Exploiting a new epigenetic regulatory mechanism for sustaining leukaemia-initiating activity
Background
Blood cancer is one of the highest causes of cancer death in Australia, claiming more lives than breast cancer and melanoma combined.
Acute myeloid leukaemia (AML) is the lethal form of blood cancer, with only 27% of patients surviving for 5 years after being diagnosed. The major cause of poor outcomes is the persistence of leukaemia-initiating cells.
These cells have the capacity to escape chemotherapy and make more of themselves indefinitely (known as self-renewal). There are currently no effective treatments to target these cells.
About the Project
Dr Jenny Wang and her team have discovered a key self-renewal pathway essential for the survival of leukaemia-initiating cells.
This project aims to evaluate the survival mechanism that these cells use to protect themselves from chemotherapy.
Dy Jenny Wang and her team will develop a therapy targeting the survival mechanism to eliminate leukaemia-initiating cells, thereby preventing therapy resistance and improving patient outcomes.
Impact
By evaluating the survival mechanism that these cells use to protect themselves from chemotherapy, this project will help the team develop a therapy targeting the survival mechanism to eliminate leukaemia-initiating cells, thereby preventing therapy resistance and tumour recurrence.
This therapy will use the teams newly developed drug, that will ensure effective translation of this therapy into the clinic to directly benefit patients who are not considered curable with current chemotherapy.
This novel therapy may also be applicable to other cancers driven by tumour-initiating cells, such as cancers of the lung, breast, prostate, colon and brain, which may share the critical survival mechanism with human leukaemia-initiating cells in blood cancer.