Publications by authors named "Owen A Ledwell"

Article Synopsis
  • * The only approved treatment, Rapamycin, offers limited benefits as lung function declines after stopping the drug, with LAM cancer stem-like cells displaying high levels of cancer-promoting protein synthesis.
  • * A new compound, RMC-5552, shows promise by effectively inhibiting LAM-associated cell growth and providing longer-lasting effects than Rapamycin, suggesting it could be a potential therapy for LAM and other conditions with mTORC1 hyperactivity.
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Lymphangioleiomyomatosis (LAM) is a progressive cystic lung disease caused by tuberous sclerosis complex 1/2 (TSC1/2) gene mutations in pulmonary mesenchymal cells, resulting in activation of the mechanistic target of rapamycin complex 1 (mTORC1). A subset of patients with LAM develop pulmonary vascular remodeling and pulmonary hypertension. Little, however, is known regarding how LAM cells communicate with endothelial cells (ECs) to trigger vascular remodeling.

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