# Josep Carreras Institute: BAF mutations let CTCF reshape DNA folding in B-cell lymphoma models

- Published: 2026-11-13 15:50 UTC
- Section: Life & Health › Medicine
- Tags: B-cell lymphoma, BAF complex mutations, CTCF protein, 3D DNA organisation, cBAF, chromatin architecture, Josep Carreras Institute, Weill Cornell Medicine, cell proliferation, lymphoma targets
- URL: https://realtech.media/news/rt-59e9d73dc237192c52c891f5_josep_carreras_institute/

**Researchers in Spain and the US showed in cell models how loss of cBAF function changes 3D DNA organisation and promotes proliferation. CTCF is a candidate target, but work is experimental.**

![Josep Carreras Institute: BAF mutations let CTCF reshape DNA folding in B-cell lymphoma models](https://realtech.media/media/2026/11/b9a044d2439555db.jpg)
*Ajay Kumar Chaurasiya, Wikimedia Commons, CC BY-SA 4.0*

An international team led by Ari Melnick, Director of the Josep Carreras Leukaemia Research Institute (Spain), and Darko Barisic of Weill Cornell Medicine (US) has described how mutations in the BAF complex alter the three-dimensional organisation of DNA in cells. According to the study published in Nature, the changes shift gene activity in ways that can favour B-cell lymphomas, cancers of B lymphocytes, as reported by EurekAlert. [1]

Mutations affecting BAF, a group of proteins that helps control gene activity, occur in many types of cancer, including B-cell lymphomas. How they contribute to cancer had not been fully understood. [1]

## How loss of cBAF changes DNA folding

Inside the nucleus, DNA is folded into a three-dimensional structure that helps determine which genes are active. BAF controls access to different DNA regions. [1]

The authors found that when a particular form of the complex, cBAF, loses function, the DNA-organising protein CTCF binds to regions it could not reach before. This changes DNA folding, disrupts some interactions that normally regulate genes and, in experimental models, was associated with increased cell proliferation. [1]

The result was unexpected. BAF is generally known for making DNA more accessible, but at sites recognised by CTCF its disruption made these regions more accessible rather than less. Melnick said the findings reveal a paradigm for how gene control is coordinated and balanced by different BAF complexes through tight control of 3D genome organisation. [1]

## CTCF as a candidate target

In experimental models, disrupting CTCF or another related protein complex reversed changes associated with the loss of cBAF function. The team also reported an association between certain CTCF alterations and better patient outcomes. [1]

Barisic said the findings establish a unifying mechanism for one of the most common classes of cancer mutations and identify CTCF and its partner proteins as candidate therapeutic targets. The findings remain at an experimental stage, and further research is needed to establish whether targeting this mechanism could lead to effective therapies. [1]

Although the work focused mainly on B-cell lymphomas, the team observed similar changes in other cell types, which suggests the mechanism may be relevant to other cancers. [1]

The study was supervised by Melnick and Barisic, with Cem Meydan of Weill Cornell Medicine as co-corresponding author. The first authors were Sonia Debek, Cem Meydan and Christopher R. Chin. Researchers from Memorial Sloan Kettering Cancer Center and The Rockefeller University also contributed. The paper is titled "SWI/SNF complexes shape 3D chromatin architecture through CTCF and cohesin." [1]

## Sources

1. [EurekAlert](https://www.eurekalert.org/news-releases/1151626)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-59e9d73dc237192c52c891f5_josep_carreras_institute/