A human genome editing-based MLL::AF4 B-cell ALL model recapitulates key cellular and molecular leukemogenic features.
Clara BuenoRaul Torres-RuízTalía Velasco-HernandezWilliam C EarnshawPaolo PetazziAlba Martinez-MorenoVirginia Carolina Rodríguez-CortezMeritxell VinyolesSandra CantilenaOwen WilliamsNerea Vega-GarcíaSandra Rodríguez-PeralesJosé Carlos SegoviaOscar Quintana-BustamanteAnindita RoyClaus MeyerRolf MarschalekAlastair L SmithThomas A MilneMario F FragaJuan Ramón Ramón TejedorPablo MenendezPublished in: Blood (2023)
The cellular ontogeny and location of the MLL-breakpoint influence the capacity of MLL-edited CD34+ HSPCs to initiate pro-B-ALL, and recapitulate the molecular features of MLL-AF4+ infant B-ALL patients. We provide key insights into the cellular-molecular leukemogenic determinants of MLL-AF4+ infant B-ALL.