I work as a postdoc in the lab of Jos Jonkers, and in short, my interest is basic and translational cancer research to understand the role of the DNA Damage Response (DDR) for cancer prevention, and in novel personalized cancer treatments. Specifically, I am using mouse models to investigate the tumour suppressor role of the hereditary breast and ovarian cancer (HBOC) gene, BRIP1/FANCJ. Tumours from these models will further be used for studying treatment response of clinically relevant drugs including novel targeted treatments. Moreover, I work on a CRISPR based functional assay for testing HBOC gene variants. Such classifications can support risk prediction for affected families, and guide treatment decisions for cancer patients.

REBBLS (Rising Entrepreneurs in BioBusiness and Life Science) is a network connecting the most dedicated, talented, and ambitious bioentrepreneurs in Denmark in order to create a forum for gaining further experience, tools, and business relations within startup in biotech and life science.

During my PhD and postdoc in the lab of Claus Storgaard Sørensen, I was part of a screen approach to identify novel factors for the ionizing radiation induced G2/M checkpoint. These screens lead to the publication of three novel factors for the regulation of the G2/M checkpoint, including the tumour suppressor BRCA2.

Ionizing radiation (IR) is often used as a cancer treatment where the tumor cells are mainly killed due to massive amounts of DNA double strand breaks (DSBs). As IR therapy normally goes along with severe side effects for the patient and as some tumors reveal IR-resistance, it is of striking importance, to get a better understanding of how the cells react upon IR. Cells exposed to DNA damage such as ionizing radiation (IR) must deal with DNA double-strand breaks (DSBs), which pose a serious threat to genome integrity. The immediate response to these DNA lesions is the block of cell cycle progression and initiation of DNA repair. In order to repair DNA DSBs, the DNA ends are resected leaving RPA-coated single-stranded DNA, which is an intermediate for further DNA repair. DNA end resection is initiated by the MRE11-RAD50-NBS1 (MRN) complex and CtIP. In my PhD project, we elucidated that IR induces an immediate checkpoint block in G2 phase of the cell cycle that occurs independently of extensive DNA end resection. However, maintenance of the G2 cell cycle checkpoint requires DNA end resection (Kousholt et al., 2012).

In my master project I performed a flow cytometry based screen for G2/M regulatory proteins using RNAi. As a research assistant, I continue the validation and characterization of the positive hits obtained.

Member of the board 2011 - 2013.Great people, great company - the future looks bright!

I did my master project under the supervision of Claus Storgaard Sørensen. See further information about Sørensens group here, http://www.bric.dk/cms/viewPage.php?id=321My project was to perform a flow cytometry based loss of function screen to identify novel genes involved in the DNA damage response to ionizing radiation.