A5037078674- RNA modifications and cancer
- Biochemical and Molecular Research
- Cancer-related gene regulation
- RNA Research and Splicing
- Signaling Pathways in Disease
- Glioma Diagnosis and Treatment
- Protein Degradation and Inhibitors
- PARP inhibition in cancer therapy
- Neuroblastoma Research and Treatments
- Nuclear Structure and Function
- Epigenetics and DNA Methylation
- Sarcoma Diagnosis and Treatment
- RNA regulation and disease
- Endoplasmic Reticulum Stress and Disease
- FOXO transcription factor regulation
- Prostate Cancer Treatment and Research
- Ethics in Clinical Research
- Prostate Cancer Diagnosis and Treatment
University of Michigan
2021-2025
Diffuse midline gliomas (DMG) are highly invasive brain tumors with rare survival beyond two years past diagnosis and limited understanding of the mechanism behind tumor invasion. Previous reports demonstrate upregulation protein ID1 H3K27M ACVR1 mutations in DMG, but this has not been confirmed human or therapeutically targeted.
PURPOSE Given challenges with randomized trials, tumor registries, and insurance claims, electronic health record data are an appealing resource for studying prostate-specific antigen (PSA) screening prostate cancer. Transparent, well-evaluated computable phenotypes that observe a stringent definition of ( v for-cause diagnosis- or symptom-directed testing) critical reproducibility comparison prospective cohorts. METHODS A cohort patients who underwent PSA testing in primary care setting at...
Abstract Ewing sarcomas are driven by EWS–ETS fusions, most commonly EWS-FLI1, which promotes widespread metabolic reprogramming, including activation of serine biosynthesis. We previously reported that biosynthesis is also activated in sarcoma the scaffolding protein menin through as yet undefined mechanisms. Here, we investigated whether EWS-FLI1 and/or orchestrate via modulation ATF4, a stress-response gene acts master transcriptional regulator other tumors. Our results show sarcoma, ATF4...
Abstract Diffuse midline gliomas (DMG) are highly invasive brain tumors with rare survival beyond two years past diagnosis. The mechanism behind tumor invasion is currently not well understood. Previous reports demonstrate upregulation of the protein ID1 H3K27M and ACVR1 mutations in DMG, but this has been confirmed human or therapeutically targeted. Whole exome, RNA, ChIP-sequencing were performed on locus DMG tissue. Scratch-assay migration transwell assays cultured cells following...
<p>Supplementary Figure S1. Real-time cell proliferation analysis of shATF4, MI-503 treatment, and dox-inducible shMEN1 knockdown in Ewing sarcoma cells.</p>
<p>shRNA sequences, plasmid information, western blot antibodies</p>
<p>Supplementary Figure S2. Effect of shFLI1 knockdown in CHLA10 Ewing sarcoma cells and Publicly Available ChIP-seq EWS-FLI1 at the ATF4 SSP Gene Promoters.</p>
<p>Supplementary Figure S3. Timecourse for the effect of MI-503 on ATF4 in Ewing sarcoma cell lines.</p>
<p>Supplementary Figure S4. Publicly Available RNA-Seq Data of EWS-FLI1 Knockdown.</p>
<p>shRNA sequences, plasmid information, western blot antibodies</p>
<p>Supplementary Figure S3. Timecourse for the effect of MI-503 on ATF4 in Ewing sarcoma cell lines.</p>
<p>Supplementary Figure S4. Publicly Available RNA-Seq Data of EWS-FLI1 Knockdown.</p>
<p>Supplementary Figure S1. Real-time cell proliferation analysis of shATF4, MI-503 treatment, and dox-inducible shMEN1 knockdown in Ewing sarcoma cells.</p>
<p>Supplementary Figure S2. Effect of shFLI1 knockdown in CHLA10 Ewing sarcoma cells and Publicly Available ChIP-seq EWS-FLI1 at the ATF4 SSP Gene Promoters.</p>
<div>Abstract<p>Ewing sarcomas are driven by EWS–ETS fusions, most commonly EWS-FLI1, which promotes widespread metabolic reprogramming, including activation of serine biosynthesis. We previously reported that biosynthesis is also activated in Ewing sarcoma the scaffolding protein menin through as yet undefined mechanisms. Here, we investigated whether EWS-FLI1 and/or orchestrate via modulation ATF4, a stress-response gene acts master transcriptional regulator other tumors. Our...
<div>Abstract<p>Ewing sarcomas are driven by EWS–ETS fusions, most commonly EWS-FLI1, which promotes widespread metabolic reprogramming, including activation of serine biosynthesis. We previously reported that biosynthesis is also activated in Ewing sarcoma the scaffolding protein menin through as yet undefined mechanisms. Here, we investigated whether EWS-FLI1 and/or orchestrate via modulation ATF4, a stress-response gene acts master transcriptional regulator other tumors. Our...