Publishing my article in Genome Biology (PMID: 40696461) and receiving the MSNZ grant to establish my own group were milestones that can be attributed to a solid scientific foundation, a supportive environment, and close interaction with clinical partners.
First, I was fortunate to work in Dresden in an ecosystem that encouraged translational thinking and provided the freedom to pursue ambitious ideas. One key lesson is that impactful science is rarely a solo effort. Mentorship, interdisciplinary collaboration, and persistence are crucial, and great ideas often rise from interdisciplinary, diverse teams. In addition, it is important to recognize one’s own limitations and to invest in potential collaborations. Another important point is (long-term) investment and trust in the next generation of scientists – e.g., by actively engaging in tutoring students of all stages in the laboratory. This way, the good high school/bachelor students of yesterday become the interested and capable PhD students of today. I have been fortunate to mentor eleven (PhD, Medical, Master’s and Bachelor’s) students throughout the past few years. Furthermore, I cannot emphasize enough the value of the excellent support I received myself, as it paved the way for everything that followed, especially from my mentors Prof. Dr. Frank Buchholz and Prof. Dr. Martin Bornhäuser, as well as Prof. Dr. Daniel Stange and Prof. Dr. Martin Wermke.
The paper recently published in Genome Biology builds on our earlier finding that correcting the TP53-R273H mutation - present in around 12,000 cancer patients annually in Germany - causes rapid depletion of cancer cells in cell lines and patient-derived organoids. Strikingly, after mutation correction, we observed a largely similar transcriptional response (through reactivation of p53 target genes), regardless of the cancer type. This result both offers a platform for identifying a mutation’s contribution to cellular fitness and the possibility for therapeutic repair of the mutated p53, a tumor suppressor protein nicknamed “the guardian of the genome”. It is important to note that strategies targeting p53 have been promising, but since p53 is a transcription factor, its defective protein has long been considered undruggable. Restoring wild-type p53 in its native context is the best approach to regain its function. We were delighted that our article was named “Paper of the Quarter” by the DG-GT.