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Gemcitabine and ATR Inhibitors Synergize to Kill PDAC Cells by Blocking DNA Damage Response
[Molecular Systems Biology] Investigators phenotypically screened 13 human PDAC cell lines against gemcitabine in combination with 146 clinical inhibitors and observed strong synergy for the ATR kinase inhibitor elimusertib in most cell lines.
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Targeting Pancreatic Cancer Glutamine Dependency Confers Vulnerability to GPX4-Dependent Ferroptosis
[Cell Reports Medicine] The authors elucidated that prolonged glutamine (Gln) restriction or treatment with the Gln antagonist, 6-diazo-5-oxo-L-norleucine, led to growth inhibition and ferroptosis program activation in PDAC.
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S100A13-Driven Interaction Between Pancreatic Adenocarcinoma Cells and Cancer-Associated Fibroblasts Promotes Tumor Progression through Calcium Signaling
[Cell Communication and Signaling] Bioinformatic analysis was employed to predict the pathogenic potential of cancer-associated fibroblasts (CAFs) and S100A13. Stable S100A13 knockdown CAFs were generated using a short hairpin RNA system.
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The Fungal Microbiota Modulate Neonatal Oxygen-Induced Lung Injury
[Microbiome] Researchers showed that the fungal microbiota modulated hyperoxia-induced lung injury severity in very low birth weight premature infants and preclinical pseudohumanized and altered fungal colonization mouse models.
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Promoting Epithelial Regeneration in Chemically Induced Acute Lung Injury through Sox9-Positive Alveolar Type 2 Epithelial Cells
[Stem Cell Research & Therapy] The authors generated Sox9flox/flox;SftpcCre−ERT2 mice and examined the effects of Sox9+ alveolar type 2 epithelial cells cells on the pathophysiology of epithelial damage during chemical-induced acute lung injury.
Cancer Stem Cell News
CD36 Enrichment in HER2-Positive Mesenchymal Stem Cells Drives Therapy Refractoriness in Breast Cancer
[Journal of Experimental & Clinical Cancer Research] Scientists elucidated whether enhanced CD36 in mesenchymal HER2 + CSCs was directly involved in anti-HER2 treatment refractoriness in HER2 + breast cancer and to design future metabolism-based approaches targeting both fatty acid reprogramming and the “root” of cancer.