To date, the mutational status of EGFR and PTEN has been shown as relevant for favoring pro- or anti-tumor functions of STAT3 in human glioblastoma multiform (GBM).

Researchers at GIGA and CHU have screened genomic data from 154 patients and have identified a strong positive correlation between STAT3 and HDAC7 expression. In addition they have shown the existence of a subpopulation of patients overexpressing HDAC7 and STAT3 that has particularly poor clinical outcome.

Using in vitro and in vivo models, they demonstrated for the first time that silencing HDAC7 can reset the tumor suppressor activity of STAT3, independently of the EGFR/PTEN/TP53 background of the GBM.

This effect could help to overcome tumor heterogeneity and could subsequently provide a new rationale for the development of specific HDAC7 inhibitors in a clinical setting.

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