No abstract available.
Bone Marrow* ; Chimerism* ; Hematologic Neoplasms* ; Recurrence*

Bone marrow (BM) microenvironment appears to play an important role in the pathogenesis of hematological malignancies. Apart from soluble factors and direct cell-cell contact, the extracellular vesicles (EVs) were identified as a third mediator for cell communication within BM microenvironment. Recently, more and more evidences have demonstrated that EVs are also involved in the dysregulation of the BM microenvironment in patients with hematological malignancies. Therefore this review focuses on the biological characteristics of EVs, the clinical value of EVs as biomarkers, the BM microenvironment reprogramming in hematological malignancies by EVs, and the potential role of EVs in drug resistance and therapy of hematological malignancies.
Bone Marrow ; Cell Communication ; Extracellular Vesicles ; Hematologic Neoplasms ; Humans

BACKGROUND: One of major challenge of cytogenetics is to obtain qualitative metaphases to achieve a meaningful analysis. Methotrexate (MTX) synchronization and the Giant Cell Tumor-Conditioned Medium (GCT-CM) have been used to improve the metaphase preparation from hematopoietic malignancies. The purpose of this study is to determine Mitotic Index (MI) of bone marrow samples under several culture conditions that may improve the quality of chromosome preparation. METHODS: Sixty nine bone marrow samples were cultured into 3 groups by traditional methods. The first group was tested for the effect of cell concentration on MI. The second, for the effect of MTX concentration on MI. The third group was classified into 4 subgroups as follows: 1) MTX only in 24 hour culture 2) MTX and GCT-CM in 24 hour culture 3) 48 hour culture without MTX 4) 48 hour culture and GCT-CM. MI was calculated as the ratio of metaphase to interphase cells in 1000 cells. Quality of metaphase was evaluated by classified the metaphase cell into 3 types. RESULTS: The first and second groups revealed no relationship between cell concentration, amount of MTX and MI, respectively. The third group showed significant differences among four subgroups. The MI increased in subgroups using GCT-CM and in the 48 hour culture, with greatest increase in group using 48 hour culture and GCT-CM simultaneously. CONCLUSIONS: The use of GCT-CM medium and prolonged culture improved the quality of metaphase cells and MI. It is therefore beneficial to use these conditions in cytogenetic studies on bone marrow in hematologic disease.
Bone Marrow* ; Cytogenetics ; Giant Cells* ; Hematologic Diseases ; Hematologic Neoplasms ; Interphase ; Metaphase ; Methotrexate ; Mitotic Index*

OBJECTIVE: To explore whether thrombopoietin (TPO) can rescue megakaryopoiesis by protecting bone marrowderived endothelial progenitor cells (BM-EPCs) in patients receiving chemotherapy for hematological malignancies. METHODS: Bone marrow samples were collected from 23 patients with hematological malignancies 30 days after chemotherapy and from 10 healthy volunteers. BM-EPCs isolated from the samples were identified by staining for CD34, CD309 and CD133, and their proliferation in response to treatment with TPO was assessed using CCK8 assay. DiL-Ac-LDL uptake and FITC-UEA-I binding assay were performed to evaluate the amount of BM-EPCs from the subjects. Tube-formation and migration experiments were used for functional assessment of the BM-EPCs. The BM-EPCs with or without TPO treatment were co-cultured with human megakaryocytes, and the proliferation of the megakaryocytes was detected with flow cytometry. RESULTS: Flow cytometry indicated that the TPO-treated cells had high expressions of CD34, CD133, and CD309. CCK8 assay demonstrated that TPO treatment enhanced the proliferation of the BM-EPCs, and the optimal concentration of TPO was 100 μg/L. Double immunofluorescence assay indicated that the number of BM-EPC was significantly higher in TPO-treated group than in the control group. The TPO-treated BM-EPCs exhibited stronger tube-formation and migration abilities ( < 0.05) and more significantly enhanced the proliferation of co-cultured human megakaryocytes than the control cells ( < 0.05). CONCLUSIONS TPO can directly stimulate megakaryopoiesis and reduce hemorrhage via protecting the function of BM-EPCs in patients following chemotherapy for hematological malignancies.
Bone Marrow ; Bone Marrow Cells ; Cells, Cultured ; Hematologic Neoplasms ; Humans ; Megakaryocytes ; Thrombopoietin

No abstract available.
Hematologic Neoplasms

Hematologic Neoplasms

No abstract available.
Hematologic Neoplasms*

Blood eosinophilia can be classified as either familial or acquired. Familial eosinophilia is a rare autosomal dominant disorder characterized by a stable eosinophil count. Acquired eosinophilia is classified further into a primary or secondary phenomenon depending on whether eosinophils are considered integral to the underlying disease. Primary eosinophilia is considered clonal in the presence of either a cytogenetic abnormality or bone marrow histological evidence of classified hematologic malignancies. Causes of secondary eosinophilia include infections, allergic or immunologic disorders, and drugs. Idiopathic eosinophilia belongs to a category of primary eosinophilia, and this is a diagnosis of exclusion. Cases with eosinophilia that lack evidence of clonality may be diagnosed as idiopathic hypereosinophilic syndrome after all causes of reactive eosinophilia have been eliminated. Genetic mutations involving the platelet-derived growth receptor genes (PDGFRA and PDGFRB) have been pathogenetically linked to clonal eosinophilia, and their presence predicts the treatment response to imatinib. In this review, I will present a clinical summary of both familial and acquired eosinophilia with emphasis on recent developments in molecular pathogenesis and treatment.
Benzamides ; Bone Marrow ; Chromosome Aberrations ; Eosinophilia ; Eosinophils ; Hematologic Neoplasms ; Hypereosinophilic Syndrome ; Piperazines ; Pyrimidines ; Imatinib Mesylate

BACKGROUND: The most noted rearrangement identified in acute promyelocytic leukemia (APL) involves the PML and RARa genes, which results in the formation of the PML/RARa gene fusion. In the fluorescence in situ hybridization (FISH) for PML/RARa, the two signals may coincidentally overlap in normal nuclei. We investigated whether a new RARa rearrangement probe could discriminate the false-positive fusion signal of the PML/RARa translocation probe. METHODS: A total of 51 cases, which showed the results from 1% to the borderline level by PML/ RARa FISH, were re-tested with the RARa rearrangement probe. Also, we compared the RARa FISH with the PML/RARa FISH on 16 patients with newly diagnosed APL and performed the RARa FISH on 20 bone marrow specimens without hematologic malignancies in order to set up the cut-off value. RESULTS: The cut-off for the RARa FISH was determined as 1.02%. For patients with newly diagnosed APL, the PML/RARa FISH showed positive signals in 95.3+/-6.5% of the cells and RARa FISH showed positive signals in 97.0+/-7.0% (r=0.83). Of a total of 41 cases consisting of hematological disorders other than APL, five cases showed results equal to or greater than 5% with PML/RARa FISH and one case showed a positive result with RARa FISH. Of 10 follow-up APL cases, seven cases showed results equal to or greater than 5% with the PML/RARa FISH and four cases showed positive results with the RARa FISH. CONCLUSIONS: The cut-off value for the RARa FISH is 1.02% and we consider RARa FISH as the proper method for follow-up of APL.
Bone Marrow ; Fluorescence* ; Follow-Up Studies* ; Gene Fusion ; Hematologic Neoplasms ; Humans ; In Situ Hybridization* ; Leukemia, Promyelocytic, Acute*

The lymphoproliferative disease multiple myeloma and the myeloproliferative disease polycythemia vera have different pathogenic mechanisms and different natural courses. Thus, the concomitant development of these two diseases in the same individual is rare. In most previously reported cases of both diseases, one disease was assumed to be a secondary malignancy caused by chemotherapy for the other primary disease. Our case was diagnosed as smoldering myeloma based on increased bone marrow plasma cell numbers and monoclonal gammopathy during a regular follow-up visit for JAK2V617F mutation-positive polycythemia vera, which had not been treated except with phlebotomy. This case provides useful clues for understanding the pathogenesis of these two hematological malignancies and the association between them. Here, we report a case of polycythemia vera with a JAK2V617F mutation combined with smoldering myeloma and discuss the clinical significance and pathogenic association between these disorders of different lineages, along with a literature review.
Bone Marrow ; Follow-Up Studies ; Hematologic Neoplasms ; Multiple Myeloma ; Paraproteinemias ; Phlebotomy ; Plasma Cells ; Polycythemia ; Polycythemia Vera