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Biology subjects

Sakemura, R. L.

Publications and source records attributed to Sakemura, R. L..

2 recordsLinked to original sources

Optimized CART Cell Therapy for Metastatic Aggressive Thyroid Cancer

Most thyroid cancer deaths are attributed to a subset of poorly differentiated, metastatic tumors. To improve treatment options for aggressive thyroid cancers, we developed a novel thyroid-stimulating hormone receptor (TSHR)-targeted chimeric antigen receptor T (CART) cell therapy, which demonstrated antigen-specific activation and antitumor efficacy against TSHR+ cell lines in vitro and in vivo. However, de-differentiated thyroid cancers downregulate TSHR. We therefore developed a potent treatment strategy by combining our novel TSHR-CART cells with mitogen-activated protein kinase (MAPK) inhibitors, which redifferentiate thyroid tumors and upregulate TSHR expression. In patient-derived anaplastic thyroid cancer xenografts, combination therapy of TSHR-CART cells and MAPK inhibitors led to increased TSHR expression on the tumor tissue and significantly enhanced antitumor efficacy and prolonged survival compared to TSHR-CART monotherapy. Based on our data, we are launching a phase I clinical trial for TSHR-CART cell therapy alone or in combination with MAPK inhibitors in patients with metastatic thyroid cancers. STATEMENT OF SIGNIFICANCEPoor target selection and antigen escape limit CART cell efficacy in solid tumors. We developed TSHR-CART cells to treat differentiated thyroid cancers but observed TSHR downregulation in dedifferentiated thyroid cancers. We found that MAPK inhibitors restored TSHR expression and sensitized these cancers to TSHR-CART cell therapy.

immunology↗

The Identification of IL-4 as a Regulator of Chimeric Antigen Receptor T Cell Exhaustion

Durable response to chimeric antigen receptor T (CART) cell therapy remains limited in part due to CART cell exhaustion. We investigated the regulation of CART cell exhaustion with three independent approaches including: a genome-wide CRISPR knockout screen using a validated in vitro model for exhaustion, RNA and ATAC sequencing on baseline and chronically stimulated CART cells, and RNA and ATAC sequencing on pre-infusion CART cell products from responders and non-responders in the ZUMA-1 clinical trial. Each of these approaches identified IL-4 as a key regulator of CART cell dysfunction. Further, when CART cells were treated with IL-4, they developed signs of exhaustion, but when CART cells were treated with an IL-4 monoclonal antibody, they showed improved antitumor efficacy and reduced signs of exhaustion in preclinical models. Therefore, our study identified both a novel role for IL-4 on CART cells and the improvement of CART cell therapy through IL-4 neutralization. Statement of SignificanceIdentifying regulators of CART cell exhaustion will not only enhance the fields understanding of therapeutic failure, but it will also provide avenues to enhance CART cell efficacy. This study reveals both a novel role for IL-4 in exhaustion and a strategy to improve CART cell activity through IL-4 neutralization.

immunology↗