Albena Dinkova-Kostova graduated in Biochemistry and Microbiology from Sofia University (Bulgaria) with MSc degree and a diploma thesis describing her research at the Institute of General and Comparative Pathology of the Bulgarian Academy of Sciences, where she was mentored by Rajna Tosheva. Albena then obtained her PhD degree in Biochemistry and Biophysics from Washington State University (USA) under the mentorship of Professor Norman G. Lewis and Dr Laurence B. Davin. She subsequently trained in Pharmacology and Molecular Sciences at Johns Hopkins University School of Medicine (USA), mentored by Professor Paul Talalay, where she continues to hold an Adjunct Professor position.

Albena joined the University of Dundee in 2007 as a Research Councils UK Academic Fellow and a research group leader. Her group collaborates with basic scientists and clinicians, and with the pharmaceutical industry. In her research, at the interface of Chemical Biology and Medicine, she is committed to understanding how cells and organisms respond to oxidative, inflammatory, and metabolic stress, and is working towards development of strategies for protection against chronic disease.

Albena is the recipient of the 2011 Arthur C. Neish Young Investigator Award of the Phytochemical Society of North America. In 2023, Albena was elected Fellow of the Royal Society of Edinburgh. In 2024, she became Fellow of the Royal Society of Biology. She was named among the top influential academics in Clarivate’s Highly Cited Researchers 2019, 2020, 2021, 2022, and 2023 lists.

The steady increase in the number of new cancer cases diagnosed each year and the relatively modest success in cancer treatment highlight the urgent need for the development of strategies for prevention. It is important to understand that the disease cancer is the process of carcinogenesis itself that begins many years, often decades, before any clinical symptoms become apparent. In animal models, protection against cancer, and many chronic diseases, can be accomplished by induction of the Keap1/Nrf2 pathway, which controls the gene expression of numerous cytoprotective enzymes (e.g., glutathione S-transferases, epoxide hydrolase, quinone oxidoreductase 1, heme oxygenase 1) that catalyze versatile reactions collectively leading to detoxification of electrophiles and oxidants. However, the Keap1/Nrf2 pathway is often upregulated in established tumors, where it contributes to cancer cell survival, metabolic adaptation, and resistance to chemo-, radio-, as well as immuno-therapy.

The expression of Nrf2-dependent genes can be elevated by a wide variety of pharmacological agents termed “inducers”, some of which are present in the human diet. Additionally, a number of endogenous compounds, which accumulate under specific conditions, can also activate Nrf2. Most well characterized inducers are electrophiles that react with specific cysteine residues of the sensor protein Keap1, thereby allowing transcription factor Nrf2 to translocate to the nucleus and activate transcription. Other inducers are Keap1-Nrf2 protein-protein interaction inhibitors. The discrete events in the regulation of the Keap1/Nrf2 pathway and the mechanism of action of these two classes of Nrf2 inducers are major objectives of our research. We are also investigating the regulation of the heat shock response, another cellular cytoprotective pathway, and the ability of small molecules, which can inhibit heat shock protein 90 (Hsp90), the most abundant cellular chaperone, to interfere with cancer cell proliferation.

We employ biochemical methods in various in vitro and cellular systems, as well as in vivo genetic and pharmacological models of human disease. Knowledge obtained from these models inform the design of clinical trials to determine the effectiveness of Nrf2 modulators for the prevention and treatment of chronic disease. Two pharmacological Nrf2 activators have entered clinical practice for the treatment of relapsing forms of multiple sclerosis (dimethyl fumarate, TECFIDERA^®) and (Friedreich's Ataxia, omaveloxolone, SKYCLARYS^®).