Could unravelling a key protein help us find new treatments for T-ALL?
By studying how TAL1 interacts with other key proteins, Dr Li aims to develop targeted therapies that disrupt this cancer-promoting network.
Dr Yang Li, from University College London (UCL), focuses on uncovering new therapeutic approaches for T-cell acute lymphoblastic leukaemia (T-ALL), a highly aggressive blood cancer often affecting children and young adults. Her research explores the role of the TAL1 gene, which is overexpressed in half of T-ALL cases, driving cancer progression. By studying how TAL1 interacts with other key proteins, Dr Li aims to develop targeted therapies that disrupt this cancer-promoting network.
The Challenge:
T-cell acute lymphoblastic leukaemia (T-ALL) is a rare but highly aggressive blood cancer that mostly affects children and young adults. While many patients achieve remission through chemotherapy, those who relapse or are resistant to initial treatments face significantly worse outcomes. Currently, no CAR-T cell therapy, a promising new treatment for other blood cancers, is available for T-ALL. This leaves a considerable gap in therapeutic options, particularly for individuals with refractory disease or relapse after treatment. The lack of effective, long-term solutions highlights the urgent need for new treatment strategies that can target the underlying causes of T-ALL, and improve survival rates for patients who do not respond to standard therapies.
The Research:
This research focuses on the protein, TAL1, which is found in higher amounts in the leukaemia cells of approximately 50% of T-ALL cases and plays a central role in driving the disease.[1] TAL1 is part of a larger ‘complex’ of different proteins which stick to each other and can drive some of the processes which go wrong in leukaemia cells. The study aims to investigate how these proteins interact and contribute to leukaemia progression. By better understanding the structural and functional relationships between these proteins, the researchers hope to identify potential therapeutic targets within the TAL1 complex. The project utilises advanced techniques to map these protein interactions, which could pave the way for developing new drugs that specifically disrupt this cancer-promoting network.
[1] Mark Hartmann, Mariam Hakobyan, Jens Langstein, Maximilian Schönung, Sina Stäble, Aurore Touzart, Justyna A. Wierzbinska, Daniel B. Lipka, Chapter 13 – Epigenetic regulation of normal hematopoiesis and its dysregulation in hematopoietic malignancies, Editor(s): Dieter Kabelitz, Jaydeep Bhat, In Translational Epigenetics, Epigenetics of the Immune System, Academic Press, Volume 16, 2020, Pages 285-313,
What difference will this research make?
By uncovering the role of TAL1 and its associated proteins, this research could lead to the development of targeted therapies for T-ALL, especially for patients who have limited options due to chemotherapy resistance or relapse. These potential new treatments would specifically attack the cancer’s core mechanisms, leaving healthy cells less affected and reducing side effects. For patients with aggressive or recurrent T-ALL, such advancements could offer improved survival rates and a better quality of life. In the future, this research may also open the door to similar treatments for other cancers where TAL1 and the proteins it works alongside are involved, broadening the impact of these findings across cancer care.