Evidence for Inhibitory and Anti-Ouabain-Like Factors in Leukaemic Blood

1981 ◽  
Vol 61 (4) ◽  
pp. 391-397 ◽  
Author(s):  
M. A. Mir

1. At a high dilution in Ringer solution (1:200), leukaemic plasma significantly (P < 0.05) decreased the ouabain-sensitive and increased ouabain-insensitive components of sodium efflux from erythrocytes. At a low dilution (1:10) leukaemic plasma predominantly decreased the total and ouabain-insensitive component of sodium efflux (P < 0.01). 2. Erythrocytes from patients with leukaemia had a high affinity for the plasma factor which inhibited the total and ouabain-insensitive efflux (inhibitory factor). 3. Washings of leukaemic erythrocytes which had been incubated in leukaemic plasma contained a factor which significantly decreased the ouabain-sensitive and increased ouabain-insensitive components of sodium efflux (the anti-ouabain-like factor). 4. These studies show that leukaemic blood contains two factors which have opposite effects on sodium efflux from erythrocytes. These factors may contribute to the high incidence of multiple electrolyte disturbances in acute myeloid leukaemia.

1975 ◽  
Vol 48 (3) ◽  
pp. 213-218
Author(s):  
M. Afzal Mir ◽  
H. Bobinski

1. Sodium transport studies were performed in erythrocytes from normal subjects and from patients with acute myeloid leukaemia. Sodium influx and efflux rates were increased in erythrocytes from leukaemic patients. 2. The ouabain-sensitive component of sodium efflux was increased in leukaemic erythrocytes. 3. The high sodium efflux from leukaemic erythrocytes was decreased when the incubation media contained leukaemic plasma, suggesting the presence of an ouabain-like factor in the plasma. Paired experiments failed to show the presence of a similar factor in normal plasma. 4. Leukaemic erythrocytes showed a significantly greater ouabain uptake than the normal cells. 5. The results are discussed in relation to the widespread electrolyte disturbances in acute myeloid leukaemia.


2011 ◽  
Vol 155 (1) ◽  
pp. 125-128 ◽  
Author(s):  
Dinesh Rakheja ◽  
Sergej Konoplev ◽  
Mu Su ◽  
David Wheeler ◽  
Donna M. Muzny ◽  
...  

1991 ◽  
Vol 79 (2) ◽  
pp. 246-255 ◽  
Author(s):  
Jon M. Gerrard ◽  
Esther D. Israels ◽  
Agnes J. Bishop ◽  
Marlis L. Schroeder ◽  
Laura L. Beattie ◽  
...  

Author(s):  
C Ward ◽  
P Cauchy ◽  
DS Walton ◽  
ML Clarke ◽  
D Blakemore ◽  
...  

ABSTRACTThe transcription factor MYB plays a pivotal role in haematopoietic homeostasis and its aberrant expression is involved in the genesis and maintenance of acute myeloid leukaemia (AML). Our previous work has demonstrated that not all AML types display the same dependency on MYB expression and that MYB dependence is dictated by the nature of the driver mutation. However, whether this difference in MYB dependency is a general trend in AML still remains to be further elucidated. In this study, we investigate the importance of MYB in human leukaemia by performing siRNA-mediated knock-down in cell line models of AML with different driver lesions. We show that the characteristic reduction in proliferation and the concomitant induction of myeloid differentiation that is observed in MLL-fusion-driven leukaemia upon MYB suppression is not seen in AML cells with a complex karyotype. By performing transcriptome analysis, we demonstrate that a strong activation of MAFB expression driven by MYB ablation is restricted to MYB-dependent cells. In line with these observations, stratification of publicly available patient data reveals a reciprocal relationship between the expression of MYB and MAFB, highlighting a novel connection between those two factors in AML.


2019 ◽  
Vol 19 (4) ◽  
pp. 233-234
Author(s):  
Jorrit Schaefer ◽  
Sorcha Cassidy ◽  
Rachel M. Webster

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