Publications by authors named "S G Kellaway"
Electrospun drug-loaded scaffolds for nervous system repair.
Wiley Interdiscip Rev Nanomed Nanobiotechnol
May 2024
Nervous system injuries, encompassing peripheral nerve injury (PNI), spinal cord injury (SCI), and traumatic brain injury (TBI), present significant challenges to patients' wellbeing. Traditional treatment approaches have limitations in addressing the complexity of neural tissue regeneration and require innovative solutions. Among emerging strategies, implantable materials, particularly electrospun drug-loaded scaffolds, have gained attention for their potential to simultaneously provide structural support and controlled release of therapeutic agents.
View Article and Find Full Text PDFAML is characterized by mutations in genes associated with growth regulation such as internal tandem duplications (ITD) in the receptor kinase FLT3. Inhibitors targeting FLT3 (FLT3i) are being used to treat patients with FLT3-ITD+ but most relapse and become resistant. To elucidate the resistance mechanism, we compared the gene regulatory networks (GRNs) of leukemic cells from patients before and after relapse, which revealed that the GRNs of drug-responsive patients were altered by rewiring their AP-1-RUNX1 axis.
View Article and Find Full Text PDFArticle Synopsis
- Acute Myeloid Leukemia (AML) results from various mutations that disrupt normal growth and differentiation of myeloid cells, leading to a dangerous increase in immature blast cells.
- Current treatments mainly involve chemotherapy, but they often fail due to the presence of dormant leukemic stem cells (LSCs) that can reactivate and cause relapse.
- This study focuses on the t(8;21) subtype of AML, revealing that LSCs in this model activate specific signaling pathways (VEGF and IL-5) that help them exit dormancy and maintain self-renewal, contributing to treatment resistance.
Article Synopsis
- Acute myeloid leukemia (AML) is a complex disease linked to various mutations, each creating its own gene regulatory network (GRN) with interacting transcription factors.
- Researchers tested the idea that important regulators for maintaining AML can be found in highly interconnected nodes of these GRNs, focusing on FLT3-ITD-mutated AML as their model.
- Their findings indicate that specific regulatory modules are essential for AML growth, and the transcription factor RUNX1 is critical, as its removal disrupts the GRN, leading to cell death.