Bart Vanhaesebroeck

This study identifies that epithelial stem cell fate, not DNA damage, determines chemoradiotherapy response in rectal cancer by analyzing patient-derived organoids and using SPARTA to validate findings.

This study shows that PTEN's protein phosphatase activity is essential for embryonic development and tumor suppression in mice, as demonstrated by mutant mice with impaired protein phosphatase activity.

This study shows that a specific PTEN mutation causes macrocephaly, lymphoid overgrowth, and late-onset cancer in mice by impairing nuclear PTEN functions, while maintaining normal PI3K/AKT signaling.

This study shows PI3Kδ is critical for dendritic cell function in intestinal immunity by linking microbial sensing to antigen presentation and T-cell activation.

This study shows that PIK3CAH1047R mutation causes clonal expansion in capillary and venous endothelial cells but not in arterial cells, revealing stage-dependent responses and a protective mechanism against arterial damage.

This study shows that VPS34 deficiency in regulatory T cells causes a fatal lymphoproliferative disorder by impairing metabolic and functional processes, despite normal development and in vitro suppression.

The paper characterizes the transcriptional dynamics of the mouse Anterior Visceral Enderm (AVE) during migration and identifies Ephrin- and Semaphorin-signalling as critical for its movement.

The paper uses single-cell analyses to show that oncogenic PIK3CAH1047R reduces IGF1 signaling specificity and enhances EGF responses, leading to increased phenotypic heterogeneity.