Our research delves into the surprising abundance of repetitive DNA found in our chromosomes, primarily from « jumping genes » known as transposable elements. These elements can move within the genome, significantly influencing human genetic diversity and contributing to various genetic conditions. Our focus is on a specific group unique to humans, the LINE-1 clade, which is active in reproductive cells, the brain, cancers, and during aging. Using innovative technologies like ATLAS-seq for deep sequencing and CRISPR-Cas9 for precise genetic editing, we aim to understand how these elements alter the human genome and epigenome, offering insights into their broad physiological effects.

Our research explores how aging affects the regeneration of epithelial tissues—like the skin, intestine, and lungs—and their progression into cancer using models ranging from mice to cellular systems. The intestine and skin frequently renew themselves, while the lungs regenerate very slowly. These tissues interact extensively with the external environment, facing significant mechanical forces that they sense and respond to at various levels. We focus particularly on how cells convert mechanical signals into biological responses during tissue regeneration. Understanding the aging process’s impact on this and stem cell behavior could lead to breakthroughs in promoting healthier aging and designing targeted cancer therapies tailored to individual needs.

Our research aims to uncover why cancer incidence increases with age, focusing on the role of telomeres, the protective caps at the ends of our chromosomes. We use zebrafish as a novel model for this study because, unlike mice, zebrafish naturally have shorter telomeres that decrease with age, affecting cell proliferation and lifespan. As telomeres shorten, they lose their protective ability, leading to cell aging and potential genome instability. Our hypothesis suggests that this telomere shortening causes cells to release inflammatory and tumor-promoting factors, creating a favorable environment for cancer development as we age. This interaction between aging cells and their environment could be key to understanding cancer’s onset in older adults.

Our research focuses on the intricate relationship between cancer cells and their surrounding environment, particularly with carcinoma-associated fibroblasts (CAF), in primary tumors. These fibroblasts play a critical role in the development and spread of cancer by remodeling the matrix and creating pathways for cancer cell invasion. We aim to understand how « normal » fibroblasts transform into pro-invasive CAFs, driven by signals from malignant cells that secrete cytokines and growth factors. This interaction significantly influences cancer progression. Building on our previous work, we are investigating the specific signaling pathways and molecules involved in this crosstalk, hoping to identify new therapeutic targets for aggressive and metastatic cancers.

Our lab is focused on uncovering the detailed mechanisms and molecular tools that define telomeres as essential parts of the nucleus and how changes in telomeres can influence cell fate, with implications for aging and medicine. Starting from the key shelterin protein TRF2, the team combines multiple scientific approaches to study its structure and function. Their goal is to use this knowledge to tackle broader issues like telomere protection, cellular aging, immune system interactions, and cancer development, and also to innovate clinical treatments for cancer and age-related diseases. Recently, they have shifted to explore how evolutionary changes in telomere biology may affect the lifespan and health of species, studying natural yeast and coral populations as part of the TARA-PACIFIC expedition, to understand the link between telomere variation and organismal health.

Our research team is dedicated to advancing the next generation of treatments for lung cancer, the world’s deadliest cancer. We are investigating the complex genetic and cellular events that contribute to lung cancer and the lack of response to current therapies. Our goal is to identify markers that predict non-response to immunotherapies and targeted therapies, and to enhance treatment effectiveness with innovative combinations of molecules. Led by Prof P. Hofman, our group is developing a new liquid biopsy technique to monitor responses to immunotherapies. Dr. V. Vouret-Craviari’s team is exploring how purinergic checkpoints can guide immune cells to fight tumors more effectively. Dr. P. Brest focuses on understanding how RNA-binding proteins within membraneless biocondensates affect protein synthesis and tumor resistance. Lastly, Dr. B. Mograbi is investigating the role of human endogenous retroviruses in cancer, suggesting they could help boost immune defenses against tumors.

Together, our multidisciplinary team is pushing the boundaries of lung cancer research to find more effective treatments and improve patient outcomes.

Our lab is dedicated to uncovering the genetic basis of human traits like cancer susceptibility and aging, using the simple organism, budding yeast (S. cerevisiae), as a model. This approach allows us to simulate complex human genetic interactions in a controlled, high-throughput environment. We aim to both model complex traits and directly explore those relevant to cancer and aging. By leveraging natural yeast variations, we investigate how genes contribute to various phenotypes, drawing on the conserved biological pathways between yeast and humans. Our findings help predict genetic variations in natural populations and understand the evolutionary forces that preserve this diversity. This research could eventually illuminate the genetic architecture of complex traits in humans, enhancing our understanding and treatment of age-related diseases and cancer.

Our research group explores how a key cell signaling pathway, known as the ERK pathway, impacts cancer development and progression, with a particular focus on its role in promoting the growth of blood vessels in tumors—a process called angiogenesis. This pathway influences the production of VEGF, a protein that helps tumors attract blood supply, which is crucial for their growth. Our studies have helped identify how changes in this pathway can indicate the severity of certain cancers, such as those in the breast and head and neck.

Additionally, we’ve linked changes in this pathway to the activity of telomeres, protective caps on chromosomes that play roles in aging and cancer development. Our team also investigates why the cancer drug Avastin (Bevacizumab) has varying success depending on the type of cancer, such as in breast, prostate, and kidney cancers, to improve how this drug is used in treatment.

Established in 1999, our group collaborates closely with doctors to translate our lab discoveries into new cancer treatments, striving to make scientific advances that can directly benefit patients.

Our research is dedicated to understanding and finding treatments for mitochondrial diseases—complex disorders caused by dysfunctions in the mitochondria, the energy-producing structures in our cells. These diseases vary widely in how and when they affect individuals, often leading to severe symptoms without currently available treatments.

One of our key findings involves the role of the MDH2 gene, which is linked to severe childhood encephalopathy, a debilitating neurological condition. We’ve also discovered that mutations in the CHCHD10 gene, which encodes a mitochondrial protein, can trigger motor neuron diseases like amyotrophic lateral sclerosis (ALS) and other neurodegenerative conditions. Our laboratory has developed mice models and used human stem cells to study these diseases, enhancing our understanding of their mechanisms.

Our team, including both physicians and scientists, collaborates closely with the Department of Medical Genetics and the Reference Centre for Mitochondrial Diseases at CHU of Nice. This partnership facilitates the detailed study of patient conditions and direct application of our research findings from the laboratory to clinical settings, aiming to bridge the gap between basic science and patient care.

The Röttinger team explores the impressive stress resistance, regenerative capacities and extreme longevity of cnidarians (sea anemones, corals) to decipher the underlying tissular, cellular and molecular mechanisms. In fact, certain cnidarians possess remarkable abilities to withstand and adapt to high levels of reactive oxygen species (ROS)—harmful byproducts that typically accelerate aging in mammals. They can also regenerate their entire bodies from just parts of themselves or even from scattered cells, and this within days. Finally, some cnidarians have been determined to be able to reach up to 4000 years of age without any signs of aging-related diseases.

Using complementary cnidarians research models, particularly the sea anemone Nematostella vectensis, the team’s focus is to uncover the molecular mechanisms responsible for this environmental stress resistance, regenerate their entire bodies from just parts of themselves or even from scattered cells, the whole-body regenerative capacity and how they prevent aging and related diseases. These insights, in collaboration with other IRCAN teams may pave the way for breakthroughs in regenerative medicine and aging research.

The Saccani lab focuses on understanding how genes are switched on and off, using a group of proteins called the NF-kB family of transcription factors as a key area of study. These proteins are essential for controlling many cellular processes, including cell survival, growth, and inflammation. Despite their widespread presence in different cell types, NF-kB proteins influence specific genes differently depending on the cell type and the environmental triggers. Our research aims to unravel why these proteins behave differently in various contexts. We explore factors like the structure of chromatin (the material that makes up chromosomes) and other proteins that interact with NF-kB, affecting its ability to turn genes on or off in certain cells. This understanding could have broad implications for developing treatments for diseases where cell behaviour goes awry, such as cancer.