Research interests

Genomic instability in cancer 

Genomic instability refers to the acquisition of changes in the DNA or chromosomes of cells. Such changes could include mutations, deletions, amplifications, the gain or loss of whole chromosomes or parts of chromosomes, or translocations (i.e., abnormal chromosome breaks followed by incorrect fusion). Genomic instability is common in cancer cells. It enables tumour cells to acquire a range of unwanted properties, such as the abilities to spread through the body, escape from the immune system or become resistant to cancer therapies.

Dr Duijf’s research focuses on identifying the causes and consequences of genomic instability in the development of cancer. He aims to translate this knowledge into the development of cancer diagnostic, therapeutic and precision medicine approaches. To achieve this, he uses a broad range of methods, including mouse modelling, genome editing, microscopy, cell and molecular biology, molecular pathology, proteomics and computational systems genomics.

As a group leader, Dr Duijf’s contributions to the research field have included:

  1. Identification of genes whose overexpression promotes genomic instability and/or tumour development (e.g., Emi1, COL17A1, CENPI and EEF1A1) and the underlying mechanisms. PMIDs: 27065322, 27891193, 28977935, 30224719.
  2. Identification of the key genomic factors that predispose to cancerous translocations (i.e., acrocentrism and open chromatin state). PMID: 29316705.
  3. Pan-cancer identification of aneuploidies that drive tumour evolution and predict good or poor patient outcome (unpublished).
  4. Using machine learning, pan-cancer identification of genomic abnormalities that predict cancer patients’ responses to a large panel of drugs, thus improving precision oncology (unpublished).

Research projects

  • The cancer biology of genomic instability in mouse models
  • Identification of pathways that cause genomic instability or aneuploidy
  • Transcriptional regulation of cell cycle genes
  • Using machine learning and systems genomics to identify aspects of tumour evolution and predict patient outcome and drug response
  • Development of strategies to specifically target aneuploid tumour cells

Researcher biography

Dr Pascal Duijf obtained a Bachelor's degree in Biology and a Master's degree in Medical Biology from the Radboud University Nijmegen in the Netherlands and was awarded two scholarships that enabled him to gain research experience in cell biology at Harvard Medical School in Boston, MA in the United States.

He then pursued a PhD degree in Human Molecular Genetics at the Radboud University Nijmegen Medical Centre. Under supervision of Professor Han Brunner and Professor Hans van Bokhoven, his research established genotype-phenotype correlations for a variety of human congenital disorders that are caused by germline mutations in the TP63 gene and are characterised by developmental abnormalities of the limbs, ectodermal structures and/or lip/palate.

For his postdoctoral research, Dr Duijf moved to the United States. At Memorial Sloan-Kettering Cancer Center in New York, he studied how chromosome instability and aneuploidy contribute to cancer development and progression. Using systems approaches, his research showed that cancer cells preferentially lose small chromosomes, although, paradoxically, gains of chromosomes predict poor prognosis in ovarian cancer. In addition, his research demonstrated that chromosome instability can be rescued in a p53 mutant mouse tumour model. This was a significant observation, as it indicates 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, Australia. His research focuses on identifying the causes and consequences of genomic instability in the development of cancer (see also 'Research Interests' below for more details). He aims to translate this knowledge into the development of cancer diagnostic, therapeutic and precision medicine approaches. To achieve this, he uses a broad range of methods, including mouse modelling, genome editing, microscopy, cell and molecular biology, molecular pathology, proteomics and computational systems genomics.

As a group leader, Dr Duijf's contributions to the research field have included:

  1. Identification of genes whose overexpression promotes genomic instability and/or tumour development (e.g., Emi1, COL17A1, CENPI and EEF1A1) and the underlying mechanisms. PMIDs: 27065322, 27891193, 28977935, 30224719.
  2. Identification of the key genomic factors that predispose to cancerous translocations (i.e., acrocentrism and open chromatin state). PMID: 29316705.
  3. Pan-cancer identification of aneuploidies that drive tumour evolution and predict good or poor patient outcome (unpublished).
  4. Using machine learning, pan-cancer identification of genomic abnormalities that predict cancer patients' responses to a large panel of chemotherapeutic drugs, thus improving precision oncology (unpublished).

Areas of research