photo credits: Marianna Kapsetaki, location New College, Oxford, graduation 2019
Dr. Steffi Kapsetaki
I’m Steffi. People also call me Stephanie, or Stefania as written in my passport. This is how I go through life, by changing identity and crossing barriers. I'm a (r)evolutionary scientist, classical music performer, and…
...a twin. I have a lifetime companion, but also... a food-absorbing friend! Coming out lighter than my sister was not easy! This may have triggered my interest in conflict and cooperation across life. Through my education at Oxford, I mastered the fields of social evolution and the evolution of multicellularity. Inside my multicellular body, I see identical cells sometimes fighting foreign cells for food. When foreign cells live with me forever, I’m called a chimera. Did I mention that I might be in my twin?! When they divide faster than other cells, they may possibly become cancer. As a Postdoctoral Researcher at Arizona State University, I’m testing this possibility in every creature on our planet.
PROJECTS I have co-authored
1. Cancer & chimerism. Major transition breakdown?
Why be interested in fagedena? Φαγέδαινα means cancer, and is the first historical record of cancer by Democritus (460 – c.370 Before Christ).
You may have seen the large stone in the entrance to this site, meteorites I think they call them. Did you feel anything as it was approaching you? Danger I suppose. Well, we usually try to avoid anything that reminds us of danger. One of these is cancer. Avoid death? Well that's on our DNA, in its energy. Mou
I am currently playing biology with the most ancient music of the universe. Follow me to find out more.
2. The evolution of multicellularity
I served as Editor-in-Chief, Co-Editor-in-Chief, Science & Society Editor, Page Editor, and Features Editor of Phenotype during my graduate studies at Oxford. Phenotype is the Oxford University Biochemistry Society journal. Feel free to explore.
4. Bacteria use flies as aeroplanes
5. Drug screening in flies
We "want" (I mean our DNA has evolved that characteristic) to "avoid death". Some bacteria may be able to kill us. Therefore one of our interests is trying to kill them. The "weapons" we use in order to kill them are called antibiotics. However, by killing them with antibiotics we promote the growth and establishment of mutant bacteria in the population, which are resistant to the antibiotics. A different approach, to avoid the build-up of unstoppable multi-drug resistant bacteria, is to not kill the bacteria, but to inhibit their communication which is important in their pathogenicity. By stopping certain of their communication pathways, we can stop the disease and not build-up antibiotic resistance. This was one of my undergraduate projects assessing the antibiotics Carbenicillin, Ciprofloxacin, Ticarcillin and Kanamycin on the model organism Drosophila melanogaster for combinatorial antimicrobial effect against the bacterium Pseudomonas aeruginosa.
7. Synergistic action of antimicrobials in the reduction of Pseudomonas-aeruginosa-14-induced-dysplasia in the posterior midgut of teg/Ras1-Act flies