Cancer Evolution (SFB 1243)
Epigenetic modifier genes such as DNMT3A and TET2 are mutated in the majority of acute myeloid leukemias (AML) and inspite of the longstanding interest in their role in leukemia, no consistent mechanism has been found yet. Here, we speculate that those genes might act as epigenetic mutators that simply accelerate the evolution of cancer by providing more raw material.
Aim 1 Classification of AML patient bone marrow cells
Aim 2 Analysis of single cell genotypes
Aim 3 Method to compare gene expression variance
-- We are developing an R-package that allows for variance estimation in complex models.
Aim 4 Measuring transcriptional dysregulation beyond gene expression levels
-- We will extend zUMIs to include alternative poly-adenylation and repeats.
Aim 5 The impact of Dnmt3a and Tet2 mutations on expression variance in Ba/F3 cells