scholarly journals Bone Marrow Dysplasia Present

2020 ◽  
Author(s):  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Dysplasia

Myelodysplastic syndromes/myeloproliferative overlap neoplasms

2020 ◽  
pp. 191-203
Author(s):  
Eric Padron ◽  
Tariq I. Mughal ◽  
David Sallman ◽  
Alan F. List
Keyword(s):  
Bone Marrow ◽  
Clinical Trials ◽  
Stem Cell ◽  
Myelodysplastic Syndromes ◽  
Peripheral Blood ◽  
Myeloproliferative Neoplasms ◽  
Bone Marrow Failure ◽  
Disease Outcomes ◽  
Genomic Landscape ◽  
Bone Marrow Dysplasia

The myelodysplastic/myeloproliferative neoplasms (MDS/MPN) are haematologically diverse stem cell malignancies sharing phenotypic features of both myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN) that display a paradoxical bone marrow phenotype hallmarked by myeloid proliferation in the context of bone marrow dysplasia and ineffective haematopoiesis. The unfolding MDS/MPN genomic landscape has revealed numerous mutations in signalling genes, such as CBL, JAK2, NRAS, KRAS, CSF3R, and others involving the spliceosome complex. These observations suggest that comutation of genes involved in dysplasia and bone marrow failure along with those of cytokine receptor signalling may, in part, explain the dual MDS/MPN phenotype. The respective MDS/MPN diseases are identified by the type of myeloid subset which predominates in the peripheral blood. Currently there are no standard treatment recommendations for most patients with MDS/MPN. To optimize efforts to improve the management and disease outcomes, it is essential to identify meaningful clinical and biologic endpoints and standardized response criteria for clinical trials.

Peripheral blood neutrophil morphology reflects bone marrow dysplasia in myelodysplastic syndromes

1995 ◽  
Vol 49 (2) ◽  
pp. 115-120 ◽  
Author(s):  
S. Widell ◽  
E. Hellström-Lindberg ◽  
Y. Kock ◽  
M. Lindberg ◽  
Å. Öst ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Myelodysplastic Syndromes ◽  
Peripheral Blood ◽  
Blood Neutrophil ◽  
Peripheral Blood Neutrophil ◽  
Bone Marrow Dysplasia

scholarly journals Reversible Bone Marrow Dysplasia in Patients with Systemic Lupus Erythematosus

2008 ◽  
Vol 47 (8) ◽  
pp. 737-742 ◽  
Author(s):  
Yumiko Oka ◽  
Junichi Kameoka ◽  
Yasuhiko Hirabayashi ◽  
Reiko Takahashi ◽  
Tomonori Ishii ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Bone Marrow ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Bone Marrow Dysplasia

Bone Marrow Dysplasia with Basophilic Cells in a Patient with Angiocentric Lymphoma

1998 ◽  
Vol 99 (2) ◽  
pp. 98-101 ◽  
Author(s):  
Akio Mori ◽  
Satoshi Hashino ◽  
Masahiro Imamura ◽  
Kaoru Kahata ◽  
Hiroshi Kawakami ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Angiocentric Lymphoma ◽  
Bone Marrow Dysplasia

The TNF-α 238A polymorphism is associated with susceptibility to persistent bone marrow dysplasia following chronic exposure to benzene

2007 ◽  
Vol 31 (11) ◽  
pp. 1479-1485 ◽  
Author(s):  
Ling Lv ◽  
Patrick Kerzic ◽  
Guowei Lin ◽  
A. Robert Schnatter ◽  
Liming Bao ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chronic Exposure ◽  
Tnf Α ◽  
Bone Marrow Dysplasia

scholarly journals SITE-1 protease ablation in the osterix-lineage results in bone marrow dysplasia with neutrophilia coupled to osteopenia

2020 ◽  
Vol 28 ◽  
pp. S110-S111
Author(s):  
D. Patra ◽  
J. Kim ◽  
Q. Zhang ◽  
E. Tycksen ◽  
L.J. Sandell
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Dysplasia

scholarly journals NUP98-HOXD13 transgenic mice develop a highly penetrant, severe myelodysplastic syndrome that progresses to acute leukemia

Blood ◽  
2005 ◽  
Vol 106 (1) ◽  
pp. 287-295 ◽  
Author(s):  
Ying-Wei Lin ◽  
Christopher Slape ◽  
Zhenhua Zhang ◽  
Peter D. Aplan
Keyword(s):  
Bone Marrow ◽  
Transgenic Mice ◽  
Acute Leukemia ◽  
Fusion Gene ◽  
Wide Spectrum ◽  
Chromosomal Translocations ◽  
Preclinical Model ◽  
Leukemic Transformation ◽  
Hematopoietic Stem ◽  
Bone Marrow Dysplasia

The myelodysplastic syndromes (MDSs) are a group of clonal hematopoietic stem-cell disorders characterized by ineffective hematopoiesis and dysplasia. A wide spectrum of genetic aberrations has been associated with MDS, including chromosomal translocations involving the NUP98 gene. Using a NUP98-HOXD13 fusion gene, we have developed a mouse model that faithfully recapitulates all of the key features of MDS, including peripheral blood cytopenias, bone marrow dysplasia, and apoptosis, and transformation to acute leukemia. The MDS that develops in NUP98-HOXD13 transgenic mice is uniformly fatal. Within 14 months, all of the mice died of either leukemic transformation or severe anemia and leucopenia as a result of progressive MDS. The NUP98-HOXD13 fusion gene inhibits megakaryocytic differentiation and increases apoptosis in the bone marrow, suggesting a mechanism leading to ineffective hematopoiesis in the presence of a hypercellular bone marrow. These mice provide an accurate preclinical model that can be used for the evaluation of MDS therapy and biology.

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