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A cellular model provides insights into the pathogenicity of the oncogenic FOXL2 somatic variant p.Cys134Trp.

Laetitia HermanAngélique AmoBerangère LegoisCaterina Di CarloReiner A VeitiaAnne Laure Todeschini
Published in: British journal of cancer (2024)
Our work, aiming at better understanding the GOF scenario, shows that the dysregulated genes and pathways are consistent with this idea. Besides, we propose that GOF might result from an enhanced interaction with SMAD3 that could underlie an ectopic capacity of mutated FOXL2 to bind SMAD4.
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