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Chromosomal Instability and Whole Genome Doubling in Cancer.

Research Summary

Normally, we store our genetic information in 23 pairs of chromosomes. However, cancer cells seldom conform to this number. Rather, cancer cells undergo whole genome doubling to duplicate all their 23 pairs of chromosomes to 46 pairs in one fell swoop. Following this, mutations and chromosomal rearrangements occur repeatedly in cancer cells, resulting in a population of highly variable chromosomal numbers. These events correlate with worse clinical outcomes, drug resistance and cancer metastasis.

Using existing population genomic and clinical data, our lab aims to functionally characterise the events that contribute to whole genome doubling and chromosomal instability. We are interested in FAT protocadherins,  a class of proteins which are often mutated in lung, breast, skin and oesophageal cancers. By understanding the role played by the FAT proteins, we aim to find novel treatment strategies

Join US!!!

Are you:

🔥Passionate about genomic and chromosomal instability?
❓Curious about the relationship between whole genome doubling, cancer evolutioN & drug resistance?
🩺Want to have close collaboration with groups that deal with clinical data?

If so, we are recruiting!!

Postdoctoral scientist (25/11/25 closing)

DPhil project available


Latest publications

Collaborators

Prof. Eileen Parkes, University of Oxford, UK

Prof. Nnennaya Kanu, University College London, UK

Prof. Fabrice André, Institut Gustave Roussy, France (SCANDARE cohort)

Prof.  Christophe Le Tourneau, Institut Curie, France (SCANDARE cohort)

Dr. Monica Arnedos, Bordeaux Institute of Oncology, France (SCANDARE cohort)

Prof. Sherene Loi, Peter MacCallum Cancer Centre,  Australia (kConFab cohort)

Dr Heather Thorne, Peter MacCallum Cancer Centre, Australia (kConFab cohort)

Related research themes