| Autor: |
Gutierrez, Catherine, Ouspenskaia, Tamara, Fu, Doris, Waddicor, Peyton, Biran, Anat, Liani, Aviv, Lazarian, Gregory, Ten Hacken, Elisa, Witten, Elizabeth, Regis, Fara Faye, Joyal, Heather, Billington, Leah, Lucas, Fabienne, Zheng, Mei, Tye, Blake, Hernandez-Sanchez, Maria, Quijada Álamo, Miguel, Li, Shuqiang, Knisbacher, Binyamin A., Lin, Ziao, Al'Khafaji, Aziz, Wang, Lili, Livak, Kenneth J., Neuberg, Donna S., Cymbalista, Florence, Getz, Gad, Churchman, Stirling, Carrasco, Ruben D., Shao, Sichen, Regev, Aviv, Wu, Catherine J. |
| Zdroj: |
Blood; November 2020, Vol. 136 Issue: 1, Number 1 Supplement 1 p28-29, 2p |
| Abstrakt: |
Amongst the novel putative drivers identified by large-scale sequencing studies of chronic lymphocytic leukemia (CLL) is the ribosomal protein RPS15. Mutated in 5.3% of CLL, it co-occurs with heterozygous TP53alterations in 36% of RPS15-mutated samples. Mutation of this mediator of ribosome maturation and translation is associated with poor disease prognosis and enriched in cohorts with del(17p) and relapsed CLL, suggesting a role in disease progression and therapeutic resistance. However, the impact of RPS15mutation on B cell function and CLL development, in the presence or absence of TP53mutation, has yet to be characterized. To this end, we developed overexpression HG3 CLL cell lines modeling four common RPS15mutations (G134R, H137Y, S138F, and S139F) and a conditional knock-in mouse model of the S138F mutation with and without heterozygous Trp53deletion (generated by crossing Rps15and Trp53mutant mice with Cd19-Cre mice). |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
