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    <title>Aging on Pierre-François Roux</title>
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    <description>Recent content in Aging on Pierre-François Roux</description>
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    <copyright>&amp;copy; 2021 Pierre-François Roux</copyright>
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      <title>ATAC-seq as an integrative assay for aging and cancer</title>
      <link>https://www.pierre-francois-roux.com/project/atac-seq-as-an-integrative-assay-for-aging-and-cancer/</link>
      <pubDate>Fri, 19 Jun 2026 00:00:00 +0000</pubDate>
      
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      <description>ATAC-seq is widely used to map chromatin accessibility, but bulk ATAC-seq libraries contain much more information than accessible regulatory elements alone. In recent work, I benchmarked ATAC-seq against matched whole-genome sequencing to evaluate whether a single assay can also recover genetic information relevant to cancer and aging biology.
Using paired datasets from patient-derived melanoma cell lines and TCGA brain tumors, we showed that ATAC-seq can support high-precision small variant detection within accessible regions, robust copy-number profiling, mitochondrial genome characterization and telomere-associated repeat quantification, while preserving its classical epigenomic readouts.</description>
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      <title>Molecular basis of cellular senescence and aging</title>
      <link>https://www.pierre-francois-roux.com/teaching/molecular-basis-of-cellular-senescence-and-aging/</link>
      <pubDate>Fri, 19 Jun 2026 00:00:00 +0000</pubDate>
      
      <guid>https://www.pierre-francois-roux.com/teaching/molecular-basis-of-cellular-senescence-and-aging/</guid>
      <description>This teaching introduces the molecular basis of cellular senescence and aging, with a focus on how stress-response pathways, chromatin regulation, metabolism and inflammatory programs interact to shape cell fate decisions.
 Université de Montpellier, Master 2 Biologie-Santé, 2021  Lecture, 4 h  The course connects fundamental mechanisms to pathophysiological contexts, including tumor suppression, tissue aging, cancer biology and metabolic homeostasis. It also uses examples from functional genomics and multi-omic studies to show how contemporary molecular biology can move from descriptive profiles to mechanistic hypotheses.</description>
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      <title>p53/E4F1-mediated metabolic and epigenetic control of senescence</title>
      <link>https://www.pierre-francois-roux.com/project/p53-e4f1-metabolic-epigenetic-control-of-senescence/</link>
      <pubDate>Fri, 19 Jun 2026 00:00:00 +0000</pubDate>
      
      <guid>https://www.pierre-francois-roux.com/project/p53-e4f1-metabolic-epigenetic-control-of-senescence/</guid>
      <description>My current research at the Montpellier Cancer Research Institute focuses on how metabolic rewiring is converted into durable chromatin and transcriptional states during senescence and aging. Cellular senescence relies on checkpoint pathways controlled by pRB and p53, but these regulators do more than arrest the cell cycle: they also control metabolic homeostasis, mitochondrial function, stress adaptation and chromatin regulation.
A central entry point of this project is E4F1, a multifunctional component of the p53/pRB network.</description>
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      <title>Toward a systems view of cellular senescence</title>
      <link>https://www.pierre-francois-roux.com/project/toward-a-systems-view-of-cellular-senescence/</link>
      <pubDate>Fri, 27 Apr 2018 00:00:00 +0000</pubDate>
      
      <guid>https://www.pierre-francois-roux.com/project/toward-a-systems-view-of-cellular-senescence/</guid>
      <description>Cellular senescence is a stress response triggered by telomere dysfunction, oncogene activation, DNA damage, oxidative stress and other insults. It leads to a durable proliferative arrest, but also to profound changes in chromatin organization, transcription, metabolism and secretory activity. This dual nature makes senescence biologically fascinating: it contributes to tumor suppression, wound healing and development, yet persistent senescent cells can also promote chronic inflammation, tissue dysfunction, cancer progression and aging-related pathologies.</description>
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