Localization of the human GM-CSF receptor β chain gene (CSF2RB) to chromosome 22q12.2→q13.1

1992 ◽  
Vol 61 (3) ◽  
pp. 175-177 ◽  
Author(s):  
Y. Shen ◽  
E. Baker ◽  
D.F. Callen ◽  
G.R. Sutherland ◽  
T.A. Willson ◽  
...  
Keyword(s):  
Gm Csf ◽  
1993 ◽  
Vol 90 (7) ◽  
pp. 2685-2689 ◽  
Author(s):  
H. Messier ◽  
T. Fuller ◽  
S. Mangal ◽  
H. Brickner ◽  
S. Igarashi ◽  
...  

Science ◽  
1989 ◽  
Vol 244 (4904) ◽  
pp. 551-556 ◽  
Author(s):  
M Hatakeyama ◽  
M Tsudo ◽  
S Minamoto ◽  
T Kono ◽  
T Doi ◽  
...  

Blood ◽  
1988 ◽  
Vol 72 (1) ◽  
pp. 234-240 ◽  
Author(s):  
P Fischer ◽  
E Nacheva ◽  
DY Mason ◽  
PD Sherrington ◽  
C Hoyle ◽  
...  

We describe the characterization of a new human cell line, Karpas 299 (K299), established from blast cells in the peripheral blood of a 25- year-old white man. His illness, which began with enlarged occipital and axillary nodes and weight loss, ended after 7 months with generalized lymphadenopathy, pleural effusion, and bone marrow involvement. A lymph node biopsy showed a large cell lymphoma mainly sinusoidal in distribution. The blast cells with pleomorphic nuclei resembled primitive histiocytes. The cells, which expressed the T-cell- associated markers CD4 and CD5, were positive for HLA-DR, epithelial membrane antigen, and CD30 (Ki-1 antigen). The karyotype was aneuploid and included a translocation 2;5. The site of translocation on chromosome 5 (at 5q35.1) is in the region of the locus of the c-fms oncogene (receptor of the monocyte-macrophage colony-stimulating factor MCSF or CSF-1). The cell line Karpas 299 has the same karyotype and pattern of antigen expression as the patient's cells. Northern blot analysis of RNA showed an active rearrangement of the T-cell receptor beta-chain gene. This is to our knowledge the first Ki-1 antigen- positive line to be established from a case of non-Hodgkin's lymphoma.


Leukemia ◽  
2021 ◽  
Author(s):  
Anne Charlet ◽  
Max Kappenstein ◽  
Philip Keye ◽  
Kathrin Kläsener ◽  
Cornelia Endres ◽  
...  

AbstractFLT3-ITD is the most predominant mutation in AML being expressed in about one-third of AML patients and is associated with a poor prognosis. Efforts to better understand FLT3-ITD downstream signaling to possibly improve therapy response are needed. We have previously described FLT3-ITD-dependent phosphorylation of CSF2RB, the common receptor beta chain of IL-3, IL-5, and GM-CSF, and therefore examined its significance for FLT3-ITD-dependent oncogenic signaling and transformation. We discovered that FLT3-ITD directly binds to CSF2RB in AML cell lines and blasts isolated from AML patients. A knockdown of CSF2RB in FLT3-ITD positive AML cell lines as well as in a xenograft model decreased STAT5 phosphorylation, attenuated cell proliferation, and sensitized to FLT3 inhibition. Bone marrow from CSF2RB-deficient mice transfected with FLT3-ITD displayed decreased colony formation capacity and delayed disease onset together with increased survival upon transplantation into lethally irradiated mice. FLT3-ITD-dependent CSF2RB phosphorylation required phosphorylation of the FLT3 juxtamembrane domain at tyrosines 589 or 591, whereas the ITD insertion site and sequence were of no relevance. Our results demonstrate that CSF2RB participates in FLT3-ITD-dependent oncogenic signaling and transformation in vitro and in vivo. Thus, CSF2RB constitutes a rational treatment target in FLT3-ITD-positive AML.


2004 ◽  
Vol 200 (1) ◽  
pp. 36-43 ◽  
Author(s):  
Robert E. Tillman ◽  
Andrea L. Wooley ◽  
Maureen M. Hughes ◽  
Bernard Khor ◽  
Barry P. Sleckman

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