Oliver Dreesen

Biography
Oliver Dreesen received his Ph.D. from the Rockefeller University in New York City, where he studied the structure and function of telomeres and telomerase in Trypanosoma brucei. In 2009, he joined the Institute of Medical Biology in Singapore to study telomeres during cellular reprogramming and in rare genetic human diseases. Dr. Dreesen was promoted to Project Leader in 2013, and to Principal Investigator and Head of the Laboratory for Cell Aging in 2016. He served as President of the Skin Research Society (Singapore) from 2019-2021  
Research interests
Age is the major risk factor for the development of chronic medical conditions. To enhance the well-being of the growing aging population, it is essential that we understand the biological processes of aging and age-related diseases. The goals of my research team at the A*STAR Skin Research Laboratories (ASRL) are to 1) elucidate fundamental mechanisms of skin cell aging, 2) identify novel biomarkers and tools to detect senescent cells within human skin and its appendages, and 3) investigate how senescence modulates the function of different skin cell types and how this in turn contributes to skin aging. 

To achieve this, we study the premature aging syndrome Hutchinson-Gilford Progeria (HGPS), a rare genetic disorder caused by a mutation in the LMNA gene. Our research provided fundamental insights on how perturbations at the of the nuclear lamina result cause human aging and disease. Moreover, by studying cells from HGPS patients, we identified novel biomarkers to detect senescent cells in vitro and in vivo. Collectively, our research lays the foundation to investigate the role of senescent cells in any age-related skin pathology, and to develop novel strategies to understand and modulate their functions.

Selected publications

Ho CY and Dreesen O (2021). Faces of Cellular Senescence in Skin Ageing. Mechanism of Ageing and Development, Sept; 198:111525.

Dreesen O and Kennedy BK (2021). Hutchinson-Gilford Progeria paves the way for novel targeted anti-aging therapies. Med (Cell Press), 2, 353-354, April 9.

Dreesen O (2020). Towards delineating the chain of events that cause premature senescence in the accelerated aging syndrome Hutchinson-Gilford progeria (HGPS). Biochemical Society Transactions, Jun 30;48(3):981-991.

Chojnowski A#, Ong PF#, Foo MXR, Liebl D, Hor LP, Stewart CL, Dreesen O (2020). Heterochromatin loss as a determinant of progerin-induced DNA damage in Hutchinson-Gilford Progeria. Aging Cell, Mar;19(3):e13108.


Aguado J, Sola-Carvajal A, Cancila V, Revêchon G, Ong PF, Jones-Weinert CW, Wallén Arzt E, Lattanzi G, Dreesen O, Tripodo C, Rossiello F, Eriksson M, d'Adda di Fagagna F. Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson-Gilford Progeria Syndrome. Nature Communications 2019 Nov 18;10(1):4990.
Wang AS, Dreesen O. Biomarkers of Cellular Senescence and Skin Aging. Frontiers in Genetics 2018 Aug 23;9:247.


Wang AS, Ong PF, Chojnowski A, Clavel C, Dreesen O. Loss of lamin B1 is a biomarker to quantify cellular senescence in photoaged skin. Scientific Reports 2017 Nov 15;7(1):15678.

Chojnowski A, Ong PF, Wong ES, Lim JS, Mutalif RA, Navasankari R, Dutta B, Yang H, Liow YY, Sze SK, Boudier T, Wright GD, Colman A, Burke B, Stewart CL, Dreesen O. Progerin reduces LAP2α-telomere association in Hutchinson-Gilford progeria.    2015 Aug 27;4:e07759.


Dreesen O, Chojnowski A, Ong PF, Zhao TY, Common JE, Lunny D, Lane EB, Lee SJ, Vardy LA, Stewart CL, Colman A. Lamin B1 fluctuations have differential effects on cellular proliferation and senescence. Journal of Cell Biololgy 2013 Mar 4;200(5):605-17.

A*STAR Open Access Repository