Background: Non-Small Cell Lung Cancer (NSCLC) is the leading cause of cancer death worldwide. Although immune checkpoint inhibitors (ICIs) have shown remarkable clinical efficacy, they can also induce a paradoxical cancer acceleration, known as hyperprogressive disease (HPD), whose causative mechanisms are still unclear.
Methods: This study investigated the mechanisms of ICI resistance in an HPD-NSCLC model.
Purpose: To describe and clarify a possible pathogenetic origin for choroidal caverns in young healthy individuals through a topographical analysis using swept-source optical coherence tomography angiography (SS-OCTA).
Methods: A cross-sectional evaluation of 44 healthy volunteers (44 eyes), aged 20-32 years with no systemic or ocular comorbidities. The topographical analysis of choroidal caverns was performed through a 15 × 15 mm volumetric scan cube using SS-OCTA (PLEX Elite 9000).
Alterations in mitochondrial function have been linked to a variety of cellular and organismal stress responses including apoptosis, aging, neurodegeneration and tumorigenesis. However, adaptation to mitochondrial dysfunction can occur through the activation of survival pathways, whose mechanisms are still poorly understood. The yeast is an invaluable model organism for studying how mitochondrial dysfunction can affect stress response and adaptation processes.
View Article and Find Full Text PDFMitochondrial (an acronym for ReTroGrade) signaling plays a cytoprotective role under various intracellular or environmental stresses. We have previously shown its contribution to osmoadaptation and capacity to sustain mitochondrial respiration in yeast. Here, we studied the interplay between , the main positive regulator of the pathway, and , encoding the catalytic subunit of the Hap2-5 complex required for the expression of many mitochondrial proteins that function in the tricarboxylic acid (TCA) cycle and electron transport, upon osmotic stress.
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