- Cancer Immunotherapy and Biomarkers
- Immunotherapy and Immune Responses
- Cancer Genomics and Diagnostics
- interferon and immune responses
- Economic and Financial Impacts of Cancer
- Immune Cell Function and Interaction
- RNA modifications and cancer
- Health Systems, Economic Evaluations, Quality of Life
- Epigenetics and DNA Methylation
- Lung Cancer Treatments and Mutations
- Ubiquitin and proteasome pathways
- CAR-T cell therapy research
- Cancer Research and Treatments
- Monoclonal and Polyclonal Antibodies Research
- Renal and related cancers
- Pharmaceutical Economics and Policy
- PARP inhibition in cancer therapy
- Mesenchymal stem cell research
- Photodynamic Therapy Research Studies
- Phagocytosis and Immune Regulation
- Renal Transplantation Outcomes and Treatments
- Lymphoma Diagnosis and Treatment
- Effects of Radiation Exposure
- Nanoplatforms for cancer theranostics
- Proteoglycans and glycosaminoglycans research
The University of Texas Southwestern Medical Center
2005-2025
Southwestern Medical Center
2007-2025
Shenzhen Bay Laboratory
2022-2024
Harold C. Simmons Comprehensive Cancer Center
2018
Northeast Normal University
2012
Ningxia Medical University
1991
Cancer Institute (WIA)
1991
Blockade of CD47, the "do not eat me" signal, has limited effects in solid tumors despite its potent antitumor hematopoietic malignancies. Taking advantage high expression cytotoxic T lymphocyte-associated protein 4 (CTLA-4) on Treg cells and abundant Fc receptor-expressing active phagocytes inside tumor microenvironment (TME), we designed tested a heterodimer combining an anti-CTLA-4 antibody, which targets cells, with CD47 ligand, signal regulatory α (SIRPα), to selectively block...
Mutations underlie all cancers, and their identification study are the foundation of cancer biology. We describe what we believe to be a novel approach mutagenesis studies based on DNA polymerase ε (POLE) ultramutator phenotype recently described in human which single amino acid substitution (most commonly P286R) proofreading domain results error-prone replication. engineered conditional PoleP286R allele mice. PoleP286R/+ embryonic fibroblasts exhibited striking mutator immortalized more...
319 Background: BRCA mutations have emerged as critical biomarkers for guiding the use of PARP inhibitors in metastatic prostate cancer. Timely access to testing remains a challenge, especially those enrolled Medicare Advantage (MA) plans, which cover more than half beneficiaries but often impose greater restrictions Traditional (TM). This study compares timeliness patients with cancer (mPCa) across these two insurance types. Methods: A retrospective cohort was conducted using Flatiron...
320 Background: Next-Generation Sequencing (NGS) testing has become a cornerstone of personalized medicine in cancer care. With Medicare Advantage (MA) now covering nearly half all beneficiaries, understanding differences access to timely NGS between MA and Traditional (TM) is crucial, particularly given MA’s potential restrictions. This study aims evaluate the effectiveness plans on patients with metastatic prostate (mPCa). Methods: retrospective cohort was based Flatiron Health...
166 Background: As MA plans gain popularity, covering over half of eligible beneficiaries in 2023, concerns have arisen about their ability to manage complex cancer care due pre-authorization requirements and limited physician networks. The study compares Traditional Medicare (TM) delivering timely hormonal intensification, specifically through addition oral novel therapy (NHT) castration therapy, which became central part treating metastatic hormone-sensitive prostate (mHSPC) by 2018....
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are a first-line therapy for rapidly killing tumors such as those associated with non-small cell lung cancer by blocking oncogenic signaling, but tumor relapse often occurs. Here, we have observed that hypofractionated EGFR TKI treatment (HypoTKI) is more potent than standard hyperfractionated (HyperTKI), and its antitumor effect preventing depends on T cells. HypoTKI triggers greater innate sensing type I IFN CXCL10...
Cancer is instigated by mutator phenotypes, including deficient mismatch repair and p53-associated chromosomal instability. More recently, a distinct class of cancers was identified with unusually high mutational loads due to heterozygous amino acid substitutions (most commonly P286R) in the proofreading domain DNA polymerase ε, leading strand replicase encoded POLE. Immunotherapy has revolutionized cancer treatment, but new model systems are needed recapitulate burdens characterizing human...
Molecular chaperone HSP70s are attractive targets for cancer therapy, but their substrate broadness and functional non-specificity have limited role in therapeutical success. Functioning as HSP70's cochaperones, HSP40s determine the client specificity of HSP70s, could be better therapy. Here we show that tumors defective HSP40 member DNAJA2 benefitted from immune-checkpoint blockade (ICB) Mechanistically, maintains centrosome homeostasis by timely degrading key centriolar satellite proteins...
Mesenchymal stem cells (MSCs) are adult with a self-renewal and multipotent capability express extensively in multitudinous tissues. We found that water channel aquaporin-5 (AQP5) is expressed bone marrow-derived MSCs (BMMSCs) the plasma membrane pattern. BMMSCs from AQP5(-/-) mice showed significantly lower permeability than those AQP5(+/+) mice. In characterizing cultured mice, we no obvious differences morphology proliferation between 2 genotypes. However, multiple differentiation...
7081 Background: FUS1 is a novel tumor suppressor gene (TSG) identified in the human chromosome 3p21.3 region that functions Apaf1-associated apoptotic pathway, and potent suppressor. We explored use of for enhancing chemotherapeutic potency Gefitnib overcoming Gefitnib-resistance both Gefitnib-sensitive resistant NSCLC cells. Methods Results: found expression wt-FUS1 by FUS1-nanoparticle-mediated transfer FUS1-deficient Gefitinib-resistant H1299, H358, H460 cells significantly sensitized...
Abstract Cancer is characterized by increased mutation rate, and recent work has led to a deeper understanding of mutator phenotypes underlying molecular mechanisms. Differences in the mutational landscape individual cancers underlie key aspects clinical behavior. For example, overall base substitution rate best predictor immune therapy response. Most genetically engineered mouse models cancer (GEMMs) reiterate few driver events but fail recapitulate high loads that are ultimate cause most...
Abstract Bispecific T-cell engagers (BiTEs) that preferentially target tumor-associated antigens (TAA) to reengage CD3 signaling have been approved treat acute B-cell lymphoblastic leukemia. However, their applications in solid tumors hampered due short half-life, weak anti-tumor activity, and severe toxicity at therapeutic doses. To explore new targets, we designed a bispecific antibody (BsAb) which simultaneously targets immune checkpoint PD-L1. Compared with conventional TAA based...
<h3>Background</h3> Although approved by FDA, anti-CTLA-4 treatment has severe side effect that limits its clinical usage. Blockade of CD47, the "don9t eat me" signal, limited effects in solid tumors despite potent anti-tumor hematopoietic malignancies. Targeted delivery immune blockers into tumor tissues are desireble. <h3>Methods</h3> Taking advantage high expression CTLA-4 on Treg cells and abundant Fc receptor+ active phagocytes inside microenvironment (TME), we design test an...