RANKINE FAMILY FELLOWSHIP IN NF1
Thanks to the generosity of Duck & Dodge supporters, the Rankine Family Fellowship in NF1 is paving the way for innovative research by training the next generation of pioneering scientists in the field of neurofibromatosis (NF1).
We are excited to report that Dr. Chris Lowden, continuing his fellowship from last year, has fully operationalized his advanced screening system and is currently conducting a comprehensive genome-wide analysis to pinpoint genes crucial for two essential processes: maintaining normal skin health and the development of skin tumours driven by the Ras/MAPK pathway, which is primarily disrupted in NF1.
Dr. Lowden has optimized the CRISPR-StAR system, enabling the screening of a vast number of genetic variations using only four animal models while producing impressively clear and accurate results. This refinement is critical, allowing for highly precise genetic screenings with fewer resources, thereby accelerating the research process. With this system now fully operational, Dr. Lowden is conducting a comprehensive genome-wide screening to identify genes essential for two key processes: maintaining normal skin health and the development of skin tumours driven by the Ras/MAPK pathway, the primary pathway disrupted in NF1.
Dr. Danian Chen is also building on his previous work, making significant headway in his exploration of NF1-linked cancer susceptibility, reinforcing the hypothesis that rapid cell division signals a heightened risk of cancer.
When the NF1 gene is lost, the KRAS gene is activated, a key driver in many cancers. Dr. Chen has been investigating how KRAS activation influences cancer initiation, particularly across different lung cell types. His research revealed that although KRAS activation affects multiple lung cell types, only certain cells become cancerous.
Dr. Chen and the team conducted further experiments, studying other cancer pathways and timing factors. One key finding emerged from investigating BRAF, another protein that drives lung cancer similarly to KRAS. They discovered that cells with BRAF mutations also exhibit faster division, reinforcing the hypothesis that rapid cell division indicates cancer susceptibility.
Ultimately, gaining insight into the mechanisms of cancer initiation, as uncovered by this research, could pave the way for strategies aimed at preventing cancer formation.
Thanks to your steadfast support that has enabled us to explore new pathways and breakthroughs, empowering scientists to uncover insights that would have remained out of reach without your support and will continue to drive this promising research forward.