Dr Pascal Duijf
Dr Pascal Duijf

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Cancer cells often missegregate their chromosomes during cell division, or mitosis. This phenomenon is termed chromosome instability. Dr Duijf’s research group focuses on identifying the mechanisms of chromosome instability in cancer cells. His research in this area is aimed at developing new approaches to improve the diagnosis and treatment of cancer.

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.


Email: p.duijf@uq.edu.au
Phone: +61 7 3443 6937

Featured Publications

 Duijf PHG#, Benezra R#. The cancer biology of whole-chromosome instability. (2013) Oncogene 32(40): 4727-4736. PMID: 23318433. # Corresponding author

Duijf PHG#, Schultz N, Benezra R#. (2013) Cancer cells preferentially lose small chromosomes. Int J Cancer 132(10): 2316-2326. PMID: 23124507. # Corresponding author
Schvartzman JM*, Duijf PHG*, Sotillo R, Coker C, Benezra R. Mad2 is a critical mediator of the chromosome instability observed upon Rb and p53 pathway inhibition. (2011) Cancer Cell 19(6): 701-714. PMID: 21665145. * Equal first authors

Cancer cells frequently missegregate their chromosomes during cell division. This phenomenon, termed chromosome instability, leads to the formation of aneuploid cells, i.e., cells with abnormal chromosome numbers. Chromosome instability is one of the most malignant features of cancer cells, because it can cause cancer, it accelerates cancer progression and it is an important mechanism for cancer cells to become resistant to cancer therapies.

The Duijf laboratory uses in vivo mouse models and in vitro cell models in order to: (1) study how chromosome instability contributes to cancer progression and (2) identify novel mechanisms that cause chromosome instability.
Chromosome missegregation has a variety of known and unknown causes and effects. Therefore, in addition to identifying new mechanisms, the group studies a range of phenomena that are known to be associated with chromosome instability, including DNA damage, mitotic checkpoint defects, sister-chromatid cohesion defects, centrosome overduplication and cytokinesis failure.
With an interest in breast and other cancers, the Duijf group’s research goals are translational in nature: to develop new approaches or enhance existing ones in order to improve the diagnosis and treatment of cancer.
  • The cancer biology of chromosome instability in mouse models
  • Identification of pathways that cause chromosome instability/aneuploidy
  • Transcriptional regulation of cell cycle genes
  • Development of strategies to specifically target aneuploid tumour cells