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Dr Rodrigo Carlessi

Senior Research Fellow
Curtin Medical School

Cancer Genomics

I have always been intrigued by the remarkable amount of information our cells store and process. My research is driven by a desire to understand how subtle molecular changes can reveal what is happening inside the body long before any symptoms appear. What inspires me most about this work is its potential impact: the idea that discoveries made at the molecular level could one day translate into tools and treatments that save lives. This research sits at the intersection of curiosity, innovation, and hope, harnessing the power of data and molecular insight to better understand disease and change the way we fight it.      

About

Dr Rodrigo’s research at the Curtin Health Innovation Research Institute centres on uncovering the molecular and metabolic mechanisms that drive liver cancer.

Liver cancer is among the most lethal cancers, responsible for nearly 10% of cancer-related deaths worldwide, and its incidence in Australia has risen by more than 425% in the past 25 years. One of the major risk factors, fatty liver disease, affects around 25% of adults, yet it remains difficult to predict which patients will progress to liver cancer.

Dr Rodrigo employs advanced molecular and computational approaches to identify the molecular signatures that determine an individual’s risk of developing liver cancer. This knowledge aims to enable early detection and timely intervention, ultimately improving treatment outcomes and survival rates.

In addition to his work on liver cancer, Dr Rodrigo has investigated the failure of insulin-producing pancreatic cells in diabetes. His contributions to this field have been recognised with awards from both the Australian Diabetes Society and the Heart Foundation.

Research Interests:

Email: Rodrigo.Carlessi@curtin.edu.au
ORCID
Google Scholar
Curtin Staff Profile

 

Research Focus

Our research group is dedicated to improving the early diagnosis and treatment of hepatocellular carcinoma (HCC) using cutting-edge molecular and genomic technologies. By integrating molecular diagnostics, genomics, and therapeutic innovation, we aim to develop new tools that transform how liver cancer is detected and managed.

Key research areas include:

Liquid biopsy development: Designing highly sensitive ctDNA-based assays to enable early detection and real-time monitoring of HCC, improving diagnostic precision and clinical outcomes.

CRISPR-Cas13 RNA therapeutics: Harnessing the RNA-targeting capabilities of CRISPR-Cas13 systems to selectively degrade cancer-promoting transcripts, creating a novel platform for targeted liver cancer therapy.

Epigenetic reprogramming: Investigating epigenetic modifiers to reverse abnormal DNA methylation patterns in HCC, with the goal of suppressing tumour growth and progression.

Through these interdisciplinary approaches, our ultimate goal is to establish integrated strategies for early detection, personalised treatment, and long-term disease management in liver cancer.

 

Research Team

Anjali Ghimire

Sessional Academic

Dinesh Thapa

Sessional Academic

Saskia Saville

PhD Student

Publications

Carlessi, R., T. J. Kendall, J. K. Olynyk, B. J. Dwyer, M. C. Wallace, J. A. Fallowfield, and J. E. Tirnitz-Parker. 2026.Disease-associated hepatocytes are predictive of outcomes and survival in MASLD beyond fibrosis staging.Gut 75 (3): 668-670.
ABSTRACT

Hepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or metabolic-dysfunction-associated steatohepatitis (MASH)1. While increasing HCC risk2, MASH triggers p53-dependent hepatocyte senescence3, which we found to parallel hypernutrition-induced DNA breaks. How this tumour-suppressive response is bypassed to license oncogenic mutagenesis and enable HCC evolution was previously unclear. Here we identified the gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP1) as a p53 target that is elevated in senescent-like MASH hepatocytes but suppressed through promoter hypermethylation and proteasomal degradation in most human HCCs. FBP1 first declines in metabolically stressed premalignant disease-associated hepatocytes and HCC progenitor cells4,5, paralleling the protumorigenic activation of AKT and NRF2. By accelerating FBP1 and p53 degradation, AKT and NRF2 enhance the proliferation and metabolic activity of previously senescent HCC progenitors. The senescence-reversing and proliferation-supportive NRF2–FBP1–AKT–p53 metabolic switch, operative in mice and humans, also enhances the accumulation of DNA-damage-induced somatic mutations needed for MASH-to-HCC progression.

Gu, L., Y. Zhu, S. P. Nandi, M. Lee, K. Watari, B. Bareng, M. Ohira, Y. Liu, S. Sakane, R. Carlessi, and 19 more contributors. 2025. FBP1 controls liver cancer evolution from senescent MASH hepatocytes.Nature 637 (8045): 461-469.

Liver Cancer biomarkers risk prediction & progression.

Dr Rodrigo Carlessi

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