC-SIGNIFICANCE | CARCINOMA | Cell Survival - drug effects | Humans | Leukemia - drug therapy | Morpholines - pharmacology | Leukemia - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Mitochondria - drug effects | Membrane Potential, Mitochondrial - drug effects | Benzoquinones - pharmacology | Drug Synergism | Signal Transduction - drug effects | K562 Cells | X-Linked Inhibitor of Apoptosis Protein - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Cell proliferation | Cellular signal transduction | Research | X-linked inhibitor of apoptosis protein | Cancer cells | Cytochrome | Drugs | Cell culture | Biotechnology | Addition polymerization | Leukemia | XIAP protein | AKT protein | Activation | Drug resistance | Kinases | Caspase-3 | Cancer therapies | Proteins | Signal transduction | Mitochondria | Cell growth | Antitumor agents | Ribose | Cleavage | Membrane potential | Inhibition | Medical research | Immunoglobulins | Quinone | Caspase | Poly(ADP-ribose) polymerase | Inflammation | Gene expression | 1-Phosphatidylinositol 3-kinase | Cytochrome c | Polymerase | Gene silencing | Inhibitors | Caspase-9 | Apoptosis
Journal Article
Blood, ISSN 1528-0020, 2011, Volume 117, Issue 23, pp. 6287 - 6296
B-cell receptor (BCR) signaling is aberrantly activated in chronic lymphocytic leukemia (CLL). Bruton tyrosine kinase (BTK) is essential to BCR signaling and... 
B-CELLS | SURVIVAL | APOPTOSIS | ACTIVATION | FLUDARABINE PLUS CYCLOPHOSPHAMIDE | RITUXIMAB | LYMPHOMA | PROLIFERATION | INHIBITOR | HEMATOLOGY | EXPRESSION | T-Lymphocytes - enzymology | Apoptosis - drug effects | Humans | Tumor Necrosis Factor-alpha - genetics | Cell Survival - genetics | Apoptosis - genetics | Male | NF-kappa B - metabolism | Neoplasm Proteins - antagonists & inhibitors | Receptors, Antigen, B-Cell - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Neoplasm Proteins - genetics | Interleukin-6 - metabolism | Cell Survival - drug effects | Drug Screening Assays, Antitumor - methods | Interleukin-6 - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Gene Expression Regulation, Leukemic - drug effects | Pyrimidines - pharmacology | Leukemia, Lymphocytic, Chronic, B-Cell - enzymology | B-Cell Activating Factor - metabolism | CD40 Ligand - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Gene Expression Regulation, Enzymologic - genetics | Cell Line, Tumor | Receptors, Antigen, B-Cell - genetics | Mice | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Mitogen-Activated Protein Kinase 1 - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Gene Expression Regulation, Leukemic - genetics | Protein-Tyrosine Kinases - genetics | CD40 Ligand - metabolism | MAP Kinase Signaling System - genetics | Female | Interleukin-4 - genetics | Protein-Tyrosine Kinases - biosynthesis | Pyrazoles - pharmacology | B-Lymphocytes - enzymology | Neoplasm Proteins - biosynthesis | Interleukin-4 - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | MAP Kinase Signaling System - drug effects | NF-kappa B - genetics | B-Cell Activating Factor - genetics | Cell Proliferation - drug effects | Lymphoid Neoplasia
Journal Article
Blood, ISSN 0006-4971, 11/2007, Volume 110, Issue 10, pp. 3695 - 3705
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 2, p. e55934
... a potential treatment option for AML. Here we show that curcumin down-regulates DNMT1 expression in AML cell lines, both in vitro and in vivo, and in primary AML cells ex vivo... 
TARGET | DECITABINE | METHYLATION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | GENES | INHIBITORS | CANCER-THERAPY | ACETYLTRANSFERASE | HYPOMETHYLATION | DELIVERY | Humans | Leukemia, Myeloid, Acute - metabolism | Antineoplastic Agents - therapeutic use | Promoter Regions, Genetic - drug effects | Transcription Factor RelA - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | Caspases - metabolism | Leukemia, Myeloid, Acute - drug therapy | Female | Antineoplastic Agents - pharmacology | Tumor Cells, Cultured | Curcumin - therapeutic use | DNA (Cytosine-5-)-Methyltransferase 1 | Leukemia, Myeloid, Acute - pathology | Curcumin - pharmacology | Down-Regulation - drug effects | DNA (Cytosine-5-)-Methyltransferases - genetics | Animals | Sp1 Transcription Factor - genetics | Mice, Nude | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | G1 Phase Cell Cycle Checkpoints - drug effects | Leukemia, Myeloid, Acute - genetics | Prevention | Care and treatment | Methyltransferases | Genes | DNA | Dietary supplements | Genetic aspects | DNA binding proteins | Methylation | Cancer | Drugs | Biotechnology | Surgical implants | Regulators | Transcription factors | Drug delivery systems | Leukemia | Activation | Phosphatase | Cancer therapies | Cell cycle | DNA methylation | Curcumin | Pharmaceutical sciences | Deoxyribonucleic acid--DNA | Hematology | Internal medicine | Myeloid leukemia | Therapeutic applications | Medical treatment | DNMT1 protein | Gene expression | Sp1 protein | Medicine | Gene silencing | Diet | Medical prognosis | Pharmacy | Epigenetics | DNA methyltransferase | Tumor suppressor genes | In vivo methods and tests | Acute myeloid leukemia | Apoptosis | Tumors | Deoxyribonucleic acid
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2002, Volume 99, Issue 25, pp. 16220 - 16225
...) including the ability to self-renew and a predominantly G cell-cycle status. Thus, although conventional chemotherapy regimens often ablate actively cycling leukemic blast cells, the primitive LSC population is likely to be drug-resistant... 
Biological Sciences | Anthracyclines | Myeloid leukemia | Stem cells | Bone marrow | Specimens | Cultured cells | Viability | Blood | Hematopoietic stem cells | Apoptosis | ABILITY IN-VITRO | PROGENITOR CELLS | ACUTE NONLYMPHOCYTIC LEUKEMIA | HEMATOPOIETIC-CELL | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | ACUTE MYELOID-LEUKEMIA | NF-KAPPA-B | PROTEASOME INHIBITORS | CYCLE ANALYSIS | CANCER-THERAPY | Leukocytes - pathology | Neoplasm Transplantation | Antibiotics, Antineoplastic - pharmacology | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Neoplasm Proteins - physiology | Recombinant Fusion Proteins - physiology | Hematopoietic Stem Cells - pathology | I-kappa B Proteins - physiology | Idarubicin - pharmacology | Neoplasm Proteins - antagonists & inhibitors | Proteasome Endopeptidase Complex | I-kappa B Proteins - genetics | Leukemia, Myeloid - pathology | Tumor Suppressor Protein p53 - physiology | Neoplastic Stem Cells - pathology | Hematopoietic Stem Cells - drug effects | Cysteine Endopeptidases | Acute Disease | NF-kappa B - antagonists & inhibitors | Gene Expression Regulation, Leukemic - drug effects | Graft Survival | Mice, SCID | Multienzyme Complexes - antagonists & inhibitors | Leupeptins - pharmacology | Animals | Cysteine Proteinase Inhibitors - pharmacology | Alleles | Leukocytes - drug effects | Mice, Inbred NOD | Mice | Physiological aspects
Journal Article
Journal Article