Protein acts as a switch for leukemia

AML switch discovered: protein responsible for leukemia

12.07.2011

Researchers at the Hannover Medical School (MHH) have discovered a kind of switch that significantly influences the development of leukemia (blood cancer). The research group led by Michael Heuser of the MHH was able to identify a specific protein as an important factor influencing the development of acute myeloid leukemia (AML). By eliminating the corresponding protein, the therapeutic procedures could be significantly improved in the future, the researchers hope.

The acute myeloid leukemia (AML), a particularly severe form of blood cancer, is mainly due to a specific protein, which acts as an artefact switch for AML, report Michael Heuser and his colleagues from the MHH in the current issue of the journal „Cancer Cell“. The researchers discovered the protein as part of their current study in the study of the blood production process of mice. Now, scientists hope to derive therapeutic procedures that enable efficient treatment or prevention of AML.

Development of leukemia in the blood production process
As part of their research work, the MHH scientists have taken a closer look at the blood production process in the laboratory. In the petri dish Michael Heuser and colleagues observed how the cells of mice developed on the way to the mature blood cell. The cells generally go through several stages until they finally take over as a mature blood cell numerous functions in the body. Stem cells become immature progenitor cells, later mature precursor cells and finally the mature blood cells. In their laboratory investigations, the researchers used mouse cells that had used a gene (MN1 gene) that can trigger the particularly aggressive acute myeloid leukemia. While observing cell development, Michael Heuser and colleagues found that only immature progenitor cells developed leukemia, whereas mature progenitor cells and mature blood cells did not tend to develop blood cancer.

Protein determines the development of leukemia cells
The fact that only the immature progenitor cells developed a leukemia, according to the MHH researchers due to a specific protein (MEIS1), which is present only in those in these cells, but is absent in the other blood stages. When the corresponding protein was used in conjunction with the leukemia-causing MN1 gene in mature progenitor cells, they also developed into leukemia cells, Michael Heuser and colleagues explained. This suggests the suspicion that „MEIS1 as a kind of switch“ acts, „It determines whether leukemia develops or not“, Heuser explained. This assumption has also been confirmed when the researchers in existing leukemic cells of mice MEIS1 switched off, write the doctors. Without MEIS1 „the cells could no longer cause leukemia in the mice“, emphasized Heuser. The results of the MHH scientists sound promising, because „the elimination of MEIS1“ could, according to Heuser „an effective therapy for many patients with different forms of leukemia“ his. As another research goal, the scientists proclaimed the search for suitable drugs to turn off or block the switches like MEIS1.

Increased chance of survival through improved therapeutic procedures
According to information from the Society of the German Epidemiological Cancer Registry (GEKID), about 10,000 people suffer from the various types of leukemia every year, and the therapeutic improvements promised by the MHH researchers could be a real ray of hope. If similar techniques are also applied to other forms of blood cancer such as acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML), the overall risk of fatal disease could be significantly reduced. According to GEKID, the relative survival rate for men is 46 percent for men and 44 percent for women after five years. Thus, approximately half of leukemia patients die within five years from the consequences of the disease. An improvement in therapeutic measures could also contribute to a significantly higher chance of survival here. (Fp)

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Picture: Johannes Höntsch