The Elias Tillandz prize 2024 was awarded to an outstanding research article which offers a possible explanation as to why higher breast density and older age increase the risk of breast cancer. The Prize was awarded to the researchers at the BioCity symposium on Thursday, 29 August 2024.
A new Finnish study from University of Turku shows that already a 30-minute exercise can increase the proportion of tumor-killing white blood cells in the bloodstream of breast cancer patients.
Treatment outcomes for breast cancer have become better over the years, but proportion of breast cancers still recur even after long periods without signs of cancer remaining dormant in the body. Finnish cancer researchers discovered a mechanism that wakes up these dormant breast cancer cells and demonstrated that preventing the mechanism can significantly improve treatment outcomes in experimental models.
Researchers have found a possible explanation as to why higher breast density and older age increase the risk of breast cancer.
Researchers at Turku University and Åbo Akademi University, Finland, have identified that finger-like cellular extensions called filopodia contribute to building a barrier surrounding breast tumours.
A research group at the University of Turku, Finland, has discovered a completely new mechanism that cells use to circulate integrins on the cell surface. Aggressive breast cancer cells exploit this mechanism to spread and metastasise to other parts of the body.
Notch proteins are key regulators of growth and differentiation of both normal and cancer cells. Researchers in Turku, Finland, have now demonstrated that the activities of distinct Notch family members are modified differently by phosphorylation. These results can be used in the development of new cancer treatments, especially for hormone-dependent breast cancer.
SORLA is a protein trafficking receptor that has been mainly studied in neurons, but it also plays a role in cancer cells. Professor Johanna Ivaska’s research group at Turku Bioscience observed that SORLA functionally contributes to the most reported therapy-resistant mechanism by which the cell-surface receptor HER3 counteracts HER2 targeting therapy in HER2-positive cancers. Removing SORLA from cancer cells sensitised anti-HER2 resistant breast cancer brain metastasis to targeted therapy.