Harnessing novel immunotherapies to restore immunity in chronic lymphocytic leukaemia
Professor David Ritchie
Chronic lymphocytic leukaemia (CLL) is the most common form of leukaemia in Western countries, and remains largely incurable. Recently a number of new drugs have shown exciting potential in clinical trials including Ibrutinib, Venetoclax and Lenalidomide. Whilst these drugs kill CLL cells via novel mechanisms, it is clear that no single drug is sufficient to cure CLL. Hence rational combinations of novel agents to maximise efficacy and minimise toxicity are required to improve cure rates for patients with CLL.
It is well known that CLL tumours can suppress the immune system via a number of mechanisms, and that some cancer drug treatments also affect this. Therefore, the ability of a patient’s immune cells to respond to cancer treatment and directly kill tumour cells can be impeded. We are investigating the ability of new CLL therapies, such as Ibrutinib, to change immune responses in patients. Additionally, we can analyse changes in gene expression in tumour and immune cells using Nanostring technology, to identify biomarkers for the treatment and outcome of CLL patients.
Ultimately our goal is to understand how novel CLL drug treatment affects both the tumour cells and individual immune cell subsets, by identifying biomarkers that may influence when and how particular treatments are given to CLL patients. Furthermore, we aim to develop a novel combination of drugs that will be used in clinical trials, which can make CLL tumours become a better target for the patient’s immune system.
- Dr Joanne Davis, Post Doctoral Research Officer
- Dr Kylie Mason, NHMRC Post Doctoral Fellow and Clinical Haematologist
- Ms Chia Sharpe, PhD student
- Dr Constantine Tam, Department of Haematology, Peter MacCallum Cancer Centre
- The Royal Melbourne Hospital Research Medal
Fight Cancer Foundation
- Davis JE, Ritchie DS. The passive-aggressive relationship between CLL-B cells and T cell immunity. Leukaemia Research, 2014 38(10):1160-1.
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