Reed M. Hawkins
A5009027945- CAR-T cell therapy research
- Immunotherapy and Immune Responses
- Cancer Immunotherapy and Biomarkers
- Prostate Cancer Treatment and Research
- Chronic Lymphocytic Leukemia Research
- Biosimilars and Bioanalytical Methods
- Silicon Carbide Semiconductor Technologies
- Immune Cell Function and Interaction
- Advancements in Semiconductor Devices and Circuit Design
- Lymphoma Diagnosis and Treatment
- Viral Infectious Diseases and Gene Expression in Insects
- Nanowire Synthesis and Applications
- Integrated Circuits and Semiconductor Failure Analysis
- Acute Lymphoblastic Leukemia research
- Virus-based gene therapy research
- T-cell and B-cell Immunology
- Cutaneous Melanoma Detection and Management
Oregon Health & Science University
2022-2024
Fred Hutch Cancer Center
2016-2022
CD19-specific chimeric antigen receptor (CAR)-modified T cells have antitumor activity in B cell malignancies, but factors that affect toxicity and efficacy been difficult to define because of differences lymphodepletion heterogeneity CAR-T administered individual patients. We conducted a clinical trial which CD19 were manufactured from defined subsets 1:1 CD4(+)/CD8(+) ratio 32 adults with relapsed and/or refractory non-Hodgkin's lymphoma after cyclophosphamide (Cy)-based chemotherapy or...
Abstract Chimeric antigen receptor (CAR) T-cell therapy has produced remarkable anti-tumor responses in patients with B-cell malignancies. However, clonal kinetics and transcriptional programs that regulate the fate of CAR-T cells after infusion remain poorly understood. Here we perform TCRB sequencing, integration site analysis, single-cell RNA sequencing (scRNA-seq) to profile CD8 + from products (IPs) blood undergoing CD19 immunotherapy. shows diversity is highest IPs declines following...
<p>Supplementary Figure 4 shows a co-culture of tumor-antigen specific T cell mediated killing tumor cells +/- AR inhibition or MHCI inhibition.</p>
<p>Supplementary Figure 3 shows validation of AR binding in MHC regulatory genes interest +/- inhibition with enzalutamide.</p>
<div>Abstract<p>Tumors escape immune detection and elimination through a variety of mechanisms. Here, we used prostate cancer as model to examine how androgen-dependent tumors undergo evasion downregulation the major histocompatibility complex class I (MHCI). We report that response immunotherapy in late-stage is associated with elevated MHC expression. To uncover mechanism, performed genome-wide CRISPR interference (CRISPRi) screen identified androgen receptor...
<p>Supplementary Figure 5 provides <i>in vivo</i> validation of enhanced T cell responses and tumor control after AR knockdown.</p>
<p>Supplementary Figure 7 is a graphical abstract of how AR regulates MHCI expression in prostate tumor cells.</p>
<p>Supplementary Figure 1 shows sgRNA validation and MHCI protein expression on tumor cell lines.</p>
<p>Supplementary Figure 6 shows clinical data analysis of neoadjuvant androgen axis inhibition in primary prostate cancer as well expression AR, MHCI, and IFNG activity mHSPC samples.</p>
<p>Supplementary Figure 2 demonstrates MHC expression following pharmacologic inhibition of AR and/or ligand withdrawal.</p>
<p>Supplementary Figure 4 shows a co-culture of tumor-antigen specific T cell mediated killing tumor cells +/- AR inhibition or MHCI inhibition.</p>
<p>Supplementary Figure 7 is a graphical abstract of how AR regulates MHCI expression in prostate tumor cells.</p>
<p>Supplementary Figure 6 shows clinical data analysis of neoadjuvant androgen axis inhibition in primary prostate cancer as well expression AR, MHCI, and IFNG activity mHSPC samples.</p>
<p>Supplementary Figure 1 shows sgRNA validation and MHCI protein expression on tumor cell lines.</p>
<p>Supplementary Figure 3 shows validation of AR binding in MHC regulatory genes interest +/- inhibition with enzalutamide.</p>
<p>Supplementary Figure 5 provides <i>in vivo</i> validation of enhanced T cell responses and tumor control after AR knockdown.</p>
<p>Supplementary Figure 2 demonstrates MHC expression following pharmacologic inhibition of AR and/or ligand withdrawal.</p>