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

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.

Flow cytometric analysis of peripheral blood neutrophil myeloperoxidase expression for ruling out myelodysplastic syndromes: a prospective validation study

2021 ◽  
Vol 100 (5) ◽  
pp. 1149-1158
Author(s):  
Tatiana Raskovalova ◽  
Marie-Christine Jacob ◽  
Claude-Eric Bulabois ◽  
Clara Mariette ◽  
Laura Scheffen ◽  
...  
Keyword(s):  
Validation Study ◽  
Myelodysplastic Syndromes ◽  
Peripheral Blood ◽  
Flow Cytometric Analysis ◽  
Blood Neutrophil ◽  
Peripheral Blood Neutrophil ◽  
Flow Cytometric

scholarly journals Normal peripheral blood neutrophil numbers accompanying ELANE whole gene deletion mutation

2019 ◽  
Vol 3 (16) ◽  
pp. 2470-2473 ◽  
Author(s):  
Marshall S. Horwitz ◽  
Mercy Y. Laurino ◽  
Siobán B. Keel
Keyword(s):  
Genome Editing ◽  
Peripheral Blood ◽  
Gene Deletion ◽  
Deletion Mutation ◽  
Blood Neutrophil ◽  
Normal Peripheral Blood ◽  
Peripheral Blood Neutrophil ◽  
Key Points ◽  
Patient Reported

Key Points The patient reported here, along with collective observations in the literature, suggest that ELANE deletion does not cause neutropenia. Potential therapeutic genome editing involving knockout of the mutant ELANE allele is therefore not expected to produce neutropenia.

The Peripheral Blood Neutrophil In Cystic Fibrosis Has An Altered Membrane Proteome Profile

2010 ◽  
Author(s):  
Elaine Hayes ◽  
David A. Bergin ◽  
Isabel Vega-Carrascal ◽  
Joanne Keenan ◽  
Martin Clynes ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Peripheral Blood ◽  
Blood Neutrophil ◽  
Membrane Proteome ◽  
Peripheral Blood Neutrophil ◽  
Proteome Profile

scholarly journals Detection of chromosome 20q deletions in bone marrow metaphases but not peripheral blood granulocytes in patients with myeloproliferative disorders or myelodysplastic syndromes

Blood ◽  
1996 ◽  
Vol 87 (4) ◽  
pp. 1561-1570 ◽  
Author(s):  
FA Asimakopoulos ◽  
TL Holloway ◽  
EP Nacheva ◽  
MA Scott ◽  
P Fenaux ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Myelodysplastic Syndromes ◽  
Peripheral Blood ◽  
Myeloproliferative Disorders ◽  
Pcr Analysis ◽  
Multipotent Progenitors ◽  
The Common ◽  
Polymerase Chain ◽  
A Minor

Myeloproliferative disorders and myelodysplastic syndromes arise in multipotent progenitors and may be associated with chromosomal deletions that can be detected in peripheral blood granulocytes. We present here seven patients with myeloproliferative disorders or myelodysplastic syndromes in whom a deletion of the long arm of chromosome 20 was detectable by G-banding and/or fluorescence in situ hybridization in most or all bone marrow metaphases. However, in each case, microsatellite polymerase chain reaction (PCR) using 15 primer pairs spanning the common deleted region on 20q showed that the deletion was absent from most peripheral blood granulocytes. The human androgen receptor clonality assay was used to show that the vast majority of peripheral blood granulocytes were clonal in all four female patients. This represents the first demonstration that the 20q deletion can arise as a second event in patients with pre-existing clonal granulopoiesis. Microsatellite PCR analysis of whole bone marrow from two patients was consistent with cytogenetic studies, a result that suggests that cytogenetic analysis was not merely selecting for a minor subclone of cells carrying the deletion. Furthermore, in one patient, the deletion was present in both erythroid and granulocyte/monocyte colonies. This implies that the absence of the deletion in most peripheral blood granulocytes did not reflect lineage restriction of the progenitors carrying the deletion but may instead result from other selective influences such as preferential retention/destruction within the bone marrow of granulocytes carrying the deletion.

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