Diet-induced obesity is a major risk factor for the development of cancer. Although alterations in inflammatory and bioenergetic pathways are critical in linking excessive weight gain to cancer, there is now sufficient evidence to also suggest disease progression may indeed have more to do with the diet itself than increased obesity per se.
The diet is shaped by multiple diverse factors such as culture, nutritional knowledge, price, availability, taste and convenience. With our current knowledge on the importance of the reciprocal interaction between host and environmental factors in selecting a microbiota that favours carcinogenesis, the food consumption is critical. Given the distinct shifts in agriculture and changes in crops, food may have a pivotal role in aggravating disease.
Our laboratory at GSH focuses on how changing diet is associated with cancer initiation and progression at a molecular and cellular level using mouse models with oncogene activation. We aim at dwelling how inflammatory cells crosstalk to host during disease progression, what sort of metabolic derangements are taking place in both host and tumor energy metabolism, whether altered post-translational modifications play a causative role or are just consequent to disease development and if/how microbiota is involved in these processes.
Once defined in depth, the next step would be to set the stage for direct interference within any of these processes and to test the possibility for developing therapeutic interventions. Our ultimate goal will be direct translation of our studies into the clinic.
Our Lab is affiliated with the Institute of Biochemistry II of Medical Faculty of Goethe University Frankfurt am Main.