Turning cancer defects into cures

With a team of 70 scientists from 22 different nations we turn cancer defects into novel treatments. Subscribe to our newsletter to stay updated about our research!

Welcome to the Helleday Laboratory

Targeting DNA Glycosylase OGG1 in inflammation

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We aim to improve science, health and society! Our commitment does not stop with science at the basics; we bring our results all the way to the patients.

The Helleday Laboratory consists of a large team of mixed professions from industry and academia; basic molecular biologists, medicinal chemists, pharmacologists, biochemists and practicing clinicians, amongst others. What brings us together is our dedication to make our basic science discoveries reach all the way to helping patients stay healthy and with their loved ones.

The Helleday Laboratory mostly focuses on metabolism and DNA repair, and recently inflammation.

The Nobel Prize laureate Otto Warburg who pioneered modern cancer metabolism research once said that “The cure of human cancer will be the resultant of biochemistry of cancer and of biochemistry of man“. We could not agree more. With today’s molecular knowledge of altered metabolic pathways in cancer cells we are making real advances in progressing cancer treatments. Read about how we target glucose metabolism and nucleotide metabolism. Chemo- and radiotherapy is still the backbone of cancer treatments, and they work by causing damage to the cancer cells DNA. We know today that cancer cells have a high load of DNA damage as compared to normal cells. Read about DNA damage and repair in cancer. Previously, the Helleday lab has exploited this and shown that PARP inhibitors selectively kill recombination defective cancers, such as inherited breast- and ovarian cancer. This is now an approved treatment and help patients across the world.


The drugs of the future will target DNA repair

Keeping up the intact DNA is vital for all organisms, and life as we know of it would not exist. Now, we know it is not black or white, but that DNA damage can also lead to imperfection leading to various diseases. Ageing is an example of a process that will damage...

When and why MTH1?

Why do cancer cells need the MTH1 protein for growing and spreading throughout the body? A new study lead by scientists from the Helleday laboratory at Karolinska Institutet together with colleagues from Stockholms University and the Heinrich-Heine University in...

Mary-Claire King visits Helleday Laboratory

Mary-Claire King visits Helleday Laboratory Lasker award winner, Nobel Peace Prize nominee and discoverer of BRCA1 Mary-Claire King visited Stockholm to give a Nobel Forum lecture. Mary-Claire King, PhD, is American Cancer Society Professor at the University of...

Thomas Helledays receives ERC Advanced Grant

Thomas Helledays receives ERC Advanced Grant Thomas Helleday is one of nine scientists receiving a grant of 2.5 million euros over five years from the European Research Council. Research proposed for funding to the ERC should aim high, both with regards to the...

“I am happy and impressed by your work. Words can not describe how grateful I am; not only for my sake but for my children and family as well. It gives me hope to break the chain of cancer in the family. I hope for the drug to reach the market soon so more patients can be treated.” Translated from Swedish



Our vision

Many diseases have alterations in metabolic pathways often leading to DNA damage that manifest or define the disease. Our strategy is to identify basic mechanisms of proteins involved in metabolism and DNA repair to gain better understanding in disease and also develop small molecule inhibitors to selectively targeting these proteins as potential therapeutics. We reach our goal through open innovation and through a foundation, securing the future for our science and ensuring long term benefit to mankind.

Our mission

We turn cancer defects into novel treatments. Cancer cells already have altered metabolic activity and a lot of DNA damage. With specific metabolic or DNA repair inhibitors we force the cancer cell into a trap where they cannot cope with the overload of DNA damage, without harming healthy cells with normal metabolic pathways.

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