MEN1 Missense Mutations Impair Sensitization to Apoptosis Induced by Wild-Type Menin in Endocrine Pancreatic Tumor Cells

Taking advantage of a new endocrine cellular model, we show a loss of function for 2 missense disease-related menin mutants and for a controversial variant as well. Furthermore, our results suggest the existence of functional interactions between p53 and menin for the control of apoptosis, which may cast new light on the mechanisms of endocrine tumorigenesis.