Louise Y Cheng

The paper shows that oncogenic outcomes of dedifferentiation in Drosophila CNS vary by region, mediated by Chinmo and ecdysone signaling.

This study shows that oenocytes in Drosophila accumulate lipids in response to tumor signals, reflecting systemic lipid metabolism changes, but do not preserve muscle function during cachexia.

This study shows that the SLC36 transporter Pathetic in Drosophila blood-brain barrier glia regulates tumour growth under nutrient restriction by modulating mTor-S6K pathway activity.

This study shows that dedifferentiated tumour neural stem cells in Drosophila generate a glial niche that supports tumour growth through dysregulated ecdysone signalling.

This study shows that depletion of the neuroepithelium stem cell pool determines the cessation of medulla NBs in Drosophila optic lobes, with multiple mechanisms contributing to their termination.

This study identifies insulin and TGF-β signaling convergence in Drosophila adipose tissue that drives ECM accumulation and muscle wasting in a tumor model.

This study identifies mitochondrial fusion and beta-oxidation as key drivers of muscle wasting in a Drosophila cancer cachexia model and shows interventions can mitigate muscle loss.

This study identifies Her6 and Prox1 as regulators of photoreceptor regeneration in zebrafish retina, showing they cross-regulate to promote differentiation.

This study shows that dedifferentiation-derived neural stem cells (NSCs) fail to express late temporal transcription factors, leading to impaired neuronal diversity and cell cycle progression.

This study shows that glial Hedgehog signaling and lipid metabolism regulate neural stem cell proliferation in Drosophila by modulating Hh signaling through lipid droplets and palmitoylation.