A5086468540- Polyomavirus and related diseases
- Bacteriophages and microbial interactions
- Plant Virus Research Studies
- Virus-based gene therapy research
- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Cancer Immunotherapy and Biomarkers
- Antenna Design and Analysis
- Full-Duplex Wireless Communications
- RNA Interference and Gene Delivery
- Microwave Engineering and Waveguides
- Herpesvirus Infections and Treatments
- Toxoplasma gondii Research Studies
- Neuroendocrine Tumor Research Advances
- Hepatocellular Carcinoma Treatment and Prognosis
- CRISPR and Genetic Engineering
- Cancer Research and Treatments
- Lung Cancer Research Studies
- Ultrasound and Hyperthermia Applications
- Immunotherapy and Immune Responses
- Colorectal Cancer Treatments and Studies
Seattle University
2021
University of Washington
2017-2020
University of Maryland, Baltimore
2009-2016
National Institutes of Health
2008
Understanding mechanisms of late/acquired cancer immunotherapy resistance is critical to improve outcomes; cellular trials offer a means probe complex tumor-immune interfaces through defined T cell/antigen interactions. We treated two patients with metastatic Merkel cell carcinoma autologous polyomavirus specific CD8+ cells and immune-checkpoint inhibitors. In both cases, dramatic remissions were associated dense infiltration activated CD8+s into the regressing tumors. However, late relapses...
Purpose: To investigate whether combining pulsed high-intensity focused ultrasound (HIFU) with the chemotherapeutic drug bortezomib could improve antitumor activity against murine squamous cell carcinoma (SCC) tumors. Materials and Methods: All experiments were conducted animal care use committee approval. Murine SCC cells implanted subcutaneously in C3H mice. When tumors reached 100 mm3, mice randomized to one of three groups for twice weekly intraperitoneal injections 1.5 mg per kilogram...
Merkel cell carcinoma (MCC) is often caused by persistent expression of polyomavirus (MCPyV) T-antigen (T-Ag). These non-self proteins comprise about 400 amino acids (AA). Clinical responses to immune checkpoint inhibitors, seen in half patients, may relate T-Ag-specific T cells. Strategies increase CD8+ T-cell number, breadth, or function could augment inhibition, but vaccines immunity must avoid delivery oncogenic domains. We probed MCC tumor-infiltrating lymphocytes (TIL) with an...
Oncolytic virotherapy is a unique cancer therapeutic that encompasses tumour cell lysis through both virus replication and programmed death (PCD) pathways. Nonetheless, clinical efficacy relatively modest, likely related to the immunosuppressive milieu. Our studies use herpes simplex type 2 (HSV-2)-based oncolytic ΔPK has documented anti-tumour activity associated with replication, PCD stem lysis. They are designed examine whether ΔPK-mediated oncolysis includes ability reverse...
Abstract Metastatic melanoma is a highly aggressive and drug resistant cancer. Oncolytic virotherapy novel therapeutic strategy designed to circumvent cancer resistance through virus replication-induced cell lysis. Unfortunately, its clinical efficacy modest, apparently related poor replication within the tumors failure stimulate inflammatory/immunotherapeutic pathways. The growth compromised herpes simplex type 2 (HSV-2) mutant ΔPK causes metastatic death activation of multiple...
<div>Abstract<p>Merkel cell carcinoma (MCC) is often caused by persistent expression of Merkel polyomavirus (MCPyV) T-antigen (T-Ag). These non-self proteins comprise about 400 amino acids (AA). Clinical responses to immune checkpoint inhibitors, seen in half patients, may relate T-Ag–specific T cells. Strategies increase CD8<sup>+</sup> T-cell number, breadth, or function could augment inhibition, but vaccines immunity must avoid delivery oncogenic domains. We probed...
<p>Sup Figures 1-13</p>
<p>Sup Figures 1-13</p>
<div>Abstract<p>Merkel cell carcinoma (MCC) is often caused by persistent expression of Merkel polyomavirus (MCPyV) T-antigen (T-Ag). These non-self proteins comprise about 400 amino acids (AA). Clinical responses to immune checkpoint inhibitors, seen in half patients, may relate T-Ag–specific T cells. Strategies increase CD8<sup>+</sup> T-cell number, breadth, or function could augment inhibition, but vaccines immunity must avoid delivery oncogenic domains. We probed...