Science at the Shine Dome 2010

Professor Roger Reddel FAA
Children’s Medical Research Institute, University of Sydney

Roger Reddel trained as a medical oncologist at Sydney’s Royal Prince Alfred Hospital and obtained a PhD in the cellular biology of breast cancer from the University of Sydney. During postdoctoral research at the National Cancer Institute, Bethesda, Maryland, he generated immortalised cell lines in order to study the role of oncogenes in human carcinogenesis. On returning to Sydney, he set up a research group to study the molecular changes required for the immortalisation of cancer cells. Roger and his team discovered the alternative lengthening of telomeres (ALT) mechanism in human cancer cells, and have made discoveries regarding the telomerase enzyme. The presence of one or other of these telomere length maintenance mechanisms – telomerase or ALT – is an almost universal characteristic of human cancer.

Roger is director of the Children’s Medical Research Institute and Lorimer Dods Professor in the University of Sydney’s Faculty of Medicine.

The immortality of cancer cells

The reason that cancer is hard to treat is that cancer cells are very similar to the normal cells from which they arise, which makes it difficult to find drugs that kill cancer cells without also damaging normal cells in the body. My research has been focusing on cellular immortality, one of the distinguishing characteristics of cancer cells. Normal human cells reproduce themselves only a limited number of times, but cancers contain populations of cells that have an unlimited capacity to proliferate and therefore are referred to as being ‘immortalised’. A major reason for the limited proliferative capacity of normal cells is that their chromosome ends (telomeres) get slightly shorter every time they reproduce themselves, and eventually their telomeres become so short that proliferation must cease. Cancer cells avoid this barrier to unlimited growth by activating a telomere length maintenance mechanism. For this purpose some cancers use an enzyme, telomerase, and others use alternative lengthening of telomeres (ALT). I will outline what we know about these two mechanisms and how we could use this information to design new treatments for cancer.