Chow Lai
Chow Lai
Chow Lai

Chow Lai

‘Towards using CRISPR-Type III for fusion oncogene detection and ablation of cancer cells in paediatric patients with acute myeloid leukaemia.’

Walter and Eliza Hall Institute of Medical Research & University of Melbourne, Vic
Awarded 2024
Co-funded by the Rotary Club of Murrumbidgee Canberra

As a paediatric haematologist/oncologist, I have seen firsthand how aggressive paediatric AML can be, and how much children with AML suffer from the treatment toxicities. From there, came a desire to find new ways to conquer the disease, and to make a difference to children and their families.”

General Health PhD Scholarship

Researcher Profile

Chow qualified as a Paediatric Haematologist, Laboratory Haematologist and Paediatric Oncologist in 2023, having trained at New Zealand, the Royal Children’s Hospital Melbourne and the Alfred Hospital, Melbourne. Despite having a busy career at Monash Children’s Hospital, his interest in science, which developed during his time at his alma mater, Imperial College London, England, continues.

Having seen how new classes of drugs impacted greatly on patients, such as tyrosine kinase inhibitors and chronic myeloid leukaemia, anti-tumour necrosis factor monoclonal antibodies and rheumatology patients, and venetoclax with a myriad of haematological malignancies, Chow aspires to follow in the footsteps of several very successful scientists and clinicians to make similar impacts in the paediatric haematological/oncological world.

Project Summary

The project aims to develop a new way to target cancer cells and eradicate them. Firstly, using a novel ‘sensing’ technique to detect certain cancer mutations, and then attempting to kill or disrupt these cancer cells by activating cell death pathways in the cancer cells.

Most cancers develop due to mutations that are acquired during rapid cell division. Some of these mutations bring tightly regulated cell signals to the proximity of another gene which is always ‘on’, resulting in lose of regulation of these cell signals. These mutations are called fusion oncogenes. Instead of turning ‘on’ and ‘off’ at appropriate times, these signals are always ‘on’, causing inappropriate cellular programmes, such as ongoing cell division and replication even when unnecessary or inappropriate. These fusion oncogenes, which are unique to the cancer and not to normal cells, would have to first be specifically detected, and once specifically detected, a way to destroy these cells without destroying other healthy cells must be developed.

For this new class of therapeutics, we would be using paediatric acute myeloid leukaemia (AML) as the disease prototype. AML is a common childhood cancer with a relatively poor prognosis and limited medication arsenal. Most paediatric AML cases also have fusion oncogenes, some of which are poor risk or more likely to relapse – hence the rationale for using this disease as a prototype.

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