- Neurofibromatosis and Schwannoma Cases
- Neuroblastoma Research and Treatments
- Sarcoma Diagnosis and Treatment
- Multiple Myeloma Research and Treatments
- Glioma Diagnosis and Treatment
- Cellular Mechanics and Interactions
- Monoclonal and Polyclonal Antibodies Research
- Epigenetics and DNA Methylation
- Advanced Proteomics Techniques and Applications
- Virus-based gene therapy research
- Cancer Immunotherapy and Biomarkers
- 3D Printing in Biomedical Research
- Mathematical Biology Tumor Growth
- Single-cell and spatial transcriptomics
- Neuroendocrine Tumor Research Advances
- Cancer Mechanisms and Therapy
- Chromatin Remodeling and Cancer
- Advanced Biosensing Techniques and Applications
- CAR-T cell therapy research
- vaccines and immunoinformatics approaches
University of Minnesota
2022-2024
University of Minnesota Medical Center
2023-2024
Masonic Cancer Center
2024
University of Minnesota System
2024
Twin Cities Orthopedics
2024
Abstract Neurofibromatosis Type 1 (NF1) is a common cancer predisposition syndrome, caused by heterozygous loss of function mutations in the tumor suppressor gene NF1 . Individuals with develop benign tumors peripheral nervous system (neurofibromas), originating from Schwann cell linage after somatic wild type allele, some which progress further to malignant nerve sheath (MPNST). There only one FDA approved targeted therapy for symptomatic plexiform neurofibromas and none MPNST. The genetic...
Background Characterizing peptide antigens, processed from tumor-specific proteoforms, and bound to the major histocompatibility complex, is critical for immuno-oncology research. Next-generation sequencing predicts candidate neoantigen peptides derived DNA mutations and/or RNA transcripts coding proteoform sequences that differ reference proteome. Mass spectrometry (MS)-based immunopeptidomics identifies predicted, MHC-bound other tumor antigens. This immunopeptidogenomic approach requires...
Abstract Background Malignant peripheral nerve sheath tumors (MPNST) are aggressive soft tissue sarcomas that often develop in patients with neurofibromatosis type 1 (NF1). To address the critical need for novel therapeutics MPNST, we aimed to establish an ex vivo 3D platform accurately captured genomic diversity of MPNST and could be utilized a medium-throughput manner drug screening studies validated using patient-derived xenografts (PDX). Methods Genomic analysis was performed on all...
Oncolytic adenoviruses (Ads) stand out as a promising strategy for the targeted infection and lysis of tumor cells, with well-established clinical utility across various malignancies. This study delves into therapeutic potential oncolytic Ads in context neurofibromatosis type 1 (NF1)-associated malignant peripheral nerve sheath tumors (MPNSTs). Specifically, we evaluate Conditionally Replicative Adenoviruses (CRAds) driven by Cyclooxygenase 2 (COX2) promoter, selective agents against MPNSTs,...
Abstract Background Glioblastoma is the most aggressive malignant brain tumor with poor survival due to its invasive nature driven by cell migration, unclear linkage transcriptomic information. The aim of this study was develop a physics-based framework connecting transcriptomics predict patient-specific glioblastoma migration. Methods and Results We applied motor-clutch model, migration simulator (CMS), parameterize cells define physical biomarkers on patient-by-patient basis. reduced...
Abstract Background Malignant peripheral nerve sheath tumors (MPNSTs) can arise from atypical neurofibromas (ANF). Loss of the polycomb repressor complex 2 (PRC2) is a common event. Previous studies on PRC2-regulated genes in MPNST used genetic add-back experiments highly aneuploid cell lines which may miss NF1-mutant ANF-like precursor cells. A set human Schwann cells (SCs) has not been defined. We hypothesized that PRC2 loss direct and indirect effects gene expression resulting MPNST, so...
Abstract Glioblastoma is the most aggressive malignant brain tumor with poor survival due to its invasive nature driven by cell migration. There still no effective treatment targeting glioma migration based on their transcriptomic information, lack of understanding in links fundamental mechanics In previous studies, we developed a physics-based motor-clutch model, simulator (CMS), identify basic mechanisms various types. this study, found that glioblastoma patient-derived (xenograft) (PD(X))...
<h3>Background</h3> Chronic stimulation of the T cell receptor (TCR) in tumor microenvironment (TME) contributes to cytotoxic CD8<sup>+</sup> exhaustion and activation-induced death, which limits effectiveness immunotherapies. Therefore, enhancing fitness TME represents a promising opportunity for improving cancer therapy. While CRISPR screens have identified factors that enhance persistence, genome-wide screen simultaneously encompassing both gain- (GOF) loss-of-function (LOF) mutants has...
Abstract Malignant peripheral nerve sheath tumors (MPNST) are aggressive soft tissue sarcomas that often develop in patients with neurofibromatosis type 1 (NF1-MPNST), but can occur sporadically. Through a multi-institution collaboration, we have developed 13 NF1-associated MPNST patient-derived xenografts (PDX). Genomic analysis of the PDX-tumor pairs identified somatic mutations NF1 (61%), SUZ12 EED (15%), and TP53 chromosome 8 (Chr8) gain (77%), consistent published data. Pre-clinical...
Abstract Central nervous system tumors account for the most childhood cancer mortality. Immunotherapies have made major contributions to treat adult cancers, but application of immunotherapy brain has been limited, in part due unique CNS microenvironment and mechanisms immune escape this context. To investigate immunologic context, we query transcriptomic profile ~700 primary released by Children’s Brain Tumor Network. An subtype classification from The Cancer Genome Atlas project reveals...
Abstract Neurofibromatosis Type 1 syndrome (NF1) is a cancer predisposition caused by inheritance of one loss function allele the NF1 gene. patients can develop malignant peripheral nerve sheath tumors (MPNST), deadly soft tissue sarcoma. MPNSTs after somatic wild-type allele, resulting in an increase Ras-GTP activated signaling. This transformation still not completely understood, but TP53 or CDKN2A/2B and polycomb repressor complex 2 (PRC2) are common events during transition to MPNST....