The CMMC is pleased to announce the three scientists of the Medical Faculty (University of Cologne) awarded with the CMMC CAP Funding.
The three awardees are:
Dr. rer. nat. Phuong-Hien Nguyen - Clinic I for Internal Medicine
Dr. med. Johannes Brägelmann - Institute for Pathology and Dept. for Translational Genomics
Dr. med. Sebastian P. Brähler - Clinic II or Internal Medicine
The CMMC´s Career Advancement Program (CAP) is a funding instrument that was established to further promote highly talented mid-career scientists to obtain preferentially a W2/W3 professorship in academia or high-quality leadership positions at non-university research institutions and organizations in the future. Based on an internal evaluation procedure the new CAP Group Leaders were selected and received CAP funding in the amount of 10.800 € per year for a three-year period with the option of a two-year prolongation after a positive external evaluation.
A new call for the submission of CAP proposals will be launched at the end of this year.
This program has been proven to be extremely successful. For further information, please visit: https://www.cmmc-uni-koeln.de/research/career-advancement-groups.
The research interest of Dr. Phuong-Hien Nguyen is to gain insights and to better understand the functional relevance and signal transduction network of protein kinases in the tumor microenvironment (TME).
Since the last decade cancer is no longer considered a disease of only malignant cells, but a highly complex tissue comprising tumor cells and their tumor microenvironment (TME). “My research is based on the finding that protein kinases are functionally essential for the formation of the tumor-promoting microenvironmental niche. The distinct pattern of substrate activation induced by each specific kinase leads to a differential activation of signaling cascades and, as a consequence, to modulation of diverse cellular functions”, Nguyen comments and adds: ”Understanding protein kinases’ functions is not only beneficial to improve cancer-killing capabilities of available kinase inhibitors, but also allows us to repurpose these inhibitors to target the cancer-associated immune and metastatic niches”.
Dr. Sebastian P. Brähler’s research interest focuses on the understanding of the B- and T-celllymphocyte attenuator (BTLA) and its role as central regulator of immunity in glomerulonephritis.
Glomerulonephritis (GN), inflammatory diseases of the glomerulus, the kidney filtering apparatus, leads to rapid loss of renal function and, ultimately, the need for chronic dialysis. “For many years my research interest is dedicated to understand the underlying molecular mechanisms causing the development of GN. T-cells and classical dendritic cells (cDC) have key functions in the pathogenesis of glomerulonephritis. Therefore, molecules governing their activity represent promising therapeutic targets. Our previous work strongly suggests that B- and T-celllymphocyte attenuator (BTLA) is such a target. The understanding of BTLA function will not only yield fundamental insight into protective mechanisms in kidney diseases but also could identify a new therapeutic principle for glomerulonephritis”.
Dr. Johannes Brägelmann’s research interest focuses on the understanding of the molecular mechanisms of tumor evolution and therapy resistance.
Large-scale genomic studies show that squamous cell lung- and head and neck cancer share substantially overlapping genetic and epigenetic backgrounds, but lack druggable drivers. Chemo- and immunotherapy thus remain a therapeutic backbone, but efficacy of these agents is limited. Accordingly, the mechanistic understanding of drug resistance represents a major translational research field. “My project therefore aims to understand and therapeutically exploit those processes to improve drug response. While we systematically assess mediators of resistance to chemotherapies using functional CRISPR-based experiments and transcriptomic/genetic profiling of chemotherapy-induced adaptations, our further goal is to identify key molecular drivers of drug response against the two main clinically relevant systemic therapies in SQLC/HNC”.