The pathogenesis of @entity788 ( @entity788 ) is poorly understood. To gain insight into the genetic mechanisms underlying this @entity5 entity, we performed genome-wide screening of 16 surgical specimens from 15 @entity1 with sporadic PNEN, combining G-band karyotyping and high resolution comparative genomic hybridization (HR-CGH). G-banding revealed abnormal karyotypes in 2 of 10 @entity5 samples analyzed. DNA copy number changes were detected in 13 samples, whereas three @entity5 showed a balanced genome. Gains were more frequent than losses in the nonfunctioning @entity5 (n=13). Common gains were scored at 5p12-13, 4q13-24, 5p15, 5q11-31, and 9q21-22. Common losses were scored at 11p11, 11p14-15, 11q23, 11p12-13, and 11q22. The average number of copy aberrations (ANCA index) was 12 for 13 nonfunctioning @entity5 , 4.8 for the nonfunctioning @entity5 with low Ki-67 (>= 5%), 21.2 for the @entity5 with high Ki-67 (<5%), 2.5 for small @entity5 (<3.5 cm), and 17.8 for large @entity5 (>= 3.5 cm). There was a statistically significant difference in the ANCA index between the groups defined by Ki-67 and @entity5 size. @entity5 with low Ki-67, no distant @entity3 and small size had few aberrations detected by HR-CGH, but frequent loss of material from chromosomal band 11p11. The present study indicates the existence of distinct cytogenetic patterns in sporadic nonfunctioning PNEN. Loss of chromosomal band 11p11 might indicate a primary pathogenetic event in these @entity5 .

Loss of 11p11 is a frequent and early event in sporadic nonfunctioning XXXX .

@entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'primary tumors', 'Nonfunctioning tumors', 'tumors'] @entity1 :: ('9606', 'Species') :: ['patients'] @entity788 :: ('MESH:D010190', 'Disease') :: ['sporadic pancreatic neuroendocrine neoplasms', 'PNENs'] @entity3 :: ('MESH:D009362', 'Disease') :: ['metastasis']
@entity788 :: (MESH:D010190,Disease) :: ['pancreatic neuroendocrine neoplasms']
