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Cancer therapies: Approach to switching off tumor development discovered

Cancer therapies: Approach to switching off tumor development discovered


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Molecular switch to destroy cancer cells identified?
In a recent study, scientists from the Albert Ludwigs University in Freiburg im Breisgau have shown how a protein prevents the uncontrolled spread of immune cells. This opens up new approaches for the treatment of various cancers, such as acute lymphoblastic leukemia (B-ALL), the most common type of tumor in children.

In their study, the researchers led by Professor Dr. Michael Reth from the Albert-Ludwigs-Universität Freiburg demonstrate how a certain protein influences the development of so-called B-lymphocytes and thus prevents the development of tumor cells. The researchers published their results in the renowned journal "Nature Immunology".

Immune cells become mature lymphocytes
The scientists explain that the human immune system consists of millions of individual cells that are produced in the bone marrow from precursor cells every day. The immune cells expand in the course of their development and differentiate into mature lymphocytes. These immune cells can recognize and remove foreign substances. Such alternating phases between multiplication and differentiation can also be seen in the maturation of the B lymphocytes, which are able to produce antibodies, the scientists explain.

Two component switch
In their current studies, the researchers examined how the “switch” that controls the change between the two phases in B lymphocytes works. "By controlling the switch between the two phases, the switch limits the expansion phase of the precursor cells, the so-called pre-B cells," the scientists report in a press release from the University of Freiburg. If these pre-B cells proliferate indefinitely, this could lead to pre-B cell leukemia. Professor Reth and colleagues have now been able to demonstrate that the switch consists of a complex with two components - the adapter protein B-cell translocation gene 2 (BTG2) and the protein arginine methyltransferase1 (PRMT1).

Tumor cell proliferation stopped
BTG2 is normally up-regulated in differentiating progenitor cells, explains Dr. Elmar Dolezal, first author of the study. If the production of BTG2 was triggered in pre-B cells, their multiplication stopped immediately. The co-author Dr. David Medgyesi explains how the BTG2 / PRMT1 complex brings the expansion of pre-B cells to a standstill: "After it binds BTG2, PRMT1 methylates the protein CDK4 and thereby prevents its function in the cell cycle and the further multiplication of the cells," reports the Expert.

BTG2 gene turned off in many tumor cells
Interestingly, according to the researchers, the loss or immobilization of the BTG2 gene can be found in many tumor cells. For example, this can hardly be found in tumors of B-cell acute lymphoblastic leukemia (B-ALL), which is the most common type of tumor in children. In the mouse model, the scientists were able to show that the reintroduction of BTG2 into such B-ALL tumor cells prevents further tumor development, which gives hope for new treatment options.

Hope for new treatment options
According to the researchers, they "discovered how BTG2 works as a tumor suppressor in pre-B cells", which leads to "better understanding and possibly better treatment of B-ALL tumor disease". In the future it will be important "to find out the exact expression and regulatory mechanisms of the BTG2 gene and to find ways of introducing BTG2 into patients in B-cell tumors and thus blocking the expansion of the tumor cells," emphasizes Professor Michael Reth. (fp)

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