DC 6: Lucas van Endert
Lucas van Endert graduated with a Bachelor’s degree in Biology from Université Paris- Saclay in 2022. He then went on to pursue a Master’s degree in Integrative Biology and Physiology at Sorbonne Université in Paris, with a specialization in neurosciences. During his Master’s studies, Lucas spent one Erasmus semester at Heidelberg University, where he followed several courses and took part in an internship at EMBL, in the Noh lab, which studies epigenetic mechanisms of neurodevelopmental diseases.
Later, he joined the Kalebic lab in February 2024 at Human Technopole Milan for his Master’s thesis internship. His work focused on elucidating the role of GPI-anchored proteins in brain cortical development by using varied in vivo and in vitro modeling approaches, high-end microscopy, and biochemistry. After graduating from his Master’s, he continued working in the Kalebic lab, continuing to work on the same project as well as starting to work with hIPSC organoid models of Down Syndrome to study how cortical development is altered in this condition.
Lucas will start working in the Mosaic Baulac lab in October 2025, focusing on the link between brain mosaicism, the mTOR pathway, and focal cortical dysplasia by integrating cutting-edge genomics and electrophysiology with patient samples as well as in vitro models.
Planned secondments: 3 months at FORTH-BRI for brain organoid modeling FCDII gene variants that alter mTORC1 activity. 3 months at Cell Signalling Technology for phospho-specific antibody development of differentially regulated proteins in mutant brains.

FORTH-BRI
3 monthsIoannina, Greece

Cell Signaling Technology
3 monthsBoston, United States
My research project
Focal Cortical Dysplasia type II (FCDII) causes severe drug-resistant pediatric epilepsy through mTOR pathway hyperactivation. FCDII-associated epilepsy is typically resistant to anti-seizure medications, and patients ultimately require neurosurgical resection of the epileptogenic zone for seizure control, allowing direct analysis of diseased tissue. The Baulac lab is one of the pioneers in the identification of brain somatic mutations in FCDII affecting various genes belonging to the mTOR pathway and which cause mTOR hyperactivation. However, there are still ~40% of FCDII cases that remain unsolved genetically. Moreover, the cell-type and developmental origin of FCDII abnormal cells remain poorly understood. DC6 will:
- discover novel FCDII-causing genes in the mTOR pathway through ultra-deep sequencing;
- identify mutation-carrying cell types and their developmental origins using single-cell approaches;
- map electrophysiological dysfunction to molecular changes via MEA recordings coupled with spatial transcriptomics from human acute cortical slices and mouse models.
PhD candidate will analyze surgical epileptic brain tissues using cutting-edge genomics (targeted panels, whole exome/genome sequencing, longread sequencing), single-nucleus RNA sequencing, laser-capture microdissection, and integrate functional electrophysiology with spatial transcriptomics.