A5093899577- Glioma Diagnosis and Treatment
- Sarcoma Diagnosis and Treatment
- Advanced biosensing and bioanalysis techniques
- Neuroblastoma Research and Treatments
- RNA modifications and cancer
- Nuclear Structure and Function
- DNA Repair Mechanisms
- Cancer-related molecular mechanisms research
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Circular RNAs in diseases
Morgan Adams Foundation
2024-2025
Children's Hospital Colorado
2024-2025
University of Colorado Denver
2024-2025
University of Colorado Anschutz Medical Campus
2024-2025
Posterior fossa molecular subtype A (PFA) ependymoma occurs in young children and is the deadliest of pediatric ependymoma. High-risk subtypes with chromosome 1q+ and/or 6q- exhibit significantly poorer outcome compared to wild-type PFA. However, 50% PFA patients relapse there a high risk gaining 1q at recurrence. We previously found constitutively active NF-κB, through loss LDOC1, led chronic IL-6 secretion an overall immunosuppressive tumor microenvironment higher subset (PFA1). In this...
Abstract Purpose: There are no effective treatment strategies for children with highest-risk posterior fossa group A ependymoma (PFA). Chromosome 1q gains (1q+) present in approximately 25% of newly diagnosed PFA tumors, and this number doubles at recurrence. Seventy percent chromosome 1q+ will die because the tumor, highlighting urgent need to develop new therapeutic population. Experimental Design: In study, we utilize vitro vivo models test efficacy combination radiation chemotherapy a...
<p>MAF-928 in vivo mice had more metastatic lesions with radiation alone.</p>
<p>MAF-811_XC in vivo survival with radiation and chemotherapy.</p>
<p>Densitometry for apoptosis proteomic array of 1q+ PFA cell lines treated with 5FU and 5Gy radiation.</p>
<p>Combination of radiation with 5FU is synergistic in 1q+ PFA cell lines.</p>
<div>AbstractPurpose:<p>There are no effective treatment strategies for children with highest-risk posterior fossa group A ependymoma (PFA). Chromosome 1q gains (1q+) present in approximately 25% of newly diagnosed PFA tumors, and this number doubles at recurrence. Seventy percent chromosome 1q+ will die because the tumor, highlighting urgent need to develop new therapeutic population.</p>Experimental Design:<p>In study, we utilize <i>in vitro</i>...
<p>Combination of radiation with 5FU is synergistic in 1q+ PFA cell lines.</p>
<p>Tretinoin (ATRA) identified as an EPN specific target</p>
<p>Densitometry for apoptosis proteomic array of 1q+ PFA cell lines treated with 5FU and 5Gy radiation.</p>
<p>5FU at 75mg/kg in combination with 10Gy radiation is too toxic vivo</p>
<p>MAF-811_XC in vivo survival with radiation and chemotherapy.</p>
<div>AbstractPurpose:<p>There are no effective treatment strategies for children with highest-risk posterior fossa group A ependymoma (PFA). Chromosome 1q gains (1q+) present in approximately 25% of newly diagnosed PFA tumors, and this number doubles at recurrence. Seventy percent chromosome 1q+ will die because the tumor, highlighting urgent need to develop new therapeutic population.</p>Experimental Design:<p>In study, we utilize <i>in vitro</i>...
<p>MDM4 gene expression with 5FU treatment</p>
<p>MAF-811_XC in vivo survival with radiation and chemotherapy.</p>
<p>MAF-928 in vivo mice had more metastatic lesions with radiation alone.</p>
<p>5FU at 75mg/kg in combination with 10Gy radiation is too toxic vivo</p>
<p>MDM4 gene expression with 5FU treatment</p>
<p>Tretinoin (ATRA) identified as an EPN specific target</p>
<p>MAF-811_XC in vivo survival with radiation and chemotherapy.</p>
Abstract BACKGROUND Gain of chromosome 1q (1q+), gives a grave prognosis in pediatric posterior fossa group A ependymoma (PFA). The prevalence 1q+ newly diagnosed PFA stands at 25%, escalating to 50% upon recurrence. Conventional therapeutic modalities, such as complete resection and radiation, exhibit minimal efficacy cases PFA, the incorporation additional chemotherapy clinical trials has failed yield substantial improvements. In this investigation, we delineate trisomy-induced...
Abstract INTRODUCTION BCL6 corepressor gene (BCOR)-altered glioma brain tumors are a newly identified entity which include cases involving fusion with histone acetyltransferase EP300. Treatment strategies for BCOR-fusion gliomas have not yet been established, largely due to their rarity. In this study we utilize established EP300::BCOR cell line identify effective FDA-approved oncology compounds in vitro. METHODS MAF-1211, from autopsy material, was molecularly defined confirm the and...
Abstract INTRODUCTION Chromosome 6q loss (6q-) has recently been identified as an ultra-high-risk factor in posterior fossa group A ependymoma (PFA). This study seeks to pinpoint the biological mechanism underlying aggressive biology of PFA 6q-. We hypothesize that chromosome gene large tumor suppressor kinase 1 (LATS1) 6q- results increased Hippo pathway activity drives malignant progression. LATS1 is a key negative regulator which may represent novel therapeutic vulnerability PFA. METHODS...
Abstract BACKGROUND Nearly all children with gain of chromosome 1q (1q+) PFA ependymoma (EPN) will die, highlighting the urgent need to develop new treatment strategies for these patients. It has recently been shown that 1q+ creates a p53 mutant-like phenotype through trisomy expression MDM4, repressor signaling. This same study found toxic uracil analogs could reverse MDM4 effect on and this was mediated another 1q-trisomy gene UCK2. We other have previously identified 5-fluorouracil (5FU)...