Telomeres and immunityHow telomere length talks to the tumour microenvironment
Non-telomeric TRF2 binding controls IL1R1 and TERT in a telomere-length-sensitive way, linking telomere state to NF-κB signalling and immune infiltration.
Cancer cell & molecular biologist
Telomeres, mitochondria and ageing in cancer, read through imaging and computation.
Welcome. I study how telomere biology and mitochondrial function, two systems that change with age, shape what cancer cells become, how they move and how they talk to the immune system. I pair hands-on molecular cell biology and super-resolution microscopy with variational optical flow, deep learning and large-scale public genomic data.
One line of my work concerns mitochondria at the leading edge of migrating cancer cells, where I identified a mitochondria-associated translational hotspot: a site of local protein synthesis at the cell front. Earlier, we showed that telomere length regulates genes far from chromosome ends through non-telomeric binding of the shelterin protein TRF2: telomere-length-dependent TRF2 occupancy at the IL1R1 promoter tunes NF-κB-driven immune signalling in breast tumours, and TRF2 at the TERT promoter controls telomerase expression itself (eLife, 2024 and 2025). I have since extended this to telomere-maintenance and senescence programmes in human immune ageing.
Alongside experiments I build quantitative and computational tools across scales: biophysical analysis of the actin cytoskeleton by variational optical flow and nematic order; pan-cancer integration of TCGA, DepMap and CPTAC with single-cell and spatial transcriptomics and proteomics; gene regulation from expression to chromatin structure, looping and transcription-factor occupancy; and image analysis from histopathology to high-content 4D light-sheet and 5D live-cell FLIM data. The thread through all of it is one question: how telomere biology, mitochondrial function and developmental (oncofetal) programmes together decide what a cancer cell becomes (tumorigenesis) and where it goes (metastasis). If that overlaps with your work, I would be glad to hear from you.
Branched actin network at the leading edgeMitochondriaLocal translation
Three papers that show the range: a co-first-author mechanism paper, a follow-up on telomerase regulation, and a sole-author quantitative study of cell migration.
My work runs on two tracks that keep meeting: experiments on telomere and mitochondrial biology in cancer cells, and computational analyses of public genomic, imaging and clinical data at pan-cancer scale.
Non-telomeric TRF2 binding controls IL1R1 and TERT in a telomere-length-sensitive way, linking telomere state to NF-κB signalling and immune infiltration.
Mitochondria positioned at the front of migrating cancer cells mark a mitochondria-associated translational hotspot, a site of local protein synthesis at the leading edge.
TV-L1 optical flow, orientational order and topological defect analysis applied to live-cell and super-resolution data, with deep-learning pipelines for microscopy.
Sole-author analyses integrating TCGA, DepMap, CPTAC, ENCODE and spatial transcriptomics to find structure that single studies miss.
Research positions and degrees, most recent first.
Research on cytoskeletal dynamics, organelle coordination and local translation in cancer cell migration. Teaching in UKE degree programmes (2026); supervised master's and PhD students in live-cell imaging, image analysis and cloning.
Telomere–immune crosstalk in the tumour microenvironment, TRF2-mediated IL1R1 regulation, TERT gene regulation, T cell ageing, machine learning for telomere length prediction from gene expression.
Single-molecule opto-genomics for immune checkpoint blockade; single-molecule imaging of T-cell receptor serial engagement.
Lineage-specific transcription factors in liver cancer, trans-differentiation, next-generation sequencing analysis.
Genetic alterations in gall bladder cancer; graph-based network analysis of tumour angiogenesis.
First division, CGPA 8.34/10. DBT Merit Scholarship.