Jemina Lehto - ESR 15

Name: Jemina Lehto

Nationality: Finland

Main Host Institution: Kancera AB / Karolinska Institutet

Academic Background:

● Master and Bachelor in Physiology and Genetics, University of Turku, Finland → Focusing in molecular biology and biomedicine, I conducted my master’s thesis research in the Department of Medical Biochemistry and Genetics in the University of Turku in Dr Riku Kiviranta’s group working with mouse models for genetic bone diseases.

● Internship in cancer drug discovery, Experimental Therapeutics Centre, A*Star, Singapore → Preclinical pharmacology under supervision of Dr Kanda Sangthongpitag

Project title: Fractalkine axis in ovarian cancer and its targeting for cancer therapy

Project background: Fractalkine is a protein on the surface of cells that works like a guide for other cells to move towards it and attach to it. To be guided by fractalkine, a cell needs to have a specific receptor that can interact with fractalkine - this is called a fractalkine receptor. Fractalkine can also detach from the cell surface and work alone outside of the cell, searching for its receptor. Binding of a cell with a fractalkine receptor to fractalkine works as a signal for the cell to for example move or divide.

Normally fractalkine works in an inflammatory response guiding blood cells, which help to battle the infection, to the site of inflammation. However in epithelial ovarian carcinoma fractalkine seems to be involved in the movement of cancer cells - also called metastasis - from the primary tumor site to other locations in the body such as internal organs. As the danger of cancer lies in the metastasis of cancer cells to vital organs, we want to block fractalkine with a drug designed to attach the receptor instead of fractalkine so that cancer cells can not move. Blocking fractalkine can also slow cancer cell division and make cancer cells more prone to be killed by other therapies such as radiation. Radiation and some cancer drugs kill cancer cells by causing their DNA unrepairable damage and a new hypothesis is that blocking fractalkine could cause more damage to the cancer cell’s DNA and kill them better than traditional therapies alone. Thus we plan to use a fractalkine blocker developed by Kancera in combination with other therapies to stop ovarian cancer cells from moving and then clear the cancer from the body.

Project Aim: The aim of this study is to get more knowledge of the role and function of fractalkine signaling in epithelial ovarian carcinoma and to contribute to the development of an effective and specific therapy for epithelial ovarian carcinoma.

Expected outcome: The drug validated in this project for EOC is expected to be used in combination with other already established therapies to yield and ultimate cancer-killing response.