Last October, The Australian Atherosclerosis Society (AAS) recognised two scientists from the
Heart Research Institute at its Annual Scientific Meeting. Dr Kate Hadfield and Dr Hamish Prosser were each awarded runners-up prizes in the ‘Young Investigators' section.
Dr Prosser (a post-doctoral scientist in the recently established Immunobiology Group) presented research showing that HDL ('good cholesterol') has the potential to be used to aid patient recovery after a heart attack by increasing the growth of new blood vessels to damaged tissue.
But in what appears to be a biology paradox, Dr Prosser's work also suggests that HDL might reduce blood vessel growth in cancer, thus limiting the supply of essential nutrients to the developing tumour and stunting growth.
"Intriguingly, in environments where there is low oxygen such as following a heart attack, HDL takes on the role of repair molecule, promoting the growth of new vessels to aid repair of damaged tissue. But in cancers, where the growth of new vessels actually promotes the spread of the tumour, HDL can inhibit this process, thus limiting the supplying of nutrients to the cancer and slowing growth", said Dr Prosser.
"This biology paradox, that the same molecule that protects us from developing heart disease might also help slow the growth of cancers, is incredibly exciting and opens up a whole new therapeutic potential for HDL", he said.
Apart from the Young Investigators' Prize, Hamish was also awarded the Early Career BioAssay LINK Award for research that shows the most potential for commercial application.
Dr Hadfield presented her findings about HOSCN - a chemical produced in the artery wall during inflammation and found in high levels in smokers. One of the ways HDL can help prevent the development of heart disease is by removing fats or cholesterols from the artery wall but Kate has discovered that HOSCN prevents this process, which may go part of the way to explaining why smokers have an increased risk of heart disease.