Abstract:
:Adoptive immunotherapy using chimeric antigen receptor (CAR) expressing T cells targeting the CD19 B lineage receptor has demonstrated marked success in relapsed pre-B-cell acute lymphoblastic leukaemia (ALL). Persisting CAR-T cells generate sustained pressure against CD19 that may drive unique mechanisms of resistance. Pre-B ALL originates from a committed pre-B cell or an earlier progenitor, with potential to reprogram into other hematopoietic lineages. Here we report changes in lineage markers including myeloid conversion in patients following CD19 CAR therapy. Using murine ALL models we study the long-term effects of CD19 CAR-T cells and demonstrate partial or complete lineage switch as a consistent mechanism of CAR resistance depending on the underlying genetic oncogenic driver. Deletion of Pax5 or Ebf1 recapitulates lineage reprogramming occurring during CD19 CAR pressure. Our findings establish lineage switch as a mechanism of CAR resistance exposing inherent plasticity in genetic subtypes of pre-B-cell ALL.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Jacoby E,Nguyen SM,Fountaine TJ,Welp K,Gryder B,Qin H,Yang Y,Chien CD,Seif AE,Lei H,Song YK,Khan J,Lee DW,Mackall CL,Gardner RA,Jensen MC,Shern JF,Fry TJdoi
10.1038/ncomms12320subject
Has Abstractpub_date
2016-07-27 00:00:00pages
12320issn
2041-1723pii
ncomms12320journal_volume
7pub_type
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