A5060421043- Advanced Breast Cancer Therapies
- PARP inhibition in cancer therapy
- Prostate Cancer Treatment and Research
- DNA Repair Mechanisms
- Fungal and yeast genetics research
- Cancer, Hypoxia, and Metabolism
- Cancer, Lipids, and Metabolism
- Endoplasmic Reticulum Stress and Disease
- Microtubule and mitosis dynamics
- Metal-Catalyzed Oxygenation Mechanisms
- Estrogen and related hormone effects
- Breast Cancer Treatment Studies
- Genetics and Neurodevelopmental Disorders
- Lung Cancer Treatments and Mutations
- RNA modifications and cancer
- Genomics and Rare Diseases
- HER2/EGFR in Cancer Research
- Metal complexes synthesis and properties
- Cellular transport and secretion
- Metabolism and Genetic Disorders
- Genomic variations and chromosomal abnormalities
- Calcium signaling and nucleotide metabolism
- Protein Degradation and Inhibitors
The University of Texas Southwestern Medical Center
2019-2024
Rhodes College
2015-2020
Asuragen (United States)
2014
PurposeFragile X CGG repeat alleles often contain one or more AGG interruptions that influence allele stability and risk of a full mutation transmission from parent to child. We have examined transmissions maternal paternal with 45–90 repeats quantify the effect on fragile instability.MethodsA novel FMR1 polymerase chain reaction assay was used determine length for 1,040 705 families.ResultsWe grouped into nine categories five by parental size found in every category, no AGGs had greatest...
Triple-negative breast cancer (TNBC) has a poor clinical outcome, due to lack of actionable therapeutic targets. Herein we define lysosomal acid lipase A (LIPA) as viable molecular target in TNBC and identify stereospecific small molecule (ERX-41) that binds LIPA. ERX-41 induces endoplasmic reticulum (ER) stress resulting cell death, this effect is on evidenced by specific LIPA mutations providing resistance. Importantly, demonstrate activity independent function but dependent its ER...
The glutamine antagonist DRP-104 blocks purine synthesis and combines with checkpoint inhibitors to promote antitumor immunity in KEAP1/NRF2-mutant lung cancers.
Abstract Background CDK4/6 inhibitors in combination with endocrine therapy (AE/AI/SERDs) are approved for the treatment of ER+ advanced breast cancer (BCa). However, not all patients benefit from therapy. We previously reported a novel therapeutic agent, ERX-11, that binds to estrogen receptor (ER) and modulates ER-coregulator interactions. Here, we tested if ERX-11 agents BCa would be more potent. Methods effect using cell line models, including those have acquired resistance tamoxifen,...
Careful regulation of the cell cycle is required for proper replication, division, and DNA repair. damage--including that induced by many anticancer drugs--results in delay or arrest, which can allow time repair lesions. Although its molecular mechanism action remains a matter debate, ruthenium complex KP1019 has been shown to bind biophysical assays damage colorectal ovarian cancer cells vitro. also induce mutations arrest Saccharomyces cerevisiae, suggesting budding yeast serve as an...
Abstract Like platinum-based chemotherapeutics, the anticancer ruthenium complex indazolium trans-[tetrachlorobis(1H-indazole)ruthenate(iii)], or KP1019, damages DNA, induces apoptosis, and causes tumor regression in animal models. Unlike drugs, KP1019 showed no dose-limiting toxicity a phase I clinical trial. Despite these advances, mechanism(s) target(s) of remain unclear. For example, drug may damage DNA directly by causing oxidative stress. Likewise, binds cytosolic proteins, suggesting...
Abstract Despite the widespread deregulation of CDK4/6 activity in non-small cell lung cancer (NSCLC), clinical trials with inhibitors (CDK4/6is) as a monotherapy have shown poor antitumor activity. However, our preclinical studies revealed significant potential for CDK4/6is to collaborate by influencing DNA damage repair pathways during radiotherapy. Given considerable upregulation PARP1 expression NSCLC, we analyzed efficacy combined PARP and inhibition NSCLC models. Our findings...