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Annals of Hematology, ISSN 0939-5555, 2/2018, Volume 97, Issue 2, pp. 309 - 317
This retrospective study attempts to establish if a correlation exists between osteoporosis and hematopoiesis before and after adjuvant chemotherapy in the... 
T-score | Hematology | TBS | Anemia | Bone marrow microenvironment | Oncology | Breast cancer | Graded toxicity of chemotherapy | Osteoporosis | Chemotherapy | Platelet | Medicine & Public Health | Trabecular bone score | Hematopoiesis | Stress hematopoiesis | Osteoblast | Neutrophil | Bone marrow adipocytes | Febrile neutropenia | SCORE TBS | BONE-MINERAL DENSITY | COLONY-STIMULATING FACTOR | POSTMENOPAUSAL WOMEN | HEMATOLOGY | STEM-CELLS | PREMENOPAUSAL WOMEN | COMPLEMENTARY APPROACH | MARROW NICHE | BLOOD-CELL COUNTS | CLINICAL-PRACTICE | Blood Platelets - immunology | Bone Density - immunology | Breast Neoplasms - immunology | Cell Count | Humans | Middle Aged | Adipocytes - drug effects | Antineoplastic Agents - administration & dosage | Hematopoiesis - drug effects | Bone Diseases, Metabolic - drug therapy | Bone Diseases, Metabolic - complications | Bone Marrow Cells - immunology | Osteoporosis - diagnostic imaging | Chemotherapy, Adjuvant | Neutropenia - immunology | Body Mass Index | Osteoporosis - immunology | Lumbar Vertebrae - diagnostic imaging | Neutrophils - drug effects | Bone Marrow Cells - pathology | Lumbar Vertebrae - drug effects | Absorptiometry, Photon | Breast Neoplasms - drug therapy | Hematopoiesis - immunology | Neutropenia - diagnostic imaging | Lumbar Vertebrae - pathology | Blood Platelets - pathology | Osteoporosis - drug therapy | Antineoplastic Agents - adverse effects | Neutropenia - pathology | Adult | Bone Marrow Cells - drug effects | Female | Retrospective Studies | Breast Neoplasms - diagnostic imaging | Blood Platelets - drug effects | Neutropenia - chemically induced | Adipocytes - immunology | Neutrophils - pathology | Bone Diseases, Metabolic - diagnostic imaging | Bone Diseases, Metabolic - immunology | Osteoblasts - drug effects | Neutrophils - immunology | Osteoblasts - immunology | Lumbar Vertebrae - immunology | Adipocytes - pathology | Breast Neoplasms - complications | Osteoblasts - pathology | Bone Density - drug effects | Osteoporosis - complications | Aged | Oncology, Experimental | Adjuvant treatment | Research | Cancer | Neutrophils | Index Medicus | Original
Journal Article
Journal of clinical oncology, ISSN 1527-7755, 2015, Volume 33, Issue 25, pp. 2803 - 2811
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 4, p. e61807
The Notch pathway can have both oncogenic and tumor suppressor roles, depending on cell context. For example, Notch signaling promotes T cell differentiation... 
PROMOTER DNA METHYLATION | LYMPHOMAS | TUMOR-SUPPRESSOR FUNCTION | MULTIDISCIPLINARY SCIENCES | ACUTE LYMPHOCYTIC-LEUKEMIA | GROWTH | GENES | TRANSCRIPTION | MALIGNANCIES | CANCER | TUMORIGENESIS | Transcription, Genetic - drug effects | Apoptosis - drug effects | Receptors, Notch - metabolism | Humans | Apoptosis - genetics | Receptors, Notch - genetics | Gene Expression Profiling | Hematopoiesis - drug effects | Basic Helix-Loop-Helix Transcription Factors - metabolism | T-Lymphocytes - metabolism | Serrate-Jagged Proteins | T-Lymphocytes - drug effects | B-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - blood | B-Lymphocytes - metabolism | Repressor Proteins - metabolism | Bone Marrow - drug effects | Jagged-1 Protein | Basic Helix-Loop-Helix Transcription Factors - genetics | Membrane Proteins - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia, B-Cell - pathology | Repressor Proteins - genetics | Hematopoiesis - genetics | Signal Transduction - genetics | Azacitidine - pharmacology | Leukemia, B-Cell - blood | Leukemia, B-Cell - genetics | Signal Transduction - drug effects | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Cell Line, Tumor | Histones - metabolism | DNA Methylation - drug effects | Calcium-Binding Proteins - genetics | Gene Silencing - drug effects | Blood Cells - metabolism | Cell Lineage - drug effects | Intercellular Signaling Peptides and Proteins - metabolism | Epigenesis, Genetic - drug effects | Membrane Proteins - metabolism | T-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology | Blood Cells - drug effects | Hydroxamic Acids - pharmacology | Cell Lineage - genetics | Calcium-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Azacitidine - analogs & derivatives | DNA Methylation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | B-Lymphocytes - drug effects | Bone Marrow - pathology | Receptor, Notch3 | Cell Proliferation - drug effects | Sulfites | Epigenetic inheritance | DNA microarrays | Genes | Genetic aspects | Genetic engineering | Acute lymphocytic leukemia | B cells | T cells | Methylation | Cell differentiation | Biotechnology | Transcription factors | Bisulfite | Pathogenesis | Leukemia | Differentiation (biology) | Lymphocytes T | Kinases | Inactivation | Signal transduction | Restoration | Lymphocytes | DNA methylation | Bone marrow | Tumorigenesis | Acetylation | Deoxyribonucleic acid--DNA | CpG islands | Acute lymphatic leukemia | Deactivation | Lymphatic leukemia | Tumor cell lines | Gene silencing | Signaling | Lymphocytes B | Regulatory mechanisms (biology) | Stem cells | Epigenetics | Ligands | Tumor suppressor genes | Leukemogenesis | Lymphomas | Notch protein | Aberration | Apoptosis | Cancer | Deoxyribonucleic acid | DNA
Journal Article
Nature communications, ISSN 2041-1723, 2016, Volume 7, Issue 1, p. 11037
Excessive activation of blood coagulation and neutrophil accumulation have been described in several human cancers. However, whether hypercoagulation and... 
COLON-CANCER | COMPLEMENT | ACTIVATION | RISK-FACTORS | VENOUS THROMBOEMBOLISM | COLORECTAL-CANCER | MULTIDISCIPLINARY SCIENCES | MOLECULAR-WEIGHT HEPARIN | MOUSE MODEL | EXTRACELLULAR DNA TRAPS | TISSUE FACTOR
Journal Article
Journal Article
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2011, Volume 332, Issue 6030, pp. 687 - 696
.... The data set allowed for an algorithmically driven assembly of related cell types defined by surface antigen expression, providing a superimposable map of cell signaling responses in combination with drug inhibition... 
T lymphocytes | Cytometry | Phosphorylation | RESEARCH ARTICLE | B lymphocytes | Stem cells | Cell lines | Bone marrow | Bone marrow cells | Cells | Hematopoietic stem cells | STEM-CELLS | ACTIVATION | LYMPHOCYTE | MULTIDISCIPLINARY SCIENCES | MYELOGENOUS LEUKEMIA | TYROSINE KINASE INHIBITOR | FLOW-CYTOMETRY | DASATINIB | IDENTIFICATION | QUANTITATIVE-ANALYSIS | SIGNALING NETWORKS | Lanthanoid Series Elements | Leukocytes, Mononuclear - metabolism | Flow Cytometry - methods | Humans | Antibodies | Lymphocyte Subsets - immunology | Lymphocyte Subsets - metabolism | T-Lymphocytes - metabolism | Hematopoiesis | Single-Cell Analysis - methods | T-Lymphocytes - drug effects | Bone Marrow Cells - immunology | Leukocytes, Mononuclear - immunology | Mass Spectrometry | Bone Marrow Cells - drug effects | B-Lymphocytes - metabolism | Dasatinib | Leukocytes, Mononuclear - drug effects | Cytokines - metabolism | Bone Marrow Cells - cytology | Lymphocyte Activation | Lymphocyte Subsets - drug effects | Immunophenotyping | Pyrimidines - pharmacology | Transition Elements | B-Lymphocytes - drug effects | Algorithms | B-Lymphocytes - immunology | Signal Transduction - drug effects | T-Lymphocytes - immunology | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Antigens, Surface - analysis | Bone Marrow Cells - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Evaluation | Flow cytometry | Immune response | Research | Immunopharmacology | Methods
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2015, Volume 112, Issue 31, pp. 9638 - 9643
Journal Article
PLoS medicine, ISSN 1549-1676, 2006, Volume 3, Issue 7, pp. e270 - 1151
The JAK2V617F allele has recently been identified in patients with polycythemia vera (PV), essential thrombocytosis (ET), and myelofibrosis with myeloid... 
Recombinant Fusion Proteins - adverse effects | Humans | Myeloproliferative Disorders - pathology | Mutation, Missense | Primary Myelofibrosis - pathology | Receptors, Cytokine - physiology | Janus Kinases - physiology | Bone Marrow Transplantation | Hematopoiesis - physiology | Myeloid Cells - drug effects | Transcription, Genetic | Colony-Forming Units Assay | Phosphorylation - drug effects | mRNA Cleavage and Polyadenylation Factors - genetics | Hematologic Neoplasms - physiopathology | Disease Models, Animal | Cells, Cultured - drug effects | Bone Marrow Cells - pathology | Hematopoiesis - genetics | Signal Transduction - genetics | Thrombocytosis - etiology | Sequence Analysis, DNA | Cell Division - drug effects | mRNA Cleavage and Polyadenylation Factors - physiology | Receptor, Platelet-Derived Growth Factor alpha - physiology | Hematologic Neoplasms - drug therapy | Mice | Mice, Inbred BALB C | Myeloid Cells - pathology | Protein Processing, Post-Translational - genetics | Myeloproliferative Disorders - genetics | Oncogene Proteins, Fusion - physiology | STAT Transcription Factors - physiology | Protein Processing, Post-Translational - drug effects | Cells, Cultured - pathology | Bone Marrow Cells - drug effects | Spleen - pathology | Thrombocytosis - pathology | Gene Expression Regulation | Janus Kinases - antagonists & inhibitors | Point Mutation | Megakaryocytes - pathology | Primary Myelofibrosis - genetics | Animals | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Receptor, Platelet-Derived Growth Factor alpha - genetics | Myeloproliferative Disorders - etiology | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Genetic Vectors | Megakaryocytes - drug effects | Cytokines - pharmacology | Amino Acid Substitution | Thrombocytosis - genetics | Genetic aspects | Myelofibrosis | Research | Hematology | Gene Therapy | Genomics | Genetics | Oncology | Cancer Biology | Hematology (including Blood Transfusion)
Journal Article
Brain, behavior, and immunity, ISSN 0889-1591, 2016, Volume 51, pp. 154 - 168
Highlights • Classical benzodiazepines ameliorated stress-induced neuroimmune responses. • Lorazepam and clonazepam blocked stress-induced neuroinflammatory... 
Psychiatry | Allergy and Immunology | Anxiety-like behavior | Social avoidance | Social defeat | Benzodiazepines | Psychosocial stress | Microglia | ACTIVATION | MONOCYTE TRAFFICKING | ANXIETY | PSYCHIATRY | IMMOBILIZATION STRESS | RECEPTOR | AGED MICE | IMMUNOLOGY | INTERLEUKIN-6 | NEUROSCIENCES | DEFEAT STRESS | GABA | GLUCOCORTICOID RESISTANCE | Anti-Anxiety Agents - administration & dosage | Male | Hippocampus - drug effects | RNA, Messenger - metabolism | Stress, Psychological - immunology | Hematopoiesis - drug effects | Microglia - immunology | Granulocytes - drug effects | Interleukin-6 - blood | Splenomegaly - etiology | Behavior, Animal - drug effects | Corticosterone - blood | Hypothalamus - drug effects | Bone Marrow - drug effects | Hypothalamus - immunology | Clonazepam - administration & dosage | Hippocampus - immunology | Microglia - drug effects | Mice, Inbred C57BL | GABA Modulators - administration & dosage | Splenomegaly - prevention & control | Lorazepam - administration & dosage | Corticotropin-Releasing Hormone - metabolism | Anxiety - immunology | Brain - drug effects | Monocytes - drug effects | Animals | Mice | CD11b Antigen - metabolism | Brain - immunology | Anxiety - etiology | Stress, Psychological - complications | Stress management | Lorazepam | Clonazepam | psychosocial stress | benzodiazepines | anxiety-like behavior | social avoidance | social defeat | microglia
Journal Article
Blood, ISSN 1528-0020, 2017, Volume 130, Issue 6, pp. 699 - 712
Journal Article