Abstract
Cancer is thought to arise from accumulation of DNA mutations. However, AML is a heterogeneous disease characterized by diverse mutations each occurring at low frequencies. Actually, AML is a subtype with a relatively low mutational load compared to other cancer types. In addition, in children, DNA is far less damaged by exposure or age. Thus, also AML might not only be driven by differences in genomic content but also by transcriptomic heterogeneity. In this thesis we aimed to study deregulated splicing in AML and uncover its role in leukemogenesis.
Original language | English |
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Qualification | Dr. |
Awarding Institution |
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Supervisors/Advisors |
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Award date | 1 Feb 2022 |
Publication status | Published - 1 Feb 2022 |
Keywords
- Alternative Splicing
- Splicing Modulation
- Splicing Deregulation
- Splicing Factor Mutation
- SF3B1
- FLT3/ITD
- Acute Myeloid Leukemia
- Pediatric Acute Myeloid Leukemia