A5072009939- Epigenetics and DNA Methylation
- Cancer, Lipids, and Metabolism
- Ferroptosis and cancer prognosis
- RNA modifications and cancer
- Lipid metabolism and biosynthesis
- Cancer-related molecular mechanisms research
- Metabolomics and Mass Spectrometry Studies
- MicroRNA in disease regulation
- Cancer Immunotherapy and Biomarkers
- Immune cells in cancer
- Cholesterol and Lipid Metabolism
Northwestern University
2022-2024
Midwestern University
2024
Fatty acids are an important source of energy and a key component phospholipids in membranes organelles. Saturated fatty (SFAs) converted into unsaturated (UFAs) by stearoyl Co-A desaturase (SCD), enzyme active cancer. Here, we studied how the dynamics between SFAs UFAs regulated SCD impacts ovarian cancer cell survival tumor progression. depletion or inhibition caused lower levels vs. altered acyl chain plasticity, as demonstrated lipidomics stimulated Raman scattering (SRS) microscopy....
BackgroundImmune checkpoint inhibitors (ICIs) have modest activity in ovarian cancer (OC). To augment their activity, we used priming with the hypomethylating agent guadecitabine a phase II study.MethodsEligible patients had platinum-resistant OC, normal organ function, measurable disease, and received up to 5 prior regimens. The treatment included (30 mg/m2) on days 1-4, pembrolizumab (200 mg i.v.) day 5, every 21 days. primary endpoint was response rate. Tumor biopsies, plasma, PBMCs were...
Abstract Platinum (Pt)‐based chemotherapy is the main treatment for ovarian cancer (OC); however, most patients develop Pt resistance (Pt‐R). This work shows that Pt‐R OC cells increase intracellular cholesterol through uptake via HDL receptor, scavenger receptor type B‐1 (SR‐B1). SR‐B1 blockade using synthetic cholesterol‐poor HDL‐like nanoparticles (HDL NPs) diminished leading to cell death and inhibition of tumor growth. Reduced accumulation in induces lipid oxidative stress reduction...
Abstract Purpose: DNA methylation causes silencing of tumor-suppressor and differentiation-associated genes, being linked to chemoresistance. Previous studies demonstrated that hypomethylating agents (HMA) resensitize ovarian cancer chemotherapy. NTX-301 is a highly potent orally bioavailable HMA, in early clinical development. Experimental Design: The antitumor effects were studied models by using cell viability, stemness ferroptosis assays, RNA sequencing, lipidomic analyses, stimulated...
High-grade serous ovarian cancer (HGSOC) is characterized by a complex genomic landscape, with both genetic and epigenetic diversity contributing to its pathogenesis, disease course, response treatment. To better understand the association between features treatment among 370 patients newly diagnosed HGSOC, we utilized multi-omic data semi-biased clustering of HGSOC specimens profiled TCGA. A Cox regression model was deployed select input based on influence recurrence. Among most...
Abstract Platinum (Pt) is the main therapy for ovarian cancer (OC); however, most patients develop Pt resistance (Pt-R). We show that Pt-R OC cells increase intracellular cholesterol through uptake via HDL receptor, scavenger receptor type B-1 (SR-B1). SR-B1 blockade using synthetic cholesterol-poor HDL-like nanoparticles (HDL NPs) diminished leading to cell death and suppressed tumor growth. Reduced accumulation induced lipid oxidative stress reduction of glutathione peroxidase 4 (GPx4)...
<p>Effects of HMAs on HDAC expression.</p>
<p>NTX301 inhibits OC tumor growth in vivo.</p>
<p>NTX-301 monotherapy inhibits PDX tumor growth.</p>
<p>NTX-301 effects in OC cells</p>
<div>AbstractPurpose:<p>DNA methylation causes silencing of tumor-suppressor and differentiation-associated genes, being linked to chemoresistance. Previous studies demonstrated that hypomethylating agents (HMA) resensitize ovarian cancer chemotherapy. NTX-301 is a highly potent orally bioavailable HMA, in early clinical development.</p>Experimental Design:<p>The antitumor effects were studied models by using cell viability, stemness ferroptosis assays, RNA...
<p>NTX301 induced transcriptome and methylome reprogramming in OC cells.</p>
<div>AbstractPurpose:<p>DNA methylation causes silencing of tumor-suppressor and differentiation-associated genes, being linked to chemoresistance. Previous studies demonstrated that hypomethylating agents (HMA) resensitize ovarian cancer chemotherapy. NTX-301 is a highly potent orally bioavailable HMA, in early clinical development.</p>Experimental Design:<p>The antitumor effects were studied models by using cell viability, stemness ferroptosis assays, RNA...