Andreas Trumpp

This study uses Perturb-seq to identify gene regulatory programs in HSPCs that link genetic regulators to cell biological processes and stem cell phenotypes.

This study links multiscale biological interactions to clinical outcomes in AML by analyzing single-cell data and developing an analytical framework.

This study uses single-cell transplantation and mathematical modeling to show that lineage biases in hematopoiesis arise from extrinsic feedback and clonal competition, not intrinsic HSC properties.

This study shows that inhibiting PTCH1 drug efflux improves chemotherapy effectiveness in triple-negative breast cancer cells by increasing drug retention and reducing cell migration.

UCS enables high-throughput single-cell proteomic analysis of blood samples, revealing disease-specific expression profiles and immune subpopulations in acute myeloid leukemia.

This study shows sodium aurothiomalate induces ferroptosis by covalently modifying GPX4 through a gold-dependent mechanism, leading to tumor growth reduction in preclinical models.

This study shows that hematopoietic Tet2 inactivation improves immune checkpoint blockade response in mice and is associated with better clinical outcomes in melanoma patients with TET2-driven clonal hematopoiesis.

This study identifies rare tumor-reactive T cells and conserved antigen repertoires in multiple myeloma and acute myeloid leukemia, developing a TCR fitness model to predict immunotherapy response.

Pyjacker detects enhancer hijacking in AML, identifying MNX1 activation via 7q deletion as a novel oncogenic mechanism.

The paper identifies PRDX6 as an alternative pathway for selenocysteine metabolism that contributes to ferroptosis resistance in cancer cells.

The paper identifies and profiles leukemic and pre-leukemic stem cells using single-cell transcriptomics combined with lineage tracing via somatic variants.

The paper integrates single-cell and spatial transcriptomics to reveal the molecular, cellular, and spatial organization of bone marrow niches.