I am a biomedical researcher with a consistent record of high-level performance across Sri Lanka and Australia, driven by a strong commitment to advancing scientific knowledge and improving human health.

My early academic direction focused on dengue epidemiology and entomology, where I conducted four research projects simultaneously. The main highlight was the large-scale community study conducted on 2000 households as a multi-disciplinary project studying Ecological-Biological-Social aspects of Dengue in Sri Lanka as a multi-country research effort funded by WHO/TDR.

In Australia, I transitioned to cancer biology supporting complex melanoma research programs and contributing to seminal work on epigenetic regulation (BET, HDAC, CDK9 and EZH2) and immunology (immune checkpoint biology and inflammasome activation). My recent work was on vascular biology and ageing, particularly the role of cellular senescence in blood–brain barrier dysfunction. I have now returned to cancer cell biology to pursue a PhD, aligning with my long-standing research passion.

Key highlights include fellowship under BioVision.Nxt programme to attend the World Life Sciences Forum 2009, interactive engagement with Nobel laureates and top researchers, NSF Postgraduate Scholarship 2008 for MPhil, co-authorship in 12 peer reviewed publications (FWCI: 2.64; Scopus) and long-term involvement in internationally funded collaborative biomedical research projects.

Men are more than twice as likely to die from cancers including melanoma compared to women. Although several reasons have been proposed to explain this observation, such as behavioural or hormonal differences, the puzzle remains unsolved. This project centres around an alternative theory, that differences in genes located on the sex chromosomes may explain differences in the ability to combat cancer between males and females.

Females genetically have two X chromosomes whereas males, only one. To equalise the numbers of genes between sexes, one copy of the female X-linked gene becomes inactivated, however there is an important exception in approximately 20% of these genes that ‘escape’ inactivation. A recent landmark study identified 4 such escape genes that have tumour suppressive functions in cancer. This effectively means that females have double the ability to fight cancer compared to males, and make sense from an evolutionary perspective of protecting eggs/offspring. Furthermore, these escape genes are known epigenetic (above genetics) controllers that have the ability to regulate hundreds of other genes involved in immune responses and cancer.

The precise mechanisms of how these genes function in melanoma is yet to be explored. This project aims to define these tumour suppressive mechanisms in Melanoma cells.  This will be achieved using gene manipulation techniques followed by determining the influence of gene manipulation on melanoma cell growth and metastases using 2D and 3D cell biological and immunological assays and identifying downstream target genes using next generation sequencing technologies and computational analyses.