Blood cancer

Myelodysplastic syndromes (MDS) are clonal blood disorders affecting mainly older adults, marked by ineffective blood cell production, chronic bone marrow inflammation, and risk of progression to acute myeloid leukaemia (AML). Patients often experience fatigue, infections, and reduced quality of life. MDS is classified into lower-risk and higher-risk forms, with higher-risk disease more likely to progress to AML. Despite ongoing research, effective treatments remain limited. Increasing evidence highlights chronic inflammation and abnormal immune signalling as key drivers of disease progression.

Our research aims to better understand how inflammatory processes influence the evolution of MDS. By integrating inflammatory profiling with molecular and genomic data, we seek to identify inflammatory signatures that predict progression from early or pre-MDS states to LR-MDS, HR-MDS, and ultimately AML. These insights will help improve risk stratification and may enable earlier, more targeted therapeutic intervention for patients with inflammation-driven disease trajectories.

Multiple Myeloma (MM) is a clonal plasma cell cancer that primarily affects older adults and remains largely incurable despite advances in treatment. Patients often relapse due to genetic diversity, clonal evolution, and resistance within the bone marrow environment, making MM a chronic condition. The disease also acts as a systemic disorder, impairing blood production and causing anaemia, immunodeficiency, and increased infection risk. Current risk models focus on genetic factors but overlook inflammation and the tumour microenvironment.

Identifying robust prognostic biomarkers of inflammation in MM represents a major opportunity to improve patient outcomes. Such biomarkers could provide mechanistic insight into disease trajectory, enable more precise risk stratification beyond genetic lesions alone, and inform personalised treatment strategies.

Thalassaemia and sickle cell disease are inherited blood disorders affecting haemoglobin and millions worldwide. Thalassaemia reduces α- or β-globin production, causing anaemia, ineffective red blood cell development, and iron overload requiring ongoing management. Sickle cell disease results from a β-globin mutation producing haemoglobin S, leading to rigid, sickle-shaped cells that block blood vessels, causing pain, inflammation, and organ damage.

Our research seeks to understand how inflammatory processes shape disease evolution in haemoglobin disorders. In particular, we investigate how abnormal haemoglobin production, chronic inflammation, and dysregulated iron metabolism alter the haematopoietic microenvironment and disrupt normal blood cell development. By integrating molecular biology, immunology, and genomic approaches, our work aims to define the mechanisms that drive disease progression and complications in these conditions. Advances in molecular medicine, gene therapy, genome editing and targeted therapeutics are creating new opportunities to translate these insights into improved treatments and, ultimately, curative strategies for individuals living with thalassaemia and sickle cell disease.

The NIK-dependent NF-kB pathway is increasingly recognised for playing an important role in the development of blood cancers like multiple myeloma, chronic lymphocytic leukaemia (CLL) and mantle cell lymphoma (MCL).  Dr Jim Vadolas and oncologist, Dr George Grigoriadis are working on understanding how this pathway affects cancer cell growth and patient survival.

AEL is an aggressive and poorly understood subtype of acute myeloid leukemia (AML) that targets the red blood cell lineage. Current treatment options are limited, and long-term survival rates remain low. Dr Catherine Carmichael has contributed to AEL’s first complete genome analysis, revealing the gene mutations driving disease development. The team is using cutting-edge gene and drug screening to find new ways to treat and diagnose patients.

There is a desperate need for improved and less invasive treatments for cancers.

Dr Daniel Garama and his research team have developed naturally derived Next Generation Photodynamic Therapy (NG-PDT) compounds that are able to target and kill tumour cells in melanoma, ovarian, lung, blood, prostate and pancreatic cancers, in both invitro and preclinical models, and also clinically in melanoma.

The next step is to move into clinical trial stages using these NG-PDT compounds with the aim of developing new non-invasive cancer treatment pathways for some of the deadliest cancers.

Team | Dr Daniel Garama, Lethica Low, Luhith Dimantha, Anurag Yadav, Dr Donald Murphy

Affiliates | Associate Professor Seb Marcuccio, Scott Carpenter, Michael Cho, Hon Cho, Alex Bennett