Researcher biography

Dr Duijf first became interested in genetics and cell biology in high school. During chemistry and biology classes, his curiosity was stimulated by the processes of DNA replication, protein synthesis and cell division. In the final year of high school, his class visited a research laboratory at the local university hospital. This environment definitively sparked his fascination for biomedical research. His desire to pursue a career in this field led to his obtaining a Bachelor's degree in Biology and a Master's degree in Medical Biology from the Radboud University Nijmegen in the Netherlands.

Subsequently, Dr Duijf successfully applied for two scholarships. Those enabled him to gain research experience in cell biology in Professor Frank McKeon's laboratory in the department of Cell Biology at Harvard Medical School in the United States.

To continue research training in cell biology and genetics, he returned to the Netherlands to pursue a PhD degree in Human Genetics at the Radboud University Nijmegen Medical Centre. His mentors included clinical geneticist Professor Han Brunner and molecular geneticist Professor Hans van Bokhoven. Under their supervision, he made important contributions to establishing genotype-phenotype correlations for a variety of human congenital disorders that are characterised by developmental abnormalities of the limbs, ectodermal structures and/or lip/palate. All of these disorders are caused by germline mutations in the p63 gene, a homologue of the p53 tumour suppressor gene. For his postdoctoral research, Dr Duijf changed research fields. In the laboratory of Professor Robert Benezra at Memorial Sloan-Kettering Cancer Center in New York, his research focussed on how chromosome instability contributes to cancer development and progression in vivo, using mouse models. With a particular interest in breast and childhood cancers, he demonstrated that p53 pathway defects, which are frequent in human cancers, lead to overexpression of the mitotic checkpoint gene Mad2 via crosstalk to the Rb (Retinoblastoma) pathway. In addition, he showed that chromosome instability can be rescued in a p53 mutant mouse tumour model. This was an important observation as it suggests that targeting chromosome instability in human tumours will be an effective strategy to treat cancer patients. In 2013, Dr Duijf established his independent research group at the University of Queensland Diamantina Institute and the Translational Research Institute in Brisbane. His group continues to study chromosome instability in mouse models in order to develop new strategies to improve cancer diagnosis and treatment.