A5006819204- Acute Lymphoblastic Leukemia research
- Cancer, Hypoxia, and Metabolism
- Acute Myeloid Leukemia Research
- Immune Cell Function and Interaction
- Glioma Diagnosis and Treatment
- Adrenal and Paraganglionic Tumors
- Epigenetics and DNA Methylation
- Childhood Cancer Survivors' Quality of Life
- Cancer-related Molecular Pathways
- T-cell and B-cell Immunology
- Chronic Myeloid Leukemia Treatments
- Chronic Lymphocytic Leukemia Research
- Cancer Genomics and Diagnostics
- PARP inhibition in cancer therapy
- Immune cells in cancer
- Neuroblastoma Research and Treatments
- Genomics and Rare Diseases
- Ubiquitin and proteasome pathways
- Viral gastroenteritis research and epidemiology
- Inflammasome and immune disorders
- Metabolism and Genetic Disorders
- interferon and immune responses
- Hippo pathway signaling and YAP/TAZ
- Pharmaceutical studies and practices
- DNA Repair Mechanisms
St. Jude Children's Research Hospital
2016-2025
Children's Research Hospital
2021
University of Tennessee Health Science Center
2001-2017
Leidos (United States)
2017
Frederick National Laboratory for Cancer Research
2017
Cohen Children's Medical Center
2017
University of Tennessee at Knoxville
1998-2013
University of California, San Francisco
2012
The University of Melbourne
2005
S.P.E.C.I.E.S.
2003
Upon antigen stimulation, the bioenergetic demands of T cells increase dramatically over resting state. Although a role for metabolic switch to glycolysis has been suggested support increased anabolic activities and facilitate cell growth proliferation, whether cellular metabolism controls lineage choices remains poorly understood. We report that glycolytic pathway is actively regulated during differentiation inflammatory TH17 Foxp3-expressing regulatory (Treg cells) fate determination. but...
Inflammation plays a key role in the pathogenesis of obesity. Chronic overfeeding leads to macrophage infiltration adipose tissue, resulting proinflammatory cytokine production. Both microbial and endogenous danger signals trigger assembly intracellular innate immune sensor Nlrp3, caspase-1 activation production cytokines IL-1β IL-18. Here, we showed that mice deficient apoptosis-associated speck-like protein, were resistant development high-fat diet-induced obesity, which correlated with...
ZBP1 activates the NLRP3 inflammasome and programmed cell death.
Retinoblastoma is an aggressive childhood cancer of the developing retina that initiated by biallelic loss RB1. Tumours progress very quickly following RB1 inactivation but underlying mechanism not known. Here we show retinoblastoma genome stable, multiple pathways can be epigenetically deregulated. To identify mutations cooperate with loss, performed whole-genome sequencing retinoblastomas. The overall mutational rate was low; only known gene mutated. We then evaluated role in stability and...
We report genetic aberrations that activate the ERK/MAP kinase pathway in 100% of posterior fossa pilocytic astrocytomas, with a high frequency gene fusions between KIAA1549 and BRAF among these tumours. These were identified from analysis focal copy number gains at 7q34, detected using Affymetrix 250K 6.0 SNP arrays. PCR sequencing confirmed presence five KIAA1549-BRAF fusion variants, along single SRGAP3 RAF1. The resulting genes lack auto-inhibitory domains RAF1, which are replaced...
Cell death provides host defense and maintains homeostasis. Zα-containing molecules are essential for these processes. Z-DNA binding protein 1 (ZBP1) activates inflammatory cell death, PANoptosis, whereas adenosine deaminase acting on RNA (ADAR1) serves as an editor to maintain Here, we identify characterize ADAR1's interaction with ZBP1, defining its role in regulation tumorigenesis. Combining interferons (IFNs) nuclear export inhibitors (NEIs) ZBP1-dependent PANoptosis. ADAR1 suppresses...
Cancer can involve non-resolving, persistent inflammation where varying numbers of tumor-associated macrophages (TAMs) infiltrate and adopt different activation states between anti-tumor M1 pro-tumor M2 phenotypes. Here, we resolve a cascade causing differential macrophage phenotypes in the tumor microenvironment. Reduction TNF mRNA production or loss type I receptor signaling resulted striking pattern enhanced expression. gene expression was driven part by IL-13 from eosinophils...