Milán Kalbfleisch, Marco
Icrea Research Professor at Institut de Recerca Biomèdica (IRB Barcelona).
Life & Medical Sciences
Short biography
Graduated in Biology at the Universidad Complutense in 1991, I obtained my PhD in the laboratory of Antonio García-Bellido at the CBM-Severo Ochoa in 1995. In 1997, I joined the laboratory of Stephen M. Cohen at the EMBL-Heidelberg where I got a position as Staff Scientist. Since 2003, I am ICREA Research Professor at the Institute for Research in Biomedicine leading the Development and Growth Control Laboratory. Since 2007, I have also been Head of the Cell and Developmental Biology (2007-2018) and Mechanisms of Disease (2018-) Programmes. I was Visiting Professor at the National University of Singapore in 2010 and I am Lecturer at the University of Barcelona since 2020. I am member of the Disease, Models and Mechanisms editorial (2016-) and European Drosophila Society (2021-) boards. I was elected EMBO Young Investigator in 2007 and EMBO member in 2023. I have directed 13 PhD theses, 17 Master theses, and published, as first or lead author, more than 75 papers.
Research interests
A balanced gene complement is crucial for proper cell function. Aneuploidy, the condition of having an imbalanced chromosome set, alters the stoichiometry of gene copy numbers and protein complexes and has dramatic consequences at the cellular and organismal levels. In humans, aneuploidy is associated with different pathological conditions including miscarriages, aging, cancer, microcephaly and mental retardation. Our lab uses Drosophila to molecularly characterize the impact of aneuploidy at the cellular, tissue-wide and organismal levels. We have established an epithelial model of Chromosomal instability (CIN), a feature of most human epithelial tumors, to unravel a leading role of aneuploidy in the emergence of tumor-like behaviors like tissue invasiveness, senescence and malignancy. We are also interested in addressing the impact of aneuploidy in other tissue types and cells, including stem cells.