Prof Brian Giulio Gabrielli

Gabrielli credits a high school chemistry teacher with inspiring him to pursue science. He went on to earn both a Bachelors and Honours degree in Biochemistry and Chemistry from James Cook University in Queensland, where his natural affinity for science opened up new opportunities. During his PhD at La Trobe University in Melbourne, Gabrielli was introduced to the world of cell cycle biology. His first post-doctoral position at the University of Colorado in the US only strengthened his interest.

“They were at the forefront of cell cycle research,” he recalls. “It was exciting and brand new. Just the sort of thing for a young post-doc.”  His work led him to the laboratory of Professor Helen Piwnica-Worms at Harvard Medical School.  Together they worked on a class of proteins called CDC25s, which were known to regulate part of the cell cycle called mitosis.  Because cancer arises from unchecked cell cycle defects that occur during mitosis, looking at key regulators was the next big thing.Gabrielli returned to Australia to characterise a new CDC25 at the Queensland Institute for Medical Research. He then moved his research team to the Pathology Department at the University of Queensland. By looking at how drugs and UV radiation affected mitosis, Gabrielli and his colleagues were able to identify new regulatory mechanisms in the cell cycle.  He admits his interest in UV was influenced in part by his Queensland location, which meant numerous colleagues were working on melanoma.In 2002, Gabrielli moved his cell cycle research to UQ’s Centre for Immunology and Cancer Research (CICR), which later became incorporated into the UQ Diamantina Institute (UQDI).  He is now an Associate Professor and Head of the Cell Cycle Group at UQDI, and his goal is to identify and target cell cycle defects in melanoma.“We want to see if we really can deliver tumour-selective, cytotoxic insults to melanoma,” he says. “We can use tools developed at UQDI to improve that targeting and we also want to identify the markers of these defects so we can identify precisely which patients can benefit from selective treatments.”Because melanomas are extremely difficult to completely eliminate, he believes the best strategy will be to integrate specific anti-tumour treatments with immunotherapies that enable long term cancer surveillance, essentially using the body’s own immune system to keep melanoma in check.Already his group has identified a defect most likely responsible for the increased mutation load in melanoma. They found that, in normal skin cells, UV radiation causes the cell cycle to pause at the ‘G2 phase-checkpoint’, just before mitosis begins. This checkpoint arrest then triggers a secondary DNA repair mechanism that fixes any damage missed by the primary repair mechanism.  Gabrielli found that this coupled checkpoint-repair mechanism is defective in a substantial number of melanoma cell lines, allowing UV-induced genetic damage to accumulate.Gabrielli believes there are numerous advantages in carrying out his melanoma research at UQDI. “The combination of Professor Matt Brown’s ability to look at coding regions of the genome together with our ability for functional assessment places us in a very unique position,” he says. Taken together with the clinical collaborations with the PA Hospital, he believes only a few places in the world can boast such a combined advantage, particularly in melanoma research.  “It’s a combination of interest, facilities, resources and expertise. On top of that,” he adds, “there’s a really good group of collaborative colleagues here to work with.”