UNASSIGNED: @entity10206 and or @entity8171 loss occur in 40% of pancreatic @entity8703 (PanNETs). PanNETs negative for @entity10206 or @entity8171 show an increased risk of relapse. The @entity5 -associated pathways activated upon @entity10206 or @entity8171 loss and how this event may induce @entity1344 ( @entity1344 ) and @entity10205 ( @entity10205 ) are still unknown. Both @entity10206 and @entity8171 are involved in DNA methylation regulation. DNA methylation of heterochromatin and of non-coding sequences is extremely important for the maintenance of genomic stability. We analysed the association of @entity10206 and or @entity8171 loss and @entity1344 with global DNA methylation in @entity1 PanNET samples and the effect of @entity10206 knock down on methylation and cell proliferation. We assessed LINE1 as well as global DNA methylation in 167 PanNETs and we found that @entity10206 and or @entity8171 negative @entity5 and @entity5 with @entity1344 were hypo-methylated. @entity10206 knock-down in PanNET cell lines blocked cells in G1/G0 phase and seemed to increase @entity1344 in QGP-1 cells. However, no direct changes in DNA methylation were observed after @entity10206 knock down in vitro. In conclusion our data indicate that epigenetic changes are crucial steps in the progression of @entity788 and suggest that DNA methylation is the mechanism via which @entity1344 is induced, allowing clonal expansion and selection.

Hypo-methylation mediates @entity1344 in XXXX .

@entity1 :: ('9606', 'Species') :: ['human'] @entity10205 :: ('MESH:C536801', 'Disease') :: ['alternative lengthening telomeres', 'ALT'] @entity788 :: ('MESH:D010190', 'Disease') :: ['PanNETs loss'] @entity8171 :: ('546', 'Gene') :: ['ATRX'] @entity8703 :: ('MESH:D004701', 'Disease') :: ['neuro-endocrine tumors'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'tumors'] @entity1344 :: ('MESH:D043171', 'Disease') :: ['chromosomal instability', 'CIN'] @entity10206 :: ('1616', 'Gene') :: ['DAXX']
@entity788 :: (MESH:D010190,Disease) :: ['pancreatic NET']
