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1. Neoplastic hematopathology
: an atlas and concise guide
by Dunphy, Cherie H
2013, ISBN 1936287633
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2. Full Text Human prostate cancer metastases target the hematopoietic stem cell niche to establish footholds in mouse bone marrow
by Shiozawa, Yusuke and Pedersen, Elisabeth A and Havens, Aaron M and Jung, Younghun and Mishra, Anjali and Joseph, Jeena and Kim, Jin Koo and Patel, Lalit R and Ying, Chi and Ziegler, Anne M and Pienta, Michael J and Song, Junhui and Wang, Jingcheng and Loberg, Robert D and Krebsbach, Paul H and Pienta, Kenneth J and Taichman, Russell S
Journal of Clinical Investigation, ISSN 0021-9738, 04/2011, Volume 121, Issue 4, pp. 1298 - 1312
HSC homing, quiescence, and self-renewal depend on the bone marrow HSC niche. A large proportion of solid tumor metastases are bone metastases, known to usurp... 
PROGENITOR CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | ADHESION | MOBILIZATION | GROWTH | MICE | INDUCTION | IDENTIFICATION | RECEPTORS | EXPRESSION | LINEAGE | Neoplasm Transplantation | Prostatic Neoplasms - pathology | Humans | Hematopoietic Stem Cells - pathology | Male | Transplantation, Heterologous | Mice, SCID | Bone Marrow Neoplasms - secondary | Osteoblasts - pathology | Animals | Bone Marrow Neoplasms - pathology | Models, Biological | Bone Marrow Transplantation | Cell Line, Tumor | Mice, Inbred NOD | Mice | Tissue Donors | Bone marrow | Genetic aspects | Metastasis | Research | Properties | Health aspects | Prostate cancer | Hematopoietic stem cells
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3. Full Text Proinflammatory S100 Proteins Regulate the Accumulation of Myeloid-Derived Suppressor Cells
by Sinha, Pratima and Okoro, Chinonyerem and Foell, Dirk and Freeze, Hudson H and Ostrand-Rosenberg, Suzanne and Srikrishna, Geetha
The Journal of Immunology, ISSN 0022-1767, 10/2008, Volume 181, Issue 7, pp. 4666 - 4675
Chronic inflammation is a complex process that promotes carcinogenesis and tumor progression; however, the mechanisms by which specific inflammatory mediators... 
INDUCED IMMUNE SUPPRESSION | IN-VITRO | TUMOR PROGRESSION | CANCER DEVELOPMENT | ENDOTHELIAL-CELLS | GENE-EXPRESSION | CARBOXYLATED GLYCANS | IMMUNOLOGY | NF-KAPPA-B | T-CELLS | GLYCATION END-PRODUCTS | Mammary Neoplasms, Experimental - immunology | Splenic Neoplasms - immunology | Calgranulin B - blood | Bone Marrow Neoplasms - immunology | Lung Neoplasms - pathology | Calgranulin A - blood | Calgranulin B - physiology | Calgranulin A - physiology | Calgranulin A - biosynthesis | Lung Neoplasms - secondary | Myeloid Cells - immunology | Mammary Neoplasms, Experimental - pathology | Inflammation Mediators - physiology | Calgranulin B - biosynthesis | Cells, Cultured | Inflammation Mediators - blood | Immunophenotyping | Mice, Transgenic | Bone Marrow Neoplasms - secondary | Lung Neoplasms - immunology | Animals | Bone Marrow Neoplasms - pathology | Splenic Neoplasms - pathology | Cell Line, Tumor | Myeloid Cells - metabolism | Mice | Mice, Inbred BALB C | Myeloid Cells - pathology | Chemotaxis, Leukocyte - immunology | Splenic Neoplasms - secondary
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4. Full Text ViSNE enables visualization of high dimensional single-cell data and reveals phenotypic heterogeneity of leukemia
by Amir, El-Ad David and Davis, Kara L and Tadmor, Michelle D and Simonds, Erin F and Levine, Jacob H and Bendall, Sean C and Shenfeld, Daniel K and Krishnaswamy, Smita and Nolan, Garry P and Pe'Er, Dana
Nature Biotechnology, ISSN 1087-0156, 06/2013, Volume 31, Issue 6, pp. 545 - 552
New high-dimensional, single-cell technologies offer unprecedented resolution in the analysis of heterogeneous tissues. However, because these technologies can... 
PROGENITORS | STEM-CELLS | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | MASS CYTOMETRY | BIOLOGY | NETWORKS | FLOW-CYTOMETRY | GUIDE | MINIMAL RESIDUAL DISEASE | HIERARCHY | Recurrence | Leukemia - pathology | Humans | Image Cytometry | Immunophenotyping | Neoplasm Recurrence, Local - diagnosis | Neoplasm Recurrence, Local - pathology | Cell Lineage | Bone Marrow Neoplasms - pathology | Single-Cell Analysis - methods | Biomarkers, Tumor - metabolism | Leukemia - diagnosis | Bone Marrow Neoplasms - diagnosis | Technology application | Flow cytometry | Usage | Leukemia | Cytology | Genetic aspects | Research | Computational biology | Genotype & phenotype | Biotechnology | Cellular biology
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5. Full Text Deletion of Tet2 in mice leads to dysregulated hematopoietic stem cells and subsequent development of myeloid malignancies
by Li, Zhe and Cai, Xiaoqiang and Cai, Chen-Leng and Wang, Jiapeng and Zhang, Wenyong and Petersen, Bruce E and Yang, Feng-Chun and Xu, Mingjiang
Blood, ISSN 0006-4971, 10/2011, Volume 118, Issue 17, pp. 4509 - 4518
TET2 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies including MDS, CMML, MPN, and AML. However, little is known regarding... 
MUTANT TET2 | 5-METHYLCYTOSINE | MOUSE | MYELOPROLIFERATIVE NEOPLASMS | 5-HYDROXYMETHYLCYTOSINE | MUTATIONS | SPECIFICATION | LEUKEMIA | MLL | HEMATOLOGY | T(10/11)(Q22,Q23) | Neoplasm Transplantation | Gene Expression Regulation, Neoplastic | Hematopoietic Stem Cells - pathology | Male | Green Fluorescent Proteins - genetics | Hematologic Neoplasms - pathology | Bone Marrow Neoplasms - genetics | DNA-Binding Proteins - metabolism | Gene Deletion | Genes, Tumor Suppressor - physiology | Female | Hematologic Neoplasms - metabolism | Disease Models, Animal | Proto-Oncogene Proteins - metabolism | DNA-Binding Proteins - physiology | Mice, Inbred C57BL | Proto-Oncogene Proteins - genetics | Hematopoietic Stem Cells - metabolism | DNA-Binding Proteins - genetics | Mice, Knockout | Animals | Bone Marrow Neoplasms - pathology | Proto-Oncogene Proteins - physiology | Hematologic Neoplasms - genetics | Mice | Plenary Paper | Myeloid Neoplasia
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6. Full Text JAK Inhibition Impairs NK Cell Function in Myeloproliferative Neoplasms
by Schönberg, Kathrin and Schönberg, Kathrin and Rudolph, Janna and Rudolph, Janna and Vonnahme, Maria and Vonnahme, Maria and Parampalli Yajnanarayana, Sowmya and Yajnanarayana, Sowmya Parampalli and Cornez, Isabelle and Cornez, Isabelle and Hejazi, Maryam and Hejazi, Maryam and Manser, Angela R and Manser, Angela R and Uhrberg, Markus and Uhrberg, Markus and Verbeek, Walter and Verbeek, Walter and Koschmieder, Steffen and Koschmieder, Steffen and Brümmendorf, Tim H and Brümmendorf, Tim H and Brossart, Peter and Brossart, Peter and Heine, Annkristin and Heine, Annkristin and Wolf, Dominik and Wolf, Dominik
Cancer research, ISSN 0008-5472, 06/2015, Volume 75, Issue 11, pp. 2187 - 2199
Ruxolitinib is a small-molecule inhibitor of the JAK kinases, which has been approved for the treatment of myelofibrosis, a rare myeloproliferative neoplasm... 
MYELOFIBROSIS | NATURAL-KILLER-CELLS | CYTOKINES | ONCOLOGY | VIRUS INFECTION | IN-VIVO | MUTATION | DISSEMINATED TUBERCULOSIS | PATIENT | FLOW-CYTOMETRY | RUXOLITINIB TREATMENT | Primary Myelofibrosis - drug therapy | Humans | Middle Aged | Male | Killer Cells, Natural - pathology | Primary Myelofibrosis - pathology | Bone Marrow Neoplasms - genetics | Neoplasms - drug therapy | Janus Kinase 3 - antagonists & inhibitors | Primary Myelofibrosis - genetics | Pyrazoles - administration & dosage | Bone Marrow Neoplasms - pathology | Neoplasms - genetics | Signal Transduction - drug effects | Janus Kinase 3 - genetics | Aged, 80 and over | Adult | Female | Aged | Bone Marrow Neoplasms - drug therapy | Cell Proliferation - drug effects | Killer Cells, Natural - drug effects | Neoplasms - pathology
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7. Full Text Revisions to the international neuroblastoma response criteria: A consensus statement from the National Cancer Institute clinical trials planning meeting
by Park, Julie R and Bagatell, Rochelle and Cohn, Susan L and Pearson, Andrew D and Villablanca, Judith G and Berthold, Frank and Burchill, Susan and Boubaker, Ariane and McHugh, Kieran and Nuchtern, Jed G and London, Wendy B and Seibel, Nita L and Lindwasser, O. Wolf and Maris, John M and Brock, Penelope and Schleiermacher, Gudrun and Ladenstein, Ruth and Matthay, Katherine K and Valteau-Couanet, Dominique
Journal of Clinical Oncology, ISSN 0732-183X, 08/2017, Volume 35, Issue 22, pp. 2580 - 2587
Purpose More than two decades ago, an international working group established the International Neuroblastoma Response Criteria (INRC) to assess treatment... 
INDUCTION CHEMOTHERAPY | ONCOLOGY | INRG TASK-FORCE | BONE-MARROW | METAIODOBENZYLGUANIDINE SCINTIGRAPHY | HIGH-RISK NEUROBLASTOMA | STEM-CELL TRANSPLANTATION | MINIMAL RESIDUAL DISEASE | PHASE-I | CHILDRENS ONCOLOGY GROUP | STAGE 4 NEUROBLASTOMA | Immunohistochemistry | 3-Iodobenzylguanidine | Soft Tissue Neoplasms - secondary | Bone Neoplasms - diagnostic imaging | Humans | Bone Neoplasms - secondary | Neuroblastoma - diagnostic imaging | Response Evaluation Criteria in Solid Tumors | Neuroblastoma - therapy | Positron-Emission Tomography | Bone Marrow Neoplasms - secondary | Consensus | Bone Marrow Neoplasms - pathology | Neuroblastoma - secondary | Soft Tissue Neoplasms - diagnostic imaging | Fluorodeoxyglucose F18 | Radiopharmaceuticals | Bone Marrow Neoplasms - diagnosis | Bone Marrow Neoplasms - chemistry | Special
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8. Full Text Two cases of histiocytic sarcoma with BCL2 translocations and occult or subsequent follicular lymphoma
by Fernandez-Pol, Sebastian and Bangs, Charles D., BS,CG(ASCP) and Cherry, Athena, PhD and Arber, Daniel A., MD and Gratzinger, Dita, MD, PhD
Human Pathology, ISSN 0046-8177, 2016, Volume 55, pp. 39 - 43
Summary Histiocytic sarcoma is rare and difficult to distinguish from histologic mimics such as myeloid sarcoma due to its relatively nonspecific... 
Pathology | Follicular lymphoma | BCL2 | Monocytic differentiation | Myeloid sarcoma | Histiocytic sarcoma | GENE REARRANGEMENTS | FREQUENCY | ACUTE MYELOID-LEUKEMIA | CELL SARCOMAS | PATHOLOGY | EXPRESSION | TRANSDIFFERENTIATION | Immunohistochemistry | Lymphoma, Follicular - chemistry | Translocation, Genetic | Lymphoma, Follicular - therapy | Prognosis | Humans | Middle Aged | Muscle Neoplasms - pathology | Male | Histiocytic Sarcoma - therapy | Liver Neoplasms - therapy | Bone Marrow Neoplasms - genetics | Liver Neoplasms - chemistry | Genes, Immunoglobulin Heavy Chain | Lymphoma, Large B-Cell, Diffuse - therapy | Muscle Neoplasms - therapy | Lymphoma, Follicular - genetics | Time Factors | Muscle Neoplasms - genetics | Lymphoma, Large B-Cell, Diffuse - chemistry | Female | Histiocytic Sarcoma - genetics | Liver Neoplasms - pathology | Histiocytic Sarcoma - pathology | Bone Marrow Neoplasms - chemistry | Bone Marrow Neoplasms - therapy | Genetic Predisposition to Disease | Liver Neoplasms - genetics | Lymphoma, Large B-Cell, Diffuse - pathology | Lymphoma, Follicular - pathology | Gene Fusion | In Situ Hybridization, Fluorescence | Bone Marrow Examination | Phenotype | Bone Marrow Neoplasms - pathology | Biopsy | Muscle Neoplasms - chemistry | Aged | Biomarkers, Tumor - genetics | Lymphoma, Large B-Cell, Diffuse - genetics | Proto-Oncogene Proteins c-bcl-2 - genetics | Sarcoma | Lymphomas | Bone marrow | Flow cytometry | Population | Leukemia
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9. Full Text Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice
by Walz, C and Ahmed, W and Lazarides, K and Betancur, M and Patel, N and Hennighausen, L and Zaleskas, VM and Van Etten, RA
BLOOD, ISSN 0006-4971, 04/2012, Volume 119, Issue 15, pp. 3550 - 3560
STAT5 proteins are constitutively activated in malignant cells from many patients with leukemia, including the myeloproliferative neoplasms (MPNs) chronic... 
STEM-CELLS | INDUCED TRANSFORMATION | LYMPHOID DEVELOPMENT | BONE-MARROW | BCR-ABL | EFFICIENT INDUCTION | GENE-EXPRESSION | HEMATOLOGY | LYMPHOBLASTIC-LEUKEMIA | CHRONIC MYELOID-LEUKEMIA | DNA-BINDING ACTIVITY | NIH 3T3 Cells | Genes, abl - genetics | Humans | STAT5 Transcription Factor - physiology | Myeloproliferative Disorders - pathology | Bone Marrow Neoplasms - genetics | Myeloproliferative Disorders - genetics | STAT5 Transcription Factor - genetics | STAT5 Transcription Factor - metabolism | Cell Transformation, Neoplastic - genetics | Myeloproliferative Disorders - metabolism | HEK293 Cells | Janus Kinase 2 - physiology | Genes, abl - physiology | Janus Kinase 2 - genetics | Mice, Transgenic | Mutation, Missense - physiology | Animals | Bone Marrow Neoplasms - pathology | Bone Marrow Neoplasms - metabolism | Phenylalanine - genetics | Valine - genetics | Mice | Mice, Congenic | Mice, Inbred BALB C | Cell Transformation, Neoplastic - pathology | Amino Acid Substitution
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10. Full Text Interleukin-6 in the bone marrow microenvironment promotes the growth and survival of neuroblastoma cells
by Ara, Tasnim and Song, Liping and Shimada, Hiroyuki and Keshelava, Nino and Russell, Heidi V and Metelitsa, Leonid S and Groshen, Susan G and Seeger, Robert C and DeClerck, Yves A
Cancer Research, ISSN 0008-5472, 01/2009, Volume 69, Issue 1, pp. 329 - 337
Neuroblastoma, the second most common solid tumor in children, frequently metastasizes to the bone marrow and the bone. Neuroblastoma cells present in the bone... 
MULTIPLE-MYELOMA | CANCER-CELLS | ONCOLOGY | SIGNALING PATHWAY | COLORECTAL-CANCER | TUMOR | OVARIAN-CANCER | HIGH-RISK NEUROBLASTOMA | STROMAL CELLS | MESENCHYMAL STEM-CELLS | IL-6 RECEPTOR | Apoptosis - drug effects | Stromal Cells - pathology | Humans | Bone Neoplasms - secondary | Cell Growth Processes - physiology | Bone Neoplasms - pathology | Bone Neoplasms - metabolism | Neuroblastoma - pathology | STAT3 Transcription Factor - metabolism | Cell Growth Processes - drug effects | Stromal Cells - metabolism | Bone Marrow Cells - pathology | Receptors, Interleukin-6 - biosynthesis | Recombinant Proteins - pharmacology | Mice, SCID | Bone Marrow Neoplasms - secondary | Animals | Bone Marrow Neoplasms - pathology | Interleukin-6 - pharmacology | Cell Line, Tumor | Interleukin-6 - biosynthesis | Mice, Inbred NOD | Mice | Neuroblastoma - metabolism | Apoptosis - physiology | Bone Marrow Cells - metabolism | Bone Marrow Neoplasms - mortality | neuroblastoma | apoptosis | STAT-3 | tumor microenvironment | cell proliferation | interleukin-6
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11. Full Text Myeloproliferative neoplasms with concurrent BCR-ABL1 translocation and JAK2 V617F mutation: A multi-institutional study from the bone marrow pathology group
by Soderquist, Craig R and Ewalt, Mark D and Czuchlewski, David R and Geyer, Julia T and Rogers, Heesun J and Hsi, Eric D and Wang, Sa A and Bueso-Ramos, Carlos E and Orazi, Attilio and Arber, Daniel A and Hexner, Elizabeth O and Babushok, Daria V and Bagg, Adam
Modern Pathology, ISSN 0893-3952, 05/2018, Volume 31, Issue 5, pp. 690 - 704
Myeloproliferative neoplasms arise from hematopoietic stem cells with somatically altered tyrosine kinase signaling. Classification of myeloproliferative... 
CHRONIC MYELOGENOUS LEUKEMIA | POLYCYTHEMIA-VERA | JAK2(V617F) MUTATION | BCR-ABL TRANSLOCATION | IMATINIB | PATIENT | JAK2V617F MUTATION | PATHOLOGY | ESSENTIAL THROMBOCYTHEMIA | CHRONIC MYELOID-LEUKEMIA | JAK2-V617F MUTATION | Humans | Middle Aged | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Male | Antineoplastic Agents - therapeutic use | Myeloproliferative Disorders - pathology | Primary Myelofibrosis - pathology | Bone Marrow Neoplasms - genetics | Myeloproliferative Disorders - genetics | Primary Myelofibrosis - blood | Myeloproliferative Disorders - blood | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Fusion Proteins, bcr-abl - blood | Aged, 80 and over | Female | Retrospective Studies | Janus Kinase 2 - antagonists & inhibitors | Primary Myelofibrosis - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - blood | Janus Kinase 2 - genetics | Myeloproliferative Disorders - drug therapy | Bone Marrow Neoplasms - blood | Enzyme Inhibitors - therapeutic use | Disease Progression | Fusion Proteins, bcr-abl - genetics | Primary Myelofibrosis - genetics | Bone Marrow Neoplasms - pathology | Multi-Institutional Systems | Bone Marrow - pathology | Fusion Proteins, bcr-abl - antagonists & inhibitors | Aged | Bone Marrow Neoplasms - drug therapy | Mutation | Janus Kinase 2 - blood | Tyrosine | BCR protein | Myelofibrosis | Myeloid leukemia | Chronic myeloid leukemia | Kinases | Hematopoietic stem cells | Disease resistance | Janus kinase 2 | Classification | Stem cells | Bone marrow | Protein-tyrosine kinase | Tumors
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12. Full Text Histiocytic cell neoplasms involving the bone marrow: summary of the workshop cases submitted to the 18th Meeting of the European Association for Haematopathology (EAHP) organized by the European Bone Marrow Working Group, Basel 2016
by Tzankov, A and Kremer, M and Leguit, R and Orazi, A and Walt, J. Van der and Gianelli, U and Hebeda, K.M
Annals of Hematology, ISSN 0939-5555, 2018, Volume 97, Issue 11, pp. 2117 - 2128
The bone marrow is a preferential site for both reactive and neoplastic histiocytic proliferations. The differential diagnosis ranges from reactive histiocyte... 
Bone marrow biopsy | EAHP workshop | Medicine & Public Health | Hematology | Oncology | Erdheim-Chester disease | Mutation | Myeloid neoplasm | Histiocytic sarcoma | ROSAI-DORFMAN-DISEASE | DENDRITIC CELL | CLASSIFICATION | FOLLICULAR LYMPHOMA | BRAF | MAP2K1 MUTATIONS | SARCOMA | JUVENILE XANTHOGRANULOMA | HEMATOLOGY | HIGH PREVALENCE | Congresses as Topic | Europe | Humans | Histiocytosis - metabolism | Mutation, Missense | Bone Marrow Neoplasms - genetics | Neoplasm Proteins - metabolism | Histiocytosis - therapy | Bone Marrow Neoplasms - pathology | MAP Kinase Signaling System - genetics | Societies, Medical | Bone Marrow Neoplasms - metabolism | Histiocytosis - genetics | Histiocytosis - pathology | Neoplasm Proteins - genetics | Bone Marrow Neoplasms - therapy | Amino Acid Substitution | Sarcoma | Conferences, meetings and seminars | Bone marrow | Tumors | Original
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13. Full Text Preventive or late administration of anti-NGF therapy attenuates tumor-induced nerve sprouting, neuroma formation, and cancer pain
by Jimenez-Andrade, Juan Miguel and Ghilardi, Joseph R and Castañeda-Corral, Gabriela and Kuskowski, Michael A and Mantyh, Patrick W
Pain, ISSN 0304-3959, 2011, Volume 152, Issue 11, pp. 2564 - 2574
As cancer cell colonies proliferate, undergo necrosis, and metastasize in bone, sensory and sympathetic nerve fibers also undergo a concomitant sprouting,... 
Neuroplasticity | Analgesia | Bone | Prostate cancer | DORSAL-HORN NEURONS | BONE METASTASES | SKELETAL PAIN | NEUROSCIENCES | CLINICAL NEUROLOGY | BREAKTHROUGH PAIN | BREAST-CANCER | MURINE MODEL | PROSTATE CARCINOMA | ANESTHESIOLOGY | HYPERALGESIA | QUALITY-OF-LIFE | GROWTH-FACTOR | Nervous System Neoplasms - drug therapy | Male | Transplantation, Heterologous | Nerve Growth Factor - antagonists & inhibitors | Nerve Growth Factor - immunology | Nervous System Neoplasms - blood supply | Pain - etiology | Nervous System Neoplasms - complications | Bone Marrow Neoplasms - complications | Disease Models, Animal | Prostatic Neoplasms - blood supply | Prostatic Neoplasms - pathology | Pain - prevention & control | Antibodies, Monoclonal - pharmacology | Neuroma - blood supply | Neuroma - drug therapy | Neoplasm Transplantation - methods | Animals | Bone Marrow Neoplasms - pathology | Mice, Nude | Dogs | Mice | Neuroma - complications | Prostatic Neoplasms - complications | Bone Marrow Neoplasms - blood supply | Care and treatment | Cancer | prostate cancer | bone | analgesia | neuroplasticity
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