Data/hora: 10/06/2024 17:26:22

Provedor de dados: 	56	
País: 	Brazil	
Título: 	CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice	
Autores: 	Lange,A.P.; Almeida,L.Y.; Araújo Silva,C.L.; Scheucher,P.S.; Chahud,F.; Krause,A.; Bohlander,S.K.; Rego,E.M.	
Data: 	2019-01-01	
Ano: 	2019	
Palavras-chave: 	Leukemia; CEBPA; CALM/AF10; Transgenic mice.	
Resumo: 	Although rare, CALM/AF10 is a chromosomal rearrangement found in immature T-cell acute lymphoblastic leukemia (T-ALL), acute myeloid leukemia, and mixed phenotype acute leukemia of T/myeloid lineages with poor prognosis. Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). However, the relevance of CEBPA low expression for CALM/AF10 leukemogenesis has not yet been evaluated. We generated double mutant mice, which express the Lck-CALM/AF10 fusion gene and are haploinsufficient for the Cebpa gene. To characterize the hematopoiesis, we quantified hematopoietic stem cells, myeloid progenitor cells, megakaryocyte-erythrocyte progenitor cells, common myeloid progenitor cells, and granulocyte-macrophage progenitor cells. No significant difference was detected in any of the progenitor subsets. Finally, we tested if Cebpa haploinsufficiency would lead to the expansion of Mac-1+/B220+/c-Kit+ cells proposed as the CALM/AF10 leukemic progenitor. Less than 1% of bone marrow cells expressed Mac-1, B220, and c-Kit with no significant difference between groups. Our results showed that the reduction of Cebpa gene expression in Lck-CALM/AF10 mice did not affect their hematopoiesis or induce leukemia. Our data corroborated previous studies suggesting that the CALM/AF10 leukemia-initiating cells are early progenitors with lymphoid/myeloid differentiating potential.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2019000600604	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20198424	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.52 n.6 2019	
Fonte: 	info:eu-repo/semantics/openAccess