I am a postdoctoral researcher in Teresa Frisan's group.
I hold a BSc in Molecular Biology and an MSc in Industrial and Commercial Biotechnology from Newcastle University. I completed my PhD in Cancer Biology at the University of Patras, Greece, where my research focused on the phenotypic and functional characterization of circulating tumor cells (CTCs) from breast cancer patients, with particular emphasis on triple-negative breast cancer (TNBC).
My doctoral work investigated key biomarkers associated with metastatic progression, including immune checkpoint molecules, EMT-related markers, and therapeutic resistance pathways. I also explored targeted therapeutic approaches and functional assays to better understand the biology of CTCs and their clinical relevance in aggressive breast cancer subtypes.
Currently, I am a postdoctoral researcher at Umeå University in Teresa Frisan lab, working on the project “Age-Dependent Immune and Spatial Biomarker Signatures Predicting Therapeutic Response in Pancreatic Ductal Adenocarcinoma (PDAC).” My current research combines spatial biology, immune profiling, and biomarker discovery to identify predictive signatures of therapeutic response in PDAC, with a particular focus on aging, tumor microenvironment dynamics, and personalized treatment strategies.
Age-Dependent Immune and Spatial Biomarker Signatures Predicting Therapeutic Response in Pancreatic Ductal Adenocarcinoma
This project investigates the interplay between host age, immune contexture, and microbiome-derived genotoxic influences in pancreatic ductal adenocarcinoma (PDAC). The study has two main objectives: (i) to characterize age-dependent immune and spatial biomarker profiles within the PDAC tumor microenvironment, and (ii) to explore how infection with genotoxin-producing Salmonella affects pancreatic tumor development and cellular responses using organoid models.
Age-Dependent Immune Landscape in PDAC
Tumors were generated in young (8 weeks) and old (30 weeks) mice using orthotopic implantation of pancreatic cancer-derived cells, alongside the inducible KPC model of spontaneous PDAC. A multiplex in situ immunofluorescence workflow was successfully established and optimized on both FFPE and fresh-frozen tissues using the LabSat platform. The staining panel included MHC-II, MPO, B220, CD3e, Ly6G, CD45, and F4/80, enabling detailed profiling of lymphoid and myeloid immune populations. Antibody stripping and restaining procedures were validated, confirming reproducibility across multiple staining rounds. Multiplex immunofluorescence has now been completed in tumors from 9 young and 7 old mice. Current analysis reveals an increased presence of B cells in the stromal regions of tumors from old mice compared with young mice, together with a trend toward higher lymphocytic aggregate formation in older animals. In contrast, macrophages (F4/80⁺) and neutrophils (Ly6G⁺) were detected at low levels across tissue compartments, suggesting that myeloid-driven inflammation is not a dominant feature in this model. The next step in this arm of the project is to extend the analysis to the KPC model.
Microbiome-Associated Mechanisms in PDAC Using Organoids
Organoid cultures representing normal (mN1), preneoplastic (mp4), and cancerous (mt4) pancreatic phenotypes were established and successfully infected under 3D conditions with either genotoxin-producing Salmonella (CdtB⁺) or its isogenic ΔcdtB mutant strain. The infection protocol was successfully optimized and maintained beyond 20 days post-infection. Immunofluorescence analyses of normal (mN1) organoids revealed condition-specific variations in DNA damage (γH2AX) and proliferation (Ki67) markers: ΔcdtB and TT-infected organoids exhibited elevated γH2AX levels, while Ki67 expression was reduced in ΔcdtB but markedly increased in TT-infected organoids. These early results may indicate divergent cellular responses to genotoxic stress and potential selection of damage-tolerant proliferative populations. In addition, immunofluorescence analyses have now also been performed in preneoplastic (mp4) and cancerous (mt4) organoids, with data analysis currently ongoing. The next objective is to complete three biological replicates across all organoid types under both 2D and 3D culture conditions to ensure robust comparative evaluation.
Overall, the project is progressing well and has already generated promising data supporting age-related immune differences in PDAC and distinct cellular responses to microbiome-associated genotoxic stress in pancreatic organoid systems.