NDLI: Loss of p19Arf in a Rag1−/− B-cell precursor population initiates acute B-lymphoblastic leukemia

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Loss of p19Arf in a Rag1−/− B-cell precursor population initiates acute B-lymphoblastic leukemia

Content Provider	Scilit
Author	Hauer, Julia Mullighan, Charles Morillon, Estelle Wang, Gary Bruneau, Julie Brousse, Nicole Lelorc'h, Marc Romana, Serge Pierrick Boudil, Amine Tiedau, Daniela Kracker, Sven Bushmann, Frederic D. Borkhardt, Arndt Fischer, Alain Bey-Abina, Salima Hacein- Cavazzana-Calvo, Marina
Copyright Year	2011
Description	In human B-acute lymphoblastic leukemia (B-ALL), RAG1-induced genomic alterations are important for disease progression. However, given that biallelic loss of the RAG1 locus is observed in a subset of cases, RAG1's role in the development of B-ALL remains unclear. We chose a p19Arf−/−Rag1−/− mouse model to confirm the previously published results concerning the contribution of CDKN2A (p19ARF /INK4a) and RAG1 copy number alterations in precursor B cells to the initiation and/or progression to B-acute lymphoblastic leukemia (B-ALL). In this murine model, we identified a new, Rag1-independent leukemia-initiating mechanism originating from a Sca1+CD19+ precursor cell population and showed that Notch1 expression accelerates the cells' self-renewal capacity in vitro. In human RAG1-deficient BM, a similar CD34+CD19+ population expressed p19ARF. These findings suggest that combined loss of p19Arf and Rag1 results in B-cell precursor leukemia in mice and may contribute to the progression of precursor B-ALL in humans.
Related Links	http://www.bloodjournal.org/content/118/3/544.full.pdf
Ending Page	553
Page Count	10
Starting Page	544
DOI	10.1182/blood-2010-09-305383
Journal	Blood
Issue Number	3
Volume Number	118
Language	English
Publisher	American Society of Hematology
Publisher Date	2011-07-21
Access Restriction	Open
Subject Keyword	Research and Experimental Medicine Acute Lymphoblastic Leukemia Rag1 P19arf Copy Number Human Cell Precursor Population Journal: Blood (Vol- 72, Issue- 3)
Content Type	Text
Resource Type	Article

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