New research published in the journal Leukemia suggests that epigenetic alterations play a key role in the development of lymphoma.
These groundbreaking findings offer deeper insight into the complex biological mechanisms that drive lymphoma and may open new pathways for treatment and prevention.
Lymphoma is a cancer affecting the immune system, primarily targeting lymphatic tissues. It is classified into several subtypes, depending on the specific immune cells from which the tumor originates.
One subtype is anaplastic large cell lymphoma (ALCL), a form of non-Hodgkin lymphoma that arises from T cells. Although ALCL progresses slowly, it can behave aggressively and is most commonly diagnosed in children and adolescents.
In this study, researchers focused on the role of histone deacetylases (HDACs) in developing ALCL. Using mouse models, they investigated the effects of entinostat, an HDAC inhibitor currently in clinical trials. Previous studies have shown that pharmacologically blocking HDAC activity can significantly delay or prevent lymphoma onset.
The researchers found that suppressing HDAC1 target gene expression in T cells led to a marked acceleration of tumor growth in mice. They believe these changes may contribute to both the initiation and progression of lymphoma.
Based on these results, the team concluded that epigenetic modifications likely play a critical role in the onset of lymphoma.
They also emphasized the urgent need for new treatment strategies, particularly in light of growing resistance to existing ALCL therapies. They also suggested that HDAC inhibitors could hold promise as future treatment options.
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