| Autor: |
Ten Hacken, Elisa, Sewastianik, Tomasz, Redd, Robert A., Fell, Geoffrey, Uduman, Mohamed, Gruber, Michaela, Yin, Shanye, Clement, Kendell, Parry, Erin Michelle, Li, Shuqiang, Hernandez-Sanchez, Maria, Billington, Leah, Witten, Elizabeth, Baranowski, Kaitlyn J, Wang, Lili, Pinello, Luca, Livak, Kenneth J., Neuberg, Donna S., Carrasco, Ruben D., Wu, Catherine J. |
| Zdroj: |
Blood; November 2020, Vol. 136 Issue: 1, Number 1 Supplement 1 p2-3, 2p |
| Abstrakt: |
Although we have gained a wealth of knowledge from large-scale DNA sequencing studies across blood cancers, we still know little about the functional interplay of the discovered putative drivers in the generation of chronic lymphocytic leukemia (CLL) and its transformation into Richter's syndrome (RS). We have previously observed that CRISPR-Cas9 in vivoB-cell editing of common CLL loss-of-function (LOF) lesions (Atm, Trp53, Chd2, Birc3, Mga, Samhd1) can increase in vitroB cell fitness, but is not sufficient to sustain in vivoB cell survival after 12 months post-transplant. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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