Mitigation of chromosome loss in clinical CRISPR-Cas9-engineered T cells

Connor A. Tsuchida(University of California, San Francisco), Nadav Brandes(University of California, San Francisco), Raymund Bueno(University of California, San Francisco), Marena Trinidad(Innovative Genomics Institute), Thomas Mazumder(University of California, San Francisco), Bingfei Yu(Parker Institute for Cancer Immunotherapy), Byungjin Hwang(University of California, San Francisco), Christopher Chang(Gladstone Institutes), Jamin Liu(University of California, San Francisco), Yang Sun(University of California, San Francisco), Caitlin R. Hopkins(Parker Institute for Cancer Immunotherapy), Kevin R. Parker(Stanford University), Yanyan Qi(Stanford University), Laura Hofman(Utrecht University), Ansuman T. Satpathy(Gladstone Institutes), Edward A. Stadtmauer(University of Pennsylvania), J.H.D. Cate(QB3), Justin Eyquem(Gladstone Institutes), Joseph A. Fraietta(Parker Institute for Cancer Immunotherapy), Carl H. June(Parker Institute for Cancer Immunotherapy), Howard Y. Chang(Howard Hughes Medical Institute), Chun Ye(Gladstone Institutes), Jennifer A. Doudna(QB3)
Cell
October 1, 2023
Cited by 184Open Access
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Abstract

CRISPR-Cas9 genome editing has enabled advanced T cell therapies, but occasional loss of the targeted chromosome remains a safety concern. To investigate whether Cas9-induced chromosome loss is a universal phenomenon and evaluate its clinical significance, we conducted a systematic analysis in primary human T cells. Arrayed and pooled CRISPR screens revealed that chromosome loss was generalizable across the genome and resulted in partial and entire loss of the targeted chromosome, including in preclinical chimeric antigen receptor T cells. T cells with chromosome loss persisted for weeks in culture, implying the potential to interfere with clinical use. A modified cell manufacturing process, employed in our first-in-human clinical trial of Cas9-engineered T cells (NCT03399448), reduced chromosome loss while largely preserving genome editing efficacy. Expression of p53 correlated with protection from chromosome loss observed in this protocol, suggesting both a mechanism and strategy for T cell engineering that mitigates this genotoxicity in the clinic.


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