Dr Francis Rodier, Ph.D.
Dept. Radiology, Radio-oncology and Nuclear Medicine, Faculty of Medicine;
Institut du cancer de Montréal, CRCHUM, Université de Montréal.
1996 B.Sc., Université de Montréal - Sciences biologiques, orientation microbiologie
1998 M.Sc., Université de Montréal - Molecular Biology Program, Dr. Anne-Marie Mes-Masson's Laboratory
2005 Ph.D., Université de Montréal - Molecular Biology Program, Dr. Anne-Marie Mes-Masson's Laboratory
2007 Post-doc., University of Berkeley - Lawrence Berkeley National Laboratory, Dr. Judith Campisi's Laboratory
2009 Post-doc., Buck Institute for Research on Aging, Dr. Judith Campisi's Laboratory
2012-2017 (co-PI) Operating grant, Canadian Institute for Health Research
“Rheumatoid arthritis and immune dysfunctions”: The role of damaged hematopoietic stem and progenitor cells”
2014-2016 (PI) New investigator grant, Terry Fox Research Institute
“Understanding the impact of cancer cell fate decisions during ovarian cancer treatment”
2011-2016 (PI) Operating grant, Canadian Institute for Health Research
“Mechanisms regulating persistent DNA damage signaling and the linked control of cell proliferation and extracellular signals”
Awards and prizes
2013-2016 Terry Fox Research Institute (TFRI) New Investigator Award
Exploring the interlaced relationship between cellular senescence, cancer and aging
Why do we get more cancer as we get older and how to treat it: The role of aging cells
Just like us, individual mammalian cells get old. This cellular aging phenomenon, termed cellular senescence, is normally a good thing. Cellular aging is hardwired into a cell genetic program and is activated in response to cellular stresses or damages that could otherwise turn a normal cell into a cancer cell. In short, cellular senescence prevents the apparition of cancer cells via activation of a stable growth arrest. But that's not the only reason why senescence exists, it is also activated by stress during tissue repair, mostly because senescent cells are adept at communicating with other cells and coordinate the repair process. Unfortunately, during normal aging or diseases associated with age, senescent cells accumulate beyond a normal threshold and disorganize tissues leading to organ dysfunctions including a paradoxical increase in tumor growth. The cellular and molecular mechanisms that regulate the accumulation and the biological functions of senescent cells remains poorly understood, which provide opportunities for discovery and room for novel therapeutic interventions.
Current projets (techniques used):
My laboratory uses human, animal and cell models to understand how aging cells contribute to tissue malfunctions and we are attempting to use this knowledge to ameliorate human healthspan. For example, one of our projects tries to understand how and why rheumatoid arthritis is associated with premature aging of the immune system. More recently, we have observed that cancer treatments like radiation or chemotherapy also activate premature cellular aging, both in normal tissues and in the treated tumors. How premature cell senescence contributes to the outcome of cancer treatment remains unappreciated providing a discovery opportunity. Taking into account the good and bad sides of cellular aging (senescence), we are focusing our discovery efforts on determining which specific aspects are good or bad and whether we can optimize beneficial effects while negating detrimental effects to improve age- associated diseases or cancer treatments.
1. Guila Delouya (MD-MSc, Collaborator, email@example.com)
2. Guillaume Cardin (MSc, Research Assistant, firstname.lastname@example.org)
3. Isabelle Clément (MSc, Research Assistant, email@example.com)
4. Julie Lafontaine (PhD, Research Assistant, firstname.lastname@example.org)
5. Maria Vlodoiu (MSc, Research Assistant, email@example.com)
6. Loïse Gilbert (TSA, Animal Tech, firstname.lastname@example.org)
7. Shuofei Cheng (PhD, Postdoc, email@example.com)
8. Nicolas Malaquin (PhD, Postdoc, firstname.lastname@example.org)
9. Yu Zhan (PhD, Postdoc, email@example.com)
10. Stéphanie Nadeau (BSc, PhD student, firstname.lastname@example.org)
11. Aurélie Martinez (MSc, PhD student, email@example.com)
12. Michael Skulimowski (MD-PhD Student, firstname.lastname@example.org)
13. Lilians Calvo Gonzalez (BSc, Master Student, email@example.com)
14. Sabrina Ghadaouia (BSc, Master Student, firstname.lastname@example.org)
15. Mireille Dessureault (BSc, Master Student, email@example.com)
16. Marc-Alexandre Olivier (BSc, Master Student, firstname.lastname@example.org)
17. Anaïs Cheblal (BSc, Master Student, email@example.com)
18. Julie Saint-Louis (COPSE BSc Intern, firstname.lastname@example.org)
19. Juliette Martin (COPSE BSc Intern, Martin.Juliette@hotmail.com)
- Gonzalez, L.C., et al., Premature aging/senescence in cancer cells facing therapy: good or bad? Biogerontology, 2016. 17(1): p. 71-87.
- O'Hagan-Wong, K., et al., Increased IL-6 secretion by aged human mesenchymal stromal cells disrupts hematopoietic stem and progenitor cells' homeostasis. Oncotarget, 2016.
- Yaswen, P., et al., Therapeutic targeting of replicative immortality. Semin Cancer Biol, 2015. 35 Suppl: p. S104-28.
- Cheng, S. and F. Rodier, Manipulating senescence in health and disease: emerging tools. Cell Cycle, 2015. 14(11): p. 1613-4.
- Malaquin, N., et al., DDR-mediated crosstalk between DNA-damaged cells and their microenvironment. Front Genet, 2015. 6: p. 94.
- Block, K.I., et al., Designing a broad-spectrum integrative approach for cancer prevention and treatment. Semin Cancer Biol, 2015. 35 Suppl: p. S276-304.
- Demaria, M., et al., An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell, 2014. 31(6): p. 722-33.
- Rodier, F., Detection of the senescence-associated secretory phenotype (SASP). Methods in molecular biology, 2013. 965: p. 165-73.
- Laberge, R.M., et al., Mitochondrial DNA damage induces apoptosis in senescent cells. Cell Death Dis, 2013. 4: p. e727.
- Rodier, F. and J. Campisi, Four Faces of cellular senescence. J Cell Biol, 2011. 192(4): p. 547-556.