5 June 19
We are pleased to announce that a study undertaken by SVI researchers Associate Professor Andrew Deans and Dr Julienne O’Rourke, in collaboration with the Children’s Medical Research Institute (CMRI) in Sydney, has identified not one, but two, potential treatment options that could help kill aggressive cells that lead to both rare children’s cancers and common cancers. Both studies were published recently in Nature Communications.
Another study by SVI undertaken with international collaborators in Portugal and Switzerland, revealed similar results. The next step in this research project will be to undertake new studies with the potential treatment options and hopefully progress to clinical trials.
Our researchers
Associate Professor Andrew Deans is the head of our DNA Stability Unit. The Unit studies familial cancer syndromes that cause predisposition to breast/ovarian cancer, leukaemias and other solid tumours. They also study the sensitivity of human tumour cell lines to cancer drugs, which impact on maintaining genome (the sets of genes we all carry in our cells) stability. Andrew is world-renowned for his work into the FANCM protein (more information about this protein is provided later in this email).
Dr Julienne O’Rourke recently completed her PhD at SVI and is on her way to the Karolinska Institutet in Sweden in the coming weeks. Julienne began her life at SVI as an Honours student in 2013, before she undertook her PhD studies. During her time at SVI, Julienne was the recipient of an SVI Top-Up Scholarship, which meant she had more time to focus on her studies. She’ll be taking her ‘just-published’ article in Nature Communications with her to Sweden – a great feat for an early career researcher!
Media activity
You may have heard about this research as in the last week, Andrew has undertaken a radio interview on 3AW, and Associate Professor Hilda Pickett from from CMRI was featured in a Channel 10 news item. Hilda also had an interview with the Chinese Government news channel.
An article has been put on our website, and Facebook, Twitter and LinkedIn posts have been made and are getting good engagement. If you are on social media, we encourage you to share our posts.
Thanks to our supporters who made this research possible
They include the SVI donors who supported Julienne’s scholarship, and Cancer Council Victoria, Cancer Council NSW and the National Breast Cancer Foundation, who provided grant funding.
The research in detail
Cells divide throughout our lives to ensure our bodies can keep on functioning; but as they divide, the structures found at the ends of chromosomes called telomeres, get shorter and shorter, until the cell eventually dies. One of the ways cancer cells find a way around this to ensure their survival, is to lengthen their telomeres. They do this through a process called “alternative lengthening of telomeres”, or ALT, in which they “copy and paste” DNA from other chromosomes that have long telomeres, onto those with short telomeres.
The researchers found that by disrupting the function of a protein (called FANCM) with either specific peptides, or an experimental drug called PIP-199, in some cancer cells that had undertaken this lengthening process, they would experience severe stress and die. As FANCM is not essential in normal cells, this suggests it could be a good target for new drugs that could eliminate cancer cells, without eliminating other healthy cells.
The stats
About 40% of soft-tissue cancers including osteosarcoma (bone cancer), liposarcoma (a cancer originating in fat cells), and angiosarcoma (blood vessel cancer), as well as 10% of other carcincoma, or hard-tissue cancers, such as breast, ovarian and prostate, occur when the ALT process is activated and the cells become cancerous.
There are currently no specific therapies for ALT-positive sarcomas. People with this type of cancer have a 50% higher rate of death, as these cancers are more resistant to current treatments.
If you have any questions about this discovery, please contact us at foundation@svi.edu.au or respond to this email.
