Oscar Fernandez-Capetillo Group
DNA damage causes cancer and ageing. Drugs that generate DNA damage or inhibit DNA repair have shown good anti-tumor efficacy, however, our knowledge of the synthetic lethal interactions enhancing their efficacy is undeveloped, leaving room for improvement. Previously, we developed DNA repair inhibitors, now towards clinical trials. At KI I want to further pursue translational activities, integrating our research with the drug development national platforms. While our research angles towards DNA damage and repair, we will also explore other health-relevant areas such as immune-modulation or new strategies to treat amyotrophic lateral sclerosis.
Our recently started laboratory at Karolinska Institutet focuses on the implementation of cell-based phenotypic screens oriented to the discovery and development of novel molecules to improve the efficiency of cancer treatments, as well as of ageing related, and other health-relevant diseases such as amyotrophic lateral sclerosis. One of the cancer-related aspects that we are interested in is replication stress, for which we are exploring chemical modulation of RNA:DNA hybrids formation, also known as R-loops. Another cancer-related branch currently in our lab is the study of immune-checkpoint modulators. We aim at the discovery of small molecules that will modulate the expression of immune-checkpoints in the surface of cancer cells. Lastly, we are interested in finding novel chemical strategies for the treatment of amyotrophic lateral sclerosis, which has currently only a palliative treatment.
|Jordi Carreras Puigvert||Project manager|
|Alba Corman||R&D trainee|
|Maria Häggblad||Research engineer|
|Louise Lidemalm||Laboratory technician|
|Per Moberg||Research coordinator|
A Genome-wide CRISPR Screen Identifies CDC25A as a Determinant of Sensitivity to ATR Inhibitors.
Mol. Cell 2016 Apr;62(2):307-13
USP7 is a SUMO deubiquitinase essential for DNA replication.
Nat. Struct. Mol. Biol. 2016 Apr;23(4):270-7
NSMCE2 suppresses cancer and aging in mice independently of its SUMO ligase activity.
EMBO J. 2015 Nov;34(21):2604-19
Increased Rrm2 gene dosage reduces fragile site breakage and prolongs survival of ATR mutant mice.
Genes Dev. 2015 Apr;29(7):690-5
The maternal side of Fanconi Anemia.
Mol. Cell 2014 Sep;55(6):803-4