Health

Breakthrough Discovery: HDAC1 Enzyme Could Be Key to Stopping Aggressive T-Cell Lymphomas!

2025-05-15

Author: Nur

What Are Lymphomas?

Lymphomas are malignant cancers that attack the immune system, primarily targeting the lymphatic system's organs. Among the various types, Anaplastic large cell lymphoma (ALCL) stands out as a rare, but particularly aggressive form of T-cell lymphoma, predominantly affecting children and young adults.

Groundbreaking Research Collaboration!

A coalition of top-tier research institutions including the Medical University of Vienna, Boston Children's Hospital, and the University of Cambridge, has unveiled critical findings about the role of epigenetic changes in the formation of ALCL. Their groundbreaking study was recently published in the esteemed journal, Leukemia.

The Power of Epigenetics!

Epigenetic changes, such as shifts in DNA methylation and chromatin structure, play a significant role in cancer progression. In fact, mutations in epigenetic factors are among the most prevalent genetic alterations found in tumors. Existing clinical treatments that inhibit epigenetic enzymes show promising results, especially for lymphoma.

Can We Delay Lymphoma Progression?

Under the guidance of Gerda Egger and lead author Maša Zrimšek from the Department of Pathology, the study focused on the effects of histone deacetylases (HDACs) on ALCL development. These enzymes are crucial in gene regulation and represent a significant target for cutting-edge cancer therapies.

Using a mouse model, researchers tested the effects of entinostat, an HDAC inhibitor currently in clinical trials. The results were promising: blocking HDAC activity notably slowed lymphoma progression and, in some cases, completely stopped it. Encouragingly, entinostat also proved effective against lymphoma cells from patients who had resisted previous treatments.

Unexpected Discoveries!

In a surprising twist, the targeted silencing of HDAC1 in T cells actually sped up tumor growth in the mouse model. This finding hints at a previously overlooked protective role of HDAC1 during specific disease stages.

Molecular analysis indicated that HDAC1 loss drastically alters genetic material packaging and gene activity in T cells, intensifying pathways that may foster lymphoma development.

A Beacon of Hope!

Study leader Gerda Egger noted, "Despite good cure rates for ALK-positive ALCL due to targeted treatments, resistance often emerges. New treatment strategies are urgently needed. Our findings provide hope for the potential use of HDAC inhibitors as viable treatment options in the near future."

A Collaborative Effort!

This groundbreaking research was made possible thanks to collaborative efforts with institutions including MedUni Vienna, the European Institute of Oncology, Boston Children's Hospital, Harvard Medical School, and the University of Cambridge.