Prof Brian Giulio Gabrielli


Lab Head

About me

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.”


Identifying the molecular basis for defective checkpoints in melanoma.

Targeting defective cell cycle responses to ultraviolet radiation and TopoII inhibitors in melanoma.

Defining the molecular changes in moles underpinning morphological changes detectable by non-invasive imaging techniques to improve their diagnostic and prognostic ability for early stage melanoma.


1.      Robyn Warrener, KeeMing Chia, William D. Warren, Kelly Brooks and Brian Gabrielli (2010) Inhibition of HDAC3 produces mitotic defects independent of alterations in histone H3 lysine 9 acetylation and methylation. Mol. Pharmacol. 78: 384-393.2.      Astuti P, Boutros R, Ducommun B, Gabrielli B. (2010) Mitotic phosphorylation of cdc25B Ser321 disrupts 14-3-3 binding to the high affinity Ser323 site. J Biol Chem. 285: 34364-34370. 3.      Astuti P, Gabrielli B. (2011) Phosphorylation of Cdc25B3 Ser169 regulates 14-3-3 binding to Ser151 and Cdc25B activity. Cell Cycle; 10:1960-7.4.      Dubravka Skalamera, Max V. Ranall1, Benjamin M. Wilson, Paul Leo, Amy S. Purdon, Carolyn Hyde, Ehsan Nourbakhsh, Sean M. Grimmond, Simon C. Barry, Brian Gabrielli, Thomas J. Gonda (2011) A High-Throughput Platform for Lentiviral Overexpression Screening of the Human ORFeome. PLoS One;6:e200575.      Brian Gabrielli, KeeMing Chia and Robyn Warrener (2011) Finally, how histone deacetylase inhibitors disrupt mitosis! Cell Cycle; 10:2658-61.6.      Giles N, Pavey S, Pinder A, Gabrielli B. (2011) Multiple melanoma susceptibility factors function in a UVR response pathway in skin. Br J Dermatol., 166:362-71.7.      Kelly Brooks, Vanessa Oakes, Brooke Edwards, Max Ranall, Paul Leo, Sandra Pavey, Alex Pinder, Heather Beamish, Pamela Mukhopadhyay, Duncan Lambie, and Brian Gabrielli. A potent Chk1 inhibitor is selectively cytotoxic in melanomas with high levels of replicative stress. Oncogene Mar 5. doi: 10.1038/onc.2012.72. [Epub ahead of print]. 8.      Matthew Wigan, Alex Pinder, Nichole Giles, Sandra Pavey, Andrew Burgess, ShuShyan Wong, Rick A. Sturm, Brian Gabrielli. A UVR-induced G2 phase checkpoint response to ssDNA gaps produced by replication fork bypass of unrepaired lesions is defective in melanoma. (2012)  J. Invest. Dermatol., 132:1681-1688.   9.      Brian Gabrielli and Melissa Brown (2012). Histone deacetylase inhibitors disrupt the mitotic spindle assembly checkpoint by targeting histone and nonhistone proteins. Adv. Cancer Res., 116:1-37.10.    Dubravka Škalamera, Mareike Dahmer, Amy S. Purdon, Benjamin M. Wilson, Max V. Ranall, Antje Blumenthal, Brian Gabrielli, and Thomas J. Gonda. (2012) Generation of a Genome Scale Lentiviral Vector Library for EF1α Promoter- Driven Expression of Human ORFs and Identification of Human Genes Affecting Viral Titer. PLoS One 7:e51733.

Research fields

Melanoma cell cycle