Ewelina Bolcun-Filas is an Associate Professor at The Jackson Laboratory in Bar Harbor, Maine. Her research aims to identify molecular mechanisms controlling development of healthy ovarian egg reserve, and how misregulation of these mechanisms can lead to infertility. Born in Poland, she received her M.Sc. in biology from Jagiellonian University in Krakow, Poland. She earned her Ph.D. from Georg-August-University in Gottingen, Germany. To pursue her interests in reproductive biology she joined MRC Human Genetics Unit in Edinburgh, Scotland as a postdoctoral fellow.
In 2008 she moved across the ocean to reunite with her family living in Connecticut and continued her research into genetic causes of infertility at Cornell University in Ithaca, NY. Her work identified an essential signaling pathway responsible for culling of abnormal oocytes and ensuring survival of only high quality eggs. She further demonstrated that the same mechanism eliminates immature eggs exposed to radiation; a common cancer therapy which can lead to premature ovarian failure and infertility in cancer survivors. Her discovery promises new approach for fertoprotective treatments for cancer patients. She joined The Jackson Laboratory in January 2015 where she continues her work investigating genetic causes of infertility and mechanisms of cancer therapy-induced ovarian toxicity. The goal of her research is to develop genetic risk prediction methods and new treatments for preservation of healthy ovarian function and fertility in female cancer survivors.
Germ cells are the only cell type that must endure extensive DNA damage in the form of programmed meiotic double-strand breaks (DSBs) during their normal development. Paradoxically, the absence of DSBs during meiosis as well as persisting unrepaired breaks are detrimental and typically result in meiotic arrest and infertility. Our research aims to understand the molecular mechanisms controlling the development of healthy gametes and how misregulation of these mechanisms can lead to reproductive disorders. In particular, we are interested in meiotic “quality checkpoints” operating in germ cells, which ensure that the correct and intact genetic information is transmitted to the next generation. The same checkpoint that monitors DSB repair during meiosis is responsible for high sensitivity of oocytes to cancer treatment. Chemo and radiation therapies can cause oocyte death and lead to premature ovarian failure and infertility. Disabling the key checkpoint kinase CHK2 preserved fertility in mice exposed to ionizing radiation, thus opening a new avenue for oncofertility research. Our goal is to further dissect the DNA damage response pathway in oocytes, helping identify additional targets for fertility preservation therapies in cancer patients.