Division - Tissue Crosstalk in Cancer Metabolism
Cancer cells gain growth advantages by re-programming their metabolism towards unlimited growth and proliferation. In addition, they also re-program the body’s metabolism in order to ensure their specific nutrient demands –with deleterious consequences for the host organism. The majority of late stage cancer patients suffer from cachexia, a multifactorial wasting disease defined by loss of adipose and muscle tissue that cannot be reversed by nutrition. Cachexia leads to severe impairment of life quality and treatment success, ultimately causing death by general weakening or organ dysfunction. It is estimated that cachexia accounts for more than 20% of cancer-related deaths. Currently there is no treatment option or cure for cachexia.
While many studies focus on the cancer cell’s metabolism, cancer-induced systemic metabolism is still relatively understudied. The aim of my group is to understand how cancer cells alter systemic metabolism to induce wasting, and how this can be prevented to prolong life. In particular, we are interested in the molecular mechanisms driving adipose tissue and muscle loss and their connection to systemic lipid and glucose homeostasis. We are investigating pancreatic function, endocrine hormones, and other circulating factors mediating these effects. We use a combination of cancer models, cell culture /co-culture systems, and state-of-the art high-throughput methods to understand the complex cancer-metabolism crosstalk, which consists of both direct tumor-mediated and indirect effects due to metabolic re-programming. By gaining knowledge about cancer-induced wasting, we expect to also find novel ways to target (A) other types of wasting diseases (e.g. sarcopenia, COPD-induced cachexia, burn injury), and (B) other metabolic diseases such as type-2-diabetes or obesity.