Fig. 6From: Centromeric cohesion failure invokes a conserved choreography of chromosomal mis-segregations in pancreatic neuroendocrine tumorProposed molecular progression mechanism for pancreatic neuroendocrine tumors. Normal islet cells acquire a mutation in MEN1, and ATRX or DAXX which leads to perturbed deposition of H3 histone variants H3.3 and CENP-A at nucleosomes in centromeric sites. This results in premature sister chromatid separation and loss of one allele, followed by a series of genome duplicationsBack to article page