Publications by authors named "Olivia L Perkins"
Article Synopsis
- Research indicates that despite existing therapies, the outlook for patients with refractory or recurrent rhabdomyosarcoma (RMS) remains poor, prompting exploration of differentiation-inducing treatments.
- In preclinical models of RAS-mutant PAX fusion-negative RMS, MEK1/2 inhibition has shown potential to encourage differentiation, slow tumor growth, and extend survival, although responses are often temporary.
- The study identifies ASAP1 and ARF1 as crucial regulators in promoting differentiation in FN-RMS cells, revealing that targeting these molecules may enhance treatment strategies by affecting key transcriptional regulators, such as WWTR1 (TAZ).
Actin-based protrusions extend from the surface of all eukaryotic cells, where they support diverse activities essential for life. Models of protrusion growth hypothesize that actin filament assembly exerts force for pushing the plasma membrane outward. However, membrane-associated myosin motors are also abundant in protrusions, although their potential for contributing, growth-promoting force remains unexplored.
View Article and Find Full Text PDFPurpose: PAX-fusion negative rhabdomyosarcoma (FN RMS) is driven by alterations in the RAS/MAP kinase pathway and is partially responsive to MEK inhibition. Overexpression of IGF1R and its ligands is also observed in FN RMS. Preclinical and clinical studies have suggested that IGF1R is itself an important target in FN RMS.
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