Related Experiment Video
Updated: Feb 13, 2026
06:48
In Ovo Xenografting of Patient-Derived Acute Lymphoblastic Leukemia (ALL) Cells (PDX-ALL)
Published on: August 1, 2025
547
The subclonal complexity of STIL-TAL1+ T-cell acute lymphoblastic leukaemia
Caroline L Furness1, Marcela B Mansur1,2, Victoria J Weston3
1Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
Leukemia
|March 21, 2018
Summary
Single-cell genetics reveal the STIL-TAL1 fusion as an early event in T-cell acute lymphoblastic leukemia (T-ALL). This study maps the evolutionary history of T-ALL, identifying key mutations and suggesting new therapeutic targets.
Area of Science:
- Hematology
- Genetics
- Oncology
Background:
- T-cell acute lymphoblastic leukemia (T-ALL) exhibits significant clonal heterogeneity.
- Understanding the mutational sequence and evolutionary dynamics is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the clonal complexity and sequence of genetic alterations in STIL-TAL1+ T-ALL.
- To elucidate the evolutionary pathways and identify founder mutations in this leukemia subtype.
Main Methods:
- Single-cell multicolour fluorescence in situ hybridization (FISH).
- Multiplex quantitative polymerase chain reaction (qPCR) and phylogenetic analysis.
- Xenografting models to assess cell propagation.
Main Results:
- The STIL-TAL1 fusion and 9p21.3 copy loss were identified as early events in T-ALL subclones.
- Secondary subclonal events included PTEN loss and mutations in NOTCH1 and PTEN, which were subclonal and recurrent.
- Genetically diverse cells were confirmed in self-renewing and propagating populations.
Conclusions:
- The STIL-TAL1 fusion is a probable founder or truncal event in T-ALL evolution.
- Targeting the TAL1 auto-regulatory complex presents a potential therapeutic avenue for T-ALL.
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