Publications by authors named "R Pineau"

Understanding how mutations arise and spread through individuals and populations is fundamental to evolutionary biology. Most organisms have a life cycle with unicellular bottlenecks during reproduction. However, some organisms like plants, fungi, or colonial animals can grow indefinitely, changing the manner in which mutations spread throughout both the individual and the population.

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  • Murine models are important in cancer research for studying glioblastoma using a specific protocol for tumor generation.
  • The protocol includes steps for preparing tumor cells, injecting them into the brain, and applying standard treatments.
  • It also covers how to monitor tumor growth with bioluminescent imaging, with further details available in the referenced study.
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  • Lung cancer is a leading cause of cancer-related deaths, necessitating advanced preclinical models to explore new treatments based on tumor genetics.
  • Researchers developed and characterized cell lines and mouse models for non-small cell lung cancer (NSCLC) to monitor tumor growth and treatment response effectively.
  • The study found that combining osimertinib and bevacizumab improves treatment outcomes for EGFR-mutated tumors, while adding afatinib helps inhibit tumor growth during treatment resistance, demonstrating the models’ utility for testing new therapies and understanding resistance mechanisms.
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The evolution of multicellular life spurred evolutionary radiations, fundamentally changing many of Earth's ecosystems. Yet little is known about how early steps in the evolution of multicellularity affect eco-evolutionary dynamics. Through long-term experimental evolution, we observed niche partitioning and the adaptive divergence of two specialized lineages from a single multicellular ancestor.

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Signalling by the Unfolded Protein Response (UPR) or by the Death Receptors (DR) are frequently activated towards pro-tumoral outputs in cancer. Herein, we demonstrate that the UPR sensor IRE1 controls the expression of the DR CD95/Fas, and its cell death-inducing ability. Both genetic and pharmacologic blunting of IRE1 activity increased CD95 expression and exacerbated CD95L-induced cell death in glioblastoma (GB) and Triple-Negative Breast Cancer (TNBC) cell lines.

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