Joseph R. Zoeller
A5030589830- RNA modifications and cancer
- DNA Repair Mechanisms
- PARP inhibition in cancer therapy
- GDF15 and Related Biomarkers
- Genetics, Bioinformatics, and Biomedical Research
- Digestive system and related health
- Nutrition, Genetics, and Disease
- Gene expression and cancer classification
- Estrogen and related hormone effects
- MicroRNA in disease regulation
- Ferroptosis and cancer prognosis
- Cell Image Analysis Techniques
- Archaeological Research and Protection
- Conservation Techniques and Studies
- RNA Research and Splicing
- Cultural Heritage Materials Analysis
- RNA and protein synthesis mechanisms
Baylor College of Medicine
2024-2025
Washington and Lee University
2019
Precision medicine relies on identifying reliable biomarkers for gene dependencies to tailor individualized therapeutic strategies. The advent of high-throughput technologies presents unprecedented opportunities explore molecular disease mechanisms but also challenges due high dimensionality and collinearity among features. Traditional statistical methods often fall short in this context, necessitating novel computational approaches that harness the full potential big data bioinformatics....
Abstract Upregulation of MYC is a hallmark cancer, wherein drives oncogenic gene expression and elevates total RNA synthesis across cancer cell transcriptomes. Although this transcriptional anabolism fuels growth survival, the consequences metabolic stresses induced by excess cellular are poorly understood. Herein, we discover that degradation downstream ribonucleotide catabolism novel mechanism MYC-induced death. Combining genetics metabolomics, find increases decay through cytoplasmic...
Reflectance imaging spectroscopy (RIS) in the visible and near infrared is revolutionizing way cultural heritage investigators may analyze paintings nondestructively. In an ongoing, highly collaborative project, authors are investigating a painting by American artist John White Alexander (1856–1915). The painting, titled A Study Pink, collection of Virginia Museum Fine Arts (VMFA). An x-radiograph taken 2014 revealed that there was another female figure, rotated 180 degrees, underneath...
<div>Abstract<p>Upregulation of MYC is a hallmark cancer, wherein drives oncogenic gene expression and elevates total RNA synthesis across cancer cell transcriptomes. Although this transcriptional anabolism fuels growth survival, the consequences metabolic stresses induced by excess cellular are poorly understood. Herein, we discover that degradation downstream ribonucleotide catabolism novel mechanism MYC-induced death. Combining genetics metabolomics, find increases decay...
<div>Abstract<p>Upregulation of MYC is a hallmark cancer, wherein drives oncogenic gene expression and elevates total RNA synthesis across cancer cell transcriptomes. Although this transcriptional anabolism fuels growth survival, the consequences metabolic stresses induced by excess cellular are poorly understood. Herein, we discover that degradation downstream ribonucleotide catabolism novel mechanism MYC-induced death. Combining genetics metabolomics, find increases decay...
<p>Table S1 is the list of candidate facilitator genes MYC-induced cell death. Table lists facilitators death discovered through MYC-specific loss function genetic screen.</p>
<p>Figure S1 shows PCA of human breast tumors, hallmark MYC signature score for expression MYC-target NECTIN4, schematic purine ribonucleotide catabolism, concentrations nucleotides in physiological conditions, prediction hypothetical nucleotide flux, MYC-induced cell death MYC-ER HMECs, and candidate facilitators death.</p>
<p>Figure S4 shows DIS3L mutation in human tumors, evolutionary action score of tumor-derived DIS3L, genomic alteration MYC and breast cancer, expression mRNA genes ribonucleotide catabolism synthesis upon knockdown.</p>
<p>Figure S5 shows expression of MCL1 upon DIS3L knockdown, effect XDH inhibition on MYC-induced cell death, xanthosine TNBC apoptosis, ROS and death HPRT1 knockdown xenografts.</p>
<p>Figure S3 shows MYC-induced apoptosis and cell death in early late timepoints, ectopic expression of BCL2 its impact on RNA decay, gene changes upon DIS3L knockdown MYC-hyperactivated conditions, exosome components MYC-induction.</p>
<p>Table S2 shows gene ontology analysis of candidate facilitator genes MYC-induced cell death.</p>
<p>Figure S6 shows 6-mercaptopurine dose curve in various cell lines, effect of on purine catabolite abundance TNBC cells, XDH knockdown induced death, and 6-mercaptopurine- viability upon nucleotide supplementation.</p>
<p>Table S3 shows evolutionary Action analysis of tumor-derived mutation in DIS3L.</p>
<p>Table S4 shows predictions of hypothetical purine nucleotide flux.</p>
<p>Figure S2 shows MYC-induced cell death in MYC-ER HMECs with DIS3L, EXOSC2, EXOSC8 and DIS3 knockdown, expression of upon EU incorporation MYC-hyperactivated conditions.</p>
<p>Figure S4 shows DIS3L mutation in human tumors, evolutionary action score of tumor-derived DIS3L, genomic alteration MYC and breast cancer, expression mRNA genes ribonucleotide catabolism synthesis upon knockdown.</p>
<p>Table S1 is the list of candidate facilitator genes MYC-induced cell death. Table lists facilitators death discovered through MYC-specific loss function genetic screen.</p>
<p>Table S2 shows gene ontology analysis of candidate facilitator genes MYC-induced cell death.</p>
<p>Figure S2 shows MYC-induced cell death in MYC-ER HMECs with DIS3L, EXOSC2, EXOSC8 and DIS3 knockdown, expression of upon EU incorporation MYC-hyperactivated conditions.</p>
<p>Figure S1 shows PCA of human breast tumors, hallmark MYC signature score for expression MYC-target NECTIN4, schematic purine ribonucleotide catabolism, concentrations nucleotides in physiological conditions, prediction hypothetical nucleotide flux, MYC-induced cell death MYC-ER HMECs, and candidate facilitators death.</p>
<p>Table S4 shows predictions of hypothetical purine nucleotide flux.</p>
<p>Figure S3 shows MYC-induced apoptosis and cell death in early late timepoints, ectopic expression of BCL2 its impact on RNA decay, gene changes upon DIS3L knockdown MYC-hyperactivated conditions, exosome components MYC-induction.</p>
<p>Figure S5 shows expression of MCL1 upon DIS3L knockdown, effect XDH inhibition on MYC-induced cell death, xanthosine TNBC apoptosis, ROS and death HPRT1 knockdown xenografts.</p>
<p>Table S3 shows evolutionary Action analysis of tumor-derived mutation in DIS3L.</p>
<p>Figure S6 shows 6-mercaptopurine dose curve in various cell lines, effect of on purine catabolite abundance TNBC cells, XDH knockdown induced death, and 6-mercaptopurine- viability upon nucleotide supplementation.</p>