New glimmer discovered in the fight against T cell lymphomas!

New glimmer discovered in the fight against T cell lymphomas!

Wien, Österreich - Vienna - A new study by research teams from the Medical University of Vienna and International Partners has created new knowledge about the role of epigenetic changes in anaplastic large cell lymphomas (ALCL). This aggressive form of T cell lymphoma often affects children and young adults and is known for their poor forecast. The results were published in the journal "Leukemia" and show how the enzyme HDAC1 acts as a potential tumor inhibitor.

lymphomas represent a group of malignant diseases of the immune system that mainly affect the lymphatic system. Among the different types of lymphomas, Alcl plays a particularly aggressive role. In particular, the alk-positive alcl cases, which in 60 to 80 percent of cases have a gene fusion of the ALK gene, urgently need new therapeutic approaches.

epigenetic mechanisms and their meaning

epigenetic changes, such as DNA methylation and chromatin structure changes, are essential factors that contribute to the development of cancer. Current research shows that such abnormalities, especially in regulators of DNA methylation and histone modifiers, shape not only the pathogenesis, but also the pathophysiology of malignant lymphomas. A review has revealed that epigenomic abnormalities can strengthen malignant clones and that hematology is a pioneer in the research of disease epigenetics.

In the specific examination, the HDAC inhibitor Entinostat was tested in the mouse model. The results indicate that the blockade of HDAC activity not only delayed the development of lymphomas, but was even able to prevent in some cases. This could open new therapeutic possibilities in the fight against Alcl, especially for patients who are resistant to former therapies.

mechanisms of alk-positive alcl

The alk gene is a strong, driving oncogen, whose reapered form, the NPM :: Alk fusion protein, occurs in the majority of the cases of alk-positive alcl. This gene fusion not only affects the DNA repair mechanisms, but also influences cellular metabolism and immune response. NPM :: ALK regulates various signal paths and thus forges the survival of tumor cells by both promoting cell proliferation and inhibits apoptosis. It also induces epigenetic deregulations that mute genes and thus contribute to tumor development.

The genetic switching off of HDAC1 into T cells has accelerated the tumor development in the mouse models, which indicates a protective role of this enzyme. A changed packaging of the genetic engineer and a changed genetic activity in the T cells reinforce signaling paths that promote lymphoma development. These findings are crucial for the future therapeutic orientation in dealing with alcl.