J Can Health Libr Assoc
August 2024
Background: In response to the COVID-19 pandemic, the Ontario-based Centre for Effective Practice (CEP) established the COVID-19 Resource Centre (CRC) in March 2020. This platform rapidly became a critical source of clinical and practice guidance for primary care providers, highlighting the importance of effective information synthesis during public health emergencies.
Description: The article discusses the development of the CRC, emphasizing the application of librarianship principles in navigating the challenges posed by the pandemic's information overload and the scarcity of evidence.
Triple-negative breast cancer (TNBC) is a difficult-to-treat, aggressive cancer type. TNBC is often associated with the cellular program of epithelial-mesenchymal transition (EMT) that confers drug resistance and metastasis. EMT and reverse mesenchymal-epithelial transition (MET) programs are regulated by several signaling pathways which converge on a group of transcription factors, EMT- TFs.
View Article and Find Full Text PDFEpithelial mesenchymal transition (EMT) and mesenchymal epithelial transition (MET) are genetic determinants of cellular plasticity. These programs operate in physiological (embryonic development, wound healing) and pathological (organ fibrosis, cancer) conditions. In cancer, EMT and MET interfere with various signalling pathways at different levels.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2022
Autophagy is a highly conserved process of cellular self-digestion that involves the formation of autophagosomes for the delivery of intracellular components and dysfunctional organelles to lysosomes. This process is induced by different signals including starvation, mitochondrial dysfunction, and DNA damage. The molecular link between autophagy and DNA damage is not well understood yet.
View Article and Find Full Text PDFThe TAM proteins TYRO3, AXL, and MER are receptor tyrosine kinases implicated in the clearance of apoptotic debris and negative regulation of innate immune responses. AXL contributes to immunosuppression by terminating the Toll-like receptor signaling in dendritic cells, and suppressing natural killer cell activity. In recent years, AXL has been intensively studied in the context of cancer.
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