Eduard Batlle joined the Institute for Research in Biomedicine (IRB Barcelona) as ICREA Research Professor and Head of the Oncology Program in 2004. His research activity has focused on the mechanisms that drive colorectal cancer (CRC) initiation and progression. Amongst other findings, his research originally identified the transcription factor Snail as a repressor of E-Cadherin gene expression during the EMT (2000); the connection between intestinal stem cells and CRC (2002-2011); and more recently a key role for TGF-beta signaling in stromal cells during metastatic colonization (2012-2015). His track record has been recognized through several awards/honors such as the Sabadell Banc Award for Biomedical Research (2010), Josef Steiner Award (2013), ERC Starting and Advanced Grants (2007, 2013, 2019), the Pezcoller foundation-EACR award (2014), the Lilly Foundation Award (2016) and the King Jaume-I award in Medicine (2021). 

The inner layer of the intestinal tube, the intestinal epithelium, is in a constant process of renewal. Hundreds of millions of terminally differentiated intestinal cells are replaced by new cells every day during the life of an adult organism. This tremendous regenerative power is ultimately sustained by a small population of intestinal stem cells. It is believed that alterations in the functioning of intestinal stem cells account for the pathophysiology of various bowel disorders. Our laboratory studies the connection between the biology of Intestinal Stem Cells and Colon Cancer. We are also interested in the process of metastasis, the cause of death of most colorectal cancer (CRC) patients. Neither conventional chemotherapy nor current targeted therapies offer significant benefits once the disease has spread to distant organs. Furthermore, current CRC staging based on histopathology and imaging has a limited ability to predict the evolution of the disease. We have recently discovered that vast majority of genes that distinguish poor prognosis CRC subtypes are expressed by stromal cells rather than by epithelial tumor cells. We proposed that metastasis relies on a tumor cell non-autonomous program driven by TGF-beta in the tumor microenvironment.