The liver is the preferred site for colorectal cancer metastases. We are looking for memory T cells that continue to target tumours over the long term – as prognostic markers and a potential basis for new immunotherapies for colorectal liver metastases

Human adenoviruses can transform cells – via the oncoprotein E1B-55K, which dysregulates cellular transcription factors such as TEAD. We are unravelling this mechanism at the molecular level and searching for new targets for cancer therapies

YAP/TAZ-TEAD inhibitors show promise in the treatment of liver cancer – but tumour cells reorganise their transcription factor complexes and circumvent the treatment. We are analysing these resistance mechanisms and searching for more effective
combination strategies.

Pancreatic cancer resists almost every form of treatment. We have discovered that tRNA wobble enzymes make tumour cells resistant to the growth inhibito mTORC1 and are investigating whether this mechanism can be targeted therapeutically.

Two-thirds of patients with gastroenteropancreatic neuroendocrine tumours do not respond to peptide receptor radionuclide therapy. We are investigating how this treatment modulates the immune system – and using these findings to develop new
biomarkers.

SHH-activated medulloblastomas are molecularly similar –yet their clinical courses are very different: curable in one case, fatal in the other. We are analysing differentiation barriers in the aggressive cases to explain the cause of these differences in prognosis.

Radiotherapy for lung cancer carries a risk of pneumotoxicity. We are training convolutional neural networks to identify individual risk factors – and aim to use this to predict toxicity more accurately than previous clinical models have been able to.

Targeted therapies against RTKPI3K- AKT signalling fail clinically in glioblastoma, even though the target structures are present. We are testing a library of specific kinase inhibitors on patient-derived tumour organoids in the tumour microenvironment.

The grading of prostate cancer remains subjective and prone to error today. We are developing AI-based analysis tools for digital histological slides, which enable a more objective assessment of tumour aggressiveness and clinical progression.

A disrupted microbiota is a key factor in inflammation-associated colorectal cancer. We are identifying IgA antibodies from innate B-cell subpopulations that modulate the gut microbiome – and are evaluating their therapeutic potential in IBD-related cancer.

PARP inhibitors have so far had little effect on urothelial carcinoma. We are combining them with BET inhibitors to induce a BRCAness-like DNA repair deficiency in tumour cells – thereby making them responsive to this class of therapy for the first time.

Tumours send extracellular vesicles to draining lymph nodes – and there prepare the pre-metastatic niche. We are investigating, using melanoma as a model, how these vesicles reprogramme lymphatic endothelial cells and macrophages for immune evasion.

Tumour cells transfer mitochondria to cancer-associated fibroblasts – thereby altering the tumour microenvironment of skin cancer. We are unravelling the mechanisms of this intercellular transfer and investigating whether it can be blocked for therapeutic purposes.

A blood test that detects cancer in several organs at the same time – even before symptoms appear? Using infrared laser technology, we analyse molecular fingerprints in blood plasma. The aim: early cancer detection via high-throughput diagnostics.

Non-alcoholic fatty liver disease significantly increases the risk of liver cancer. We are investigating how specific fatty acids impair the anti-tumour function of MAIT cells – and thereby weaken the immune system of this metabolically stressed organ.

Helicobacter pylori is a trigger for gastric cancer – but what happens in the tumour stroma afterwards? We are investigating how the microbiota and immune cells interact in various histological subtypes of gastric adenocarcinoma and influence tumour progression.

Tumour blood vessels require considerable amounts of energy for growth and branching. We show that this metabolic demand is met by mitochondrial activity – and investigate whether this energy metabolism can be used as a therapeutic target.

HPV-negative head and neck tumours resist chemoradiotherapy and show little immune response. We are investigating how CD98hc reprogrammes tumour cell metabolism and inhibits anti-tumour immunity – and whether this pathway is therapeutically vulnerable.

Anti-hormone therapy for prostate cancer drives tumour cells into lineage plasticity – they change their identity in order to evade the therapy. We are investigating chromatin remodelling mechanisms that regulate this plasticity as new target structures.

Small-cell lung cancer metastasises early and aggressively. In our analyses, metastases lose MHCI – an indication of active immune evasion. We are investigating the mechanisms behind this and looking for targets for immunotherapy strategies.

CT, MRI and radiology findings combined in a single AI model: We are developing a multimodal foundation model that uses contrastive learning to generate generalisable tumour representations – across different organs and without the need for retraining.

Carbon ions, protons or photons: How does each type of radiation affect prostate tumour cells? We are carrying out a comprehensive proteome analysis on 220 tissue samples and deciphering radiation-type-specific molecular signatures and resistance mechanisms.

Chromosomal instability occurs in 60–80 % of all carcinomas – and is particularly pronounced in gastric carcinoma. We model CIN in the laboratory to address the resulting growth advantages, immune evasion and metastatic potential from a
therapeutic perspective.

In chronic lymphocytic leukaemia checkpoint inhibitors and CAR-T cells, which are effective in other lymphomas, fail. We are investigating DUSP1/6 inhibition as a strategy to overcome the tumour’s own immunosuppression in CLL.

T cells targeting lymphomas require two activation signals – TCR/ CD3 and co-stimulation via CD28. We are developing trispecific antibodies that modulate both signals in a tumourrestricted manner: precise immunotherapy rather than systemic T-cell activation.

Recurrence is a clinically significant problem in hormone-receptor-positive breast cancer. We use patients’ own tumour organoids to determine the effectiveness of CDK4/6 inhibitors in the early stages – to inform more personalised treatment decisions.

KRAS is mutated in 90 % of pancreatic cancers – and was long considered untreatable. New mutation-specific inhibitors are now available, but tumour cells adapt their metabolism accordingly. We are unravelling these transcription-induced resistance
adaptations.

Genotoxic E. coli strains containing the pks operon are linked to the development of colorectal cancer. We are investigating how extracellular vesicles from these bacteria damage intestinal epithelial cells and what role the microbiome plays in carcinogenesis.

Meningiomas are the most common intracranial primary tumours – some progress despite resection and radiotherapy. We use DNA hypermethylation signatures as a molecular fingerprint to develop new targeted therapeutic strategies.

Cancer treatments have a lasting effect on the immune system – though not always for the better. Elevated Th17 levels following treatment are associated with recurrences of cervical and vulvar cancer. We are characterising the role of succinate in this process.

The mechanics of the basement membrane influence how lung adenocarcinomas develop and progress – an underestimated factor. We are investigating the biomechanical properties of the extracellular matrixas a new therapeutic target in lung
cancer.

p53 is mutated in one in every two tumours – and was long considered untreatable. We are developing tailored DARPin proteins, which correct structural hotspot mutations in the p53 DNA-binding domain and reactivate the tumour suppressor.

Gliomas respond very little to immunotherapies – too few antigens, too severe immunosuppression. We are developing pan-HLA-reactive T-cell receptors for adoptive T-cell therapy, which can be used regardless of the patients’ HLA type.

CAT6A fusion oncogenes affect epigenetic regulators and drive rare, highly aggressive leukaemias. We are investigating, for the first time, the leukaemogenesis of these entities and examine whether targeted inhibition opens a clinically relevant therapeutic approach.

The surgical removal of early-stage oesophageal cancer carries significant risks – organ-preserving endoscopy is an attractive alternative. We are conducting a wide analysis of risk factors for recurrence to refine the selection criteria for this treatment.

Ductal adenocarcinoma of the pancreas is almost impossible to control despite chemotherapy – desmoplastic stroma and progranulin promote resistance. We are investigating progranulin as a target to make the tumour microenvironment more
accessible to chemotherapy.

CAR-T cell therapies work – but random genomic integration carries risks. We are developing a sequence-specific ‘Sleeping Beauty’ transposon system for the targeted, safe integration of CAR genes: genomically safe cell therapy of the next generation.

Clear-cell renal cell carcinomas often remain incurable at the metastatic stage. We have identified that tumour cells exploit aberrant tubular repair mechanisms – and are investigating whether this vulnerability can be exploited for new therapeutic
approaches.