A5038530353- Telomeres, Telomerase, and Senescence
- Science, Research, and Medicine
- Neuroblastoma Research and Treatments
- PARP inhibition in cancer therapy
- Cell death mechanisms and regulation
- Radiation Therapy and Dosimetry
- Glioma Diagnosis and Treatment
- Epigenetics and DNA Methylation
- Advanced biosensing and bioanalysis techniques
- Cancer, Hypoxia, and Metabolism
- Dermatological and COVID-19 studies
- Cancer-related Molecular Pathways
- Hematological disorders and diagnostics
- Cancer Research and Treatments
- Microplastics and Plastic Pollution
- Leprosy Research and Treatment
- RNA Interference and Gene Delivery
- DNA Repair Mechanisms
Texas Tech University Health Sciences Center
2021-2024
Texas Tech University
2021-2024
National Cancer Institute
2024
ATM activation at telomeres confers chemoresistance in ALT neuroblastoma and is reversible preclinical models by knockdown or inhibition.
A subset of cancers across multiple histologies with predominantly poor outcomes use the alternative lengthening telomeres (ALT) mechanism to maintain telomere length, which can be identified robust biomarkers. ALT has been reported prevalent in high-risk neuroblastoma and certain sarcomas, are a major clinical challenge that lack targeted therapeutic approaches. Here, we found variety pediatric adult cancer histologies, including carcinomas. Patient-derived cell lines from neuroblastomas,...
Introduction Alternative lengthening of telomeres (ALT) occurs in sarcomas and ALT cancers share common mechanisms therapy resistance or sensitivity. Telomeric DNA C-circles are self-primed circular telomeric repeats detected with a PCR assay that provide sensitive specific biomarker exclusive to cancers. We have previously shown 23% high-risk neuroblastomas the phenotype. Here, we investigate frequency Ewing’s family sarcoma (EFS), rhabdomyosarcoma (RMS), osteosarcoma (OS) by analyzing from...
Abstract Background: Overall survival (OS) of high-risk neuroblastoma (HRNB) patients with alternative lengthening telomeres (ALT) tumors (∼23% patients) is low. Event-free (EFS) HRNB in COG ANBL0532 was higher for tandem relative to single ASCT.We sought determine if ALT on benefited from ASCT. Methods:We assessed telomere maintenance mechanisms (TMM), defined as per Cancer Res 80:2663, 2020, 204 primary TERT+ (high TERT mRNA), (positive telomeric DNA C-circle assay) or ultrabright foci...
Background: Alternative lengthening of telomeres (ALT) occurs in sarcomas and ALT cancers share common mechanisms therapy resistance or sensitivity. Telomeric DNA C-circles are self-primed circular telomeric repeats detected with a PCR assay that provide sensitive specific biomarker exclusive to cancers. We have previously shown 23% high-risk neuroblastomas the phenotype. Here, we investigate frequency Ewing’s family sarcoma (EFS), rhabdomyosarcoma (RMS), osteosarcoma (OS) by analyzing from...
Abstract BACKGROUND High-grade gliomas (HGG) comprise ~10% of pediatric brain tumors; 40% HGG use the alternative lengthening telomeres (ALT) mechanism to maintain replicative immortality. ALT cancers share a unique biology providing potential therapeutic targets. Extrachromosomal telomere DNA repeats, termed C-circles, can be detected by PCR assay, sensitive and specific biomarker for cancers. C-circles have been in tumors serum patients. We adapted C-circle assay (CCA) provide with cfDNA...
Abstract Cancers overcome replicative immortality by activating either telomerase or an alternative lengthening of telomeres (ALT) mechanism. ALT occurs in ∼ 25% high-risk neuroblastomas and relapse progression neuroblastoma patients during after front-line therapy is frequent almost uniformly fatal. Temozolomide + irinotecan commonly used as salvage for neuroblastoma. Patient-derived cell-lines xenografts established from relapsed demonstrated de novo resistance to temozolomide (as SN-38...
<div>Abstract<p>A subset of cancers across multiple histologies with predominantly poor outcomes use the alternative lengthening telomeres (ALT) mechanism to maintain telomere length, which can be identified robust biomarkers. ALT has been reported prevalent in high-risk neuroblastoma and certain sarcomas, are a major clinical challenge that lack targeted therapeutic approaches. Here, we found variety pediatric adult cancer histologies, including carcinomas. Patient-derived cell...
Supplementary Data from Alternative Lengthening of Telomeres in Cancer Confers a Vulnerability to Reactivation p53 Function
Supplementary Data from Alternative Lengthening of Telomeres in Cancer Confers a Vulnerability to Reactivation p53 Function
Supplementary Data from Alternative Lengthening of Telomeres in Cancer Confers a Vulnerability to Reactivation p53 Function
Supplementary Data from Alternative Lengthening of Telomeres in Cancer Confers a Vulnerability to Reactivation p53 Function
<div>Abstract<p>A subset of cancers across multiple histologies with predominantly poor outcomes use the alternative lengthening telomeres (ALT) mechanism to maintain telomere length, which can be identified robust biomarkers. ALT has been reported prevalent in high-risk neuroblastoma and certain sarcomas, are a major clinical challenge that lack targeted therapeutic approaches. Here, we found variety pediatric adult cancer histologies, including carcinomas. Patient-derived cell...
Abstract Introduction: Most cancers proliferate by activating telomerase (TA+) while 10% of utilize alternate lengthening telomeres (ALT). ALT has been associated with resistance to DNA damaging agents, p53 loss-of-function (p53LOF), ATRX mutations, and very poor survival. ATM kinase, which activates functional p53, is constitutively activated in (Science Translational Medicine 18:eabd5750, 2021). We hypothesized that the constitutive activation kinase would confer high sensitivity...