Publications by authors named "Maria Quiles Del Rey"

Objectives: Disparities in cancer incidence and outcomes across race, ethnicity, gender, socioeconomic status, and geography are well-documented, but their etiologies are often poorly understood and multifactorial. Clinical informatics can provide tools to better understand and address these disparities by enabling high-throughput analysis of multiple types of data. Here, we review recent efforts in clinical informatics to study and measure disparities in cancer.

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Unlabelled: Pancreatic ductal adenocarcinomas (PDAC) depend on autophagy for survival; however, the metabolic substrates that autophagy provides to drive PDAC progression are unclear. Ferritin, the cellular iron storage complex, is targeted for lysosomal degradation (ferritinophagy) by the selective autophagy adaptor NCOA4, resulting in release of iron for cellular utilization. Using patient-derived and murine models of PDAC, we demonstrate that ferritinophagy is upregulated in PDAC to sustain iron availability, thereby promoting tumor progression.

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Article Synopsis
  • Some tumors don’t respond well to treatments because they lose important signals (MHC class I) needed for immune cells to recognize them.
  • A new treatment involving specific proteins (cIAP1/2 antagonists) can help the immune system fight these tumors by changing how certain immune cells (macrophages) attack.
  • Using this new treatment alongside another therapy (CD47 blockade) might work even better against tough tumors that usually resist other types of treatments.
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Article Synopsis
  • Rodent's incisors have special enamel rich in iron that keeps growing as they age, making them interesting for studying how iron works in the body.
  • Scientists removed a specific gene (ATG7) in mice that helps make enamel, which caused the teeth to turn white instead of yellow due to less iron moving into the enamel.
  • The absence of ATG7 also led to extra teeth growing in places where they shouldn't, showing that healthy enamel growth in rodents relies on this gene's activity.
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NCOA4 (Nuclear receptor coactivator 4) mediates the selective autophagic degradation of ferritin, the cellular cytosolic iron storage complex, thereby playing a critical role in intracellular and systemic iron homeostasis. Disruptions in iron homeostasis and autophagy are observed in several neurodegenerative disorders raising the possibility that NCOA4-mediated ferritinophagy links these two observations and may underlie, in part, the pathophysiology of neurodegeneration. Here, we review the available evidence detailing the molecular mechanisms of NCOA4-mediated ferritinophagy and recent studies examining its role in systemic iron homeostasis and erythropoiesis.

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Ncoa4 mediates autophagic degradation of ferritin, the cytosolic iron storage complex, to maintain intracellular iron homeostasis. Recent evidence also supports a role for Ncoa4 in systemic iron homeostasis and erythropoiesis. However, the specific contribution and temporal importance of Ncoa4-mediated ferritinophagy in regulating systemic iron homeostasis and erythropoiesis is unclear.

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Pancreatic ductal adenocarcinoma is a notoriously difficult-to-treat cancer and patients are in need of novel therapies. We have shown previously that these tumours have altered metabolic requirements, making them highly reliant on a number of adaptations including a non-canonical glutamine (Gln) metabolic pathway and that inhibition of downstream components of Gln metabolism leads to a decrease in tumour growth. Here we test whether recently developed inhibitors of glutaminase (GLS), which mediates an early step in Gln metabolism, represent a viable therapeutic strategy.

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The PI3K/mTOR pathway is commonly deregulated in cancer. mTOR inhibitors are registered for the treatment of several solid tumors and novel inhibitors are explored clinically. Notably, this pathway also plays an important role in immunoregulation.

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Rationale: Several lines of evidence indicate that the regulation of microRNA (miRNA) levels by different stimuli may contribute to the modulation of stimulus-induced responses. The miR-17-92 cluster has been linked to tumor development and angiogenesis, but its role in vascular endothelial growth factor-induced endothelial cell (EC) functions is unclear and its regulation is unknown.

Objective: The purpose of this study was to elucidate the mechanism by which VEGF regulates the expression of miR-17-92 cluster in ECs and determine its contribution to the regulation of endothelial angiogenic functions, both in vitro and in vivo.

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