{Publications
Take a look at our recent publications
- Negative Hyperselection of Resistance Mutations for Panitumumab Maintenance in RAS Wild-Type Metastatic Colorectal Cancer (PanaMa Phase II Trial, AIO KRK 0212)
- Serial Analysis of Gene Mutations and Gene Expression during First-Line Chemotherapy against Metastatic Colorectal Cancer: Identification of Potentially Actionable Targets within the Multicenter Prospective Biomarker Study REVEAL
- A RAS-Independent Biomarker Panel to Reliably Predict Response to MEK Inhibition in Colorectal Cancer
- Clonality and timing of relapsing colorectal cancer metastasis revealed through whole-genome single-cell sequencing
- DNA methylation reveals distinct cells of origin for pancreatic neuroendocrine carcinomas and pancreatic neuroendocrine tumors
- Mitogen-activated protein kinase activity drives cell trajectories in colorectal cancer
- Correction to: The majority of β-catenin mutations in colorectal cancer is homozygous
- The majority of β-catenin mutations in colorectal cancer is homozygous
- Malignant transformation and genetic alterations are uncoupled in early colorectal cancer progression
- Reduced replication origin licensing selectively kills KRAS-mutant colorectal cancer cells via mitotic catastrophe
- DNA methylation profiling reliably distinguishes pulmonary enteric adenocarcinoma from metastatic colorectal cancer
- Robust in-silico identification of Cancer Cell Lines based on RNA and targeted DNA sequencing data
- DNA copy number changes define spatial patterns of heterogeneity in colorectal cancer
- SoFIA: a data integration framework for annotating high-throughput datasets
- Loss of prolyl hydroxylase-2 in myeloid cells and T-lymphocytes impairs tumor development
- Loss of epithelial hypoxia-inducible factor prolyl hydroxylase 2 accelerates skin wound healing in mice
- HIF prolyl hydroxylase 2 (PHD2) is a critical regulator of hematopoietic stem cell maintenance during steady-state and stress
- HIF-1α is a protective factor in conditional PHD2-deficient mice suffering from severe HIF-2α-induced excessive erythropoiesis
- Hypoxia-inducible factors as key regulators of tumor inflammation
- Inhibition of HIF prolyl hydroxylase-2 blocks tumor growth in mice through the antiproliferative activity of TGFβ
- Irradiated breast cancer patients demonstrate subgroup-specific regularities in protein expression patterns of circulating leukocytes