Cell-Intrinsic Factors (Area A)
How internal mechanisms shape malignant cell plasticity
Studying the molecular programs driving malignant plasticity.
Cancer cells undergo dynamic changes driven not only by genetic mutations, but also by reversible molecular programs. Area A investigates cellular mechanisms inside leukemic cells — including RNA modification, metabolism, epigenetics and lineage identity — to understand how these internal factors promote plasticity, therapy resistance and disease progression.
Using nanopore sequencing of single native RNA molecules from primary samples project A01 will comprehensively identify…
Project A02 will map and quantify m1G levels in mitochondrial- and nuclear-encoded tRNAs in healthy hematopoietic…
Project A03 will identify key metabolic features (e.g., OXPHOS, FAO, glycolysis, ROS, etc.) of primary AML…
Project A04 proposes that loss of KDM5D, a chromosome Y-specific histone H3 lysine-4 demethylase, associates with…
In project A05 single cell multi-omics will be applied to analyze triplet primary AML samples (diagnosis,…
Using primary patient AML samples, PDX mouse models, single-cell/bulk omics profiling and integrative data analysis A06…
Project A07 will explore regulatory networks shaping the immunopeptidome produced by AML blasts and analyzes the…
Area B — Cell-Extrinsic Factors
How the microenvironment and therapeutic stress drive adaptation
How external cues shape leukemic cell states.
Beyond cell-intrinsic processes, leukemic cells respond to external cues such as inflammation, niche interactions, immune pressure and therapeutic stress. Area B explores how extrinsic influences shape malignant states, enable immune evasion, induce lineage changes and contribute to treatment failure — and how these mechanisms can be targeted.
Project B01 will analyze variability of AML blasts as determinants of response to venetoclax and azacytidine…
Project B02 will analyze the JAK2-inhibitor-mediated modulation of the plastic state of dormancy during the transition…
Project B03 will apply multi-modal proteomics to understand and overcome adaptive drug-resistance mechanisms in FLT3-mutated AML….
Project B04 will characterize the impact of the inflammatory AML environment and identify mechanisms of AML…
Project B05 will characterize lineage plasticity of KMT2A-rearranged acute leukemia under therapeutic pressure from CAR-T cells….
Project B06 aims to identify cellular states of resistant AML blasts in first complete remission. Extended…
Project B07 will apply single-cell and imaging technologies to characterize BM niche plasticity in AML during…
Project B08 will unravel the spatial and epigenetic plasticity during leukemia development and targeted therapeutic intervention…
By using AdvSM patient samples at different stages of the disease (pre-treatment, remission, primary resistance, and…
Using innovative techniques, including dynamic differentiation and fate tracking, 3D co-culture models, and clone tracing, project…
Project B11 aims to systematically study the role of donor-host interactions in mediating therapy outcome in…
Core Projects
Our Core Projects provide advanced analytical systems, cross-project technology access and centralized data integration.These platforms enable single-cell multi-omics, proteomics, PDX models, biobanking, AI-based analysis and computational data infrastructure — forming the backbone of CRC 1709’s interdisciplinary research.
The CRC 1709 aims to integrate multi-dimensional data from compatible shared disease models regarding myeloid plasticity….
Efficient coordination and management of the CRC activities is instrumental for the success of the consortium….
Within project Z02 all PIs of the CRC will be provided with (1) shared primary myeloid…
Transcriptomic, epigenomic and proteomic profiling are key technologies across the CRC to investigate and understand cell…
Events
Advancing cancer research through collaborative events
SFB 1709 hosts seminars, workshops, and symposia that bring together experts from basic science, clinical research, computational biology, and translational oncology. These events foster interdisciplinary exchange, highlight emerging insights into cancer cell plasticity, and support the development of innovative therapeutic approaches.
By decoding the plasticity of myeloid malignancies, we aim to fundamentally change how we understand and treat aggressive blood cancers.
Prof. Carsten Müller-Tidow
Speaker, CRC 1709 – Cellular Plasticity in Myeloid Malignancies
