Genetic differences in endocrine pancreatic tumor subtypes detected by comparative genomic hybridization.

摘要: The molecular pathogenesis as well histogenesis of endocrine pancreatic tumors (EPTs) is not understood, and the clinical behavior EPTs difficult to predict using current morphological criteria. Thus, more accurate markers risk better understanding tumor initiation progression are needed allow a precise classification EPTs. We have studied 44 benign malignant by comparative genomic hybridization correlate overall number genetic alterations with histopathological parameters identify chromosomal regions which might harbor genes involved in EPT progression. Aberrations were found 36 EPTs, losses (mean, 5.3) slightly frequent than gains 4.6). most Y (45% male EPTs), 6q (39%), 11q (36%), 3p, 3q, 11p (each 30%), 6p (27%), 10q Xq 25%), whereas common included 7q (43%), 17q (41%), 5q 14q 32%), 7p, 9q, 17p, 20q 27%), 12q Xp 25%). A correlation was between total changes per both size disease stage. In particular, 3p 6 be associated metastatic disease. Furthermore, characteristic patterns various subtypes, eg, loss insulinomas, indicating that these groups evolve along genetically different pathways. highlighted aberrations, including newly involvement sex chromosome alterations, should stimulate further analysis regions, may lead discovery novel important tumorigenesis evolution