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Hendel, A.

Publications and source records attributed to Hendel, A..

2 recordsLinked to original sources

Development of a Fully Non-Viral 1XX-enhanced BCMA CAR-T Cell Therapy for Multiple Myeloma

Multiple myeloma (MM) is a clonal plasma cell malignancy characterized by bone marrow infiltration, monoclonal immunoglobulin production, and microenvironmental dysregulation that leads to systemic organ damage. The advent of B-cell maturation antigen (BCMA)-directed chimeric antigen receptor (CAR) T-cell therapy has induced unprecedented responses and durability for patients with relapsed/refractory MM. These outcomes are rarely observed with prior salvage strategies, although relapse remains the predominant long-term challenge for most patients. The two currently approved BCMA CAR-T cell products use viral vectors to semi-randomly insert the CAR gene, which results in heterogeneous genomic composition and variability in efficacy, safety, and product consistency. To address these challenges, we integrated targeted CRISPR genome engineering with precise CAR transgene insertion at the T-cell receptor alpha constant (TRAC) locus, 1XX CAR signaling architecture to enhance potency and durability, and non-viral manufacturing with a single-stranded DNA repair template to improve efficiency and yield. This approach confers physiological CAR expression, reduces insertional mutagenesis, and improves persistence by mitigating tonic signaling and exhaustion. Our GMP manufacturing process consistently achieved high CAR integration (37.7-72.7%) and yields across all full-scale runs and met predefined release criteria for identity, purity, safety, and quality. In NSG mouse models of MM, the UCCT-BCMA-1 product exhibited exceptionally potent tumor control, CAR-T cell expansion 100-1000-fold greater than that of lentiviral constructs, and durable clearance of myeloma cells after multiple rechallenges. These findings establish a CRISPR-edited, fully non-viral manufacturing platform for next-generation 1XX-BCMA CAR-T therapies with enhanced persistence, safety, and efficacy. One Sentence SummaryCRISPR-engineered, TRAC-targeted 1XX-BCMA CAR-T therapy with improved safety, potency, and persistence in relapsed and refractory multiple myeloma.

cancer biology↗

Multiplex HDR for Disease and Correction Modeling of SCID by CRISPR Genome Editing in Human HSPCs

Severe combined immunodeficiency (SCID) is a group of monogenic primary immunodeficiencies caused by mutations in genes involved in the process of lymphocyte maturation and function. CRISPR-Cas9 gene editing of the patients own hematopoietic stem and progenitor cells (HSPCs) ex vivo could provide a therapeutic alternative to allogeneic hematopoietic stem cell transplantation (HSCT), the current gold standard for treatment of SCID. Using CRISPR-Cas9/rAAV6 gene-editing, we engineered genotypes in healthy donor (HD)-derived CD34+ HSPCs, thus eliminating the need for rare patient samples, to model both SCID and the therapeutic outcomes of gene-editing therapies for SCID via multiplexed homology directed repair (HDR). Firstly, we developed a SCID disease model via knock-out of both alleles of genes critical to the development of lymphocytes; and secondly, we established a knock-in/knock-out (KI-KO) strategy to develop a proof-of-concept single-allelic gene correction. Since SCID is a recessive disorder, correction of only one allele is enough to cure the patient. Based on these results, we performed gene correction of RAG2-SCID patient-derived CD34+ HSPCs that successfully developed into CD3+ T cells with diverse TCR repertoires in an in vitro T-cell differentiation (IVTD) platform. By using CRISPR-Cas9, multiplexed HDR, HD-derived CD34+ HSPCs, and an IVTD system we outline an approach for the study of human lymphopoiesis. We present both a way for researchers to determine the optimal configuration for CRISPR-Cas9 gene correction of SCID and other recessive blood disorders, and the feasibility of translating these techniques to perform gene correction in patient-derived CD34+ HSPCs.

bioengineering↗