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March 18

We had the honor to host

Dr. Catarina Brito from ITQB NOVA who gave a talk on:

Development and application of an innate immunocompetent hiPSC-derived neurosphere model, to capture the early CNS response to rAAV”

and

Dr. Daria Bunina from Max Delbrück Center  who  gave a talk on:

Chromatin malfunction in neurodevelopmental and cardiovascular disorders”

 

Dr Catarina Brito Short Bio

I have led the Advanced Cell Models Lab of ITQB NOVA and iBET since 2014 and have been a principal investigator at ITQB since 2023. My research is primarily preclinical and translational, focusing on the microenvironment-driven modulation during targeted therapy response. My group pioneered cell-based strategies to address challenges in cancer immunotherapies and viral vector-based gene therapies. Our research centers on two main research lines: 1) Macrophage-tumor cell crosstalk within the tumor microenvironment in immunosuppression and resistance to immunomodulatory therapies; 2) Neuron-glia crosstalk in neuroinflammation and innate immune response to viral vector-based gene therapies.

Dr Daria Bunina Short Bio

Dr. Daria Bunina is a Group Leader at the Max Delbrück Center (MDC) in Berlin, Germany since 2022. She earned her PhD in Biomedical Sciences from Heidelberg University in 2016, where she investigated antisense transcription effects on protein abundance in S. cerevisiae. She then pursued postdoctoral research at EMBL Heidelberg, where she trained in experimental and computational epigenomics, focusing on chromatin dynamics and gene regulation in the context of cell differentiation. Her current work explores how chromatin malfunction affects gene regulatory networks, particularly in neurodevelopmental and cardiovascular disorders. Bunina lab is using human stem cell-derived 2D and 3D in vitro models of cardiovascular and neuronal differentiation and a systemic approach combining bulk and single-cell “omics” technologies and novel data integration methods to dissect gene regulatory networks and identify molecular pathways perturbed in human disease.