1 May 2018

DFF research project 1 grants to Kristian Helin and to Kim Bak Jensen


DanStem Professor Kristian Helin and affiliated Associate Professor Kim Bak Jensen obtained the Independent Research Fund Denmark (DFF) grants, respectively.

Kim Bak Jensen granted project: Exploiting new treatment opportunities for patients with inflammatory bowel disease

Inflammatory bowel disease covers a number of diseases, including ulcerative colitis and Crohn's disease, in which patients suffer from chronic intestinal inflammation and wounds that do not heal normally. These wounds can cause major abdominal pain, bleeding diarrhea and an increased risk of developing colon cancer. Currently, there are limited options for curing the disease, and the symptoms are most often treated with steroids and drugs that reduce inflammation. If this does not help, parts of the intestinal tract will be removed operatively. The intestinal surface is coated with a layer of epithelial cells which are responsible for absorption of protein and sugars.These cells also form a protective skin against the many bacteria present in the intestine. Therefore, if the skin is damaged it is important that it is quickly repaired to reduce the spread of bacteria to the rest of the body. This spread is a contributing factor to the chronic inflammatory condition of the intestine. If treatment can kickstart repair of the protective skin, bacterial access to the rest of the body will be reduced, allowing the body to fight the chronic inflammatory condition. In this project scientists led by Kim Jensen will develop methods for kickstart repair of the intestine. This knowledge will be used to establish new complementary treatment methods for inflammatory bowel disease, to be tested in various experimental models of colitis

Kristian Helin granted project: Understanding the role of TET2 in normal hematopoiesis and how its loss of function can lead to AML

Acute myeloid leukemia (AML) is a cancerous disease in the blood-forming cells of the bone marrow. The disease causes the normal blood-producing cells of the bone marrow to be displaced and replaced by leukemia cells. This is often a fatal disease.AML patients are treated with high-dose chemotherapy, depending on the subtype and age, including bone marrow transplantation. The 5-year survival rate for AML patients is approximately 25% and has not increased for many years. Therefore, increased efforts are required to improve the treatment of AML patients, which requires better understanding of why the disease develops, in order to develop new therapies. The gene encoding the TET2 enzyme is often mutated in AML patients, as well as in other types of blood cancer. TET2 is an enzyme that works by binding to DNA and removing a methyl group, and we know that the loss of TET2 leads to an increase in the cell's DNA methylation, which contributes to cancer development. However, it is still unclear why TET2 is necessary for the growth of normal blood cells and what happens when the cell lacks TET2. To investigate this, the group led by Kristian Helin will use some newly developed methods to map the TET2 enzyme DNA binding in cells, as well as a mouse model where the loss of TET2 causes the development of AML. The results from these studies will subsequently be verified in cell samples from AML patients. Scientists expect that this research will contribute to a better understanding of how the loss of TET2 contributes to cancer development.
Independent Research Fund Denmark funds specific research activities within all scientific areas that are based on the researchers' own initiatives and that improve the quality and internationalisation of Danish research.