Such discrepancies could be explained, at least in part, by the increased sensitivity of the SNP-array vs. iFISH studies in the identification of small interstitial changes . A more detailed analysis of the most SB431542 frequently altered chromosomal regions shows that they contain multiple cancerassociated genes, including several genes which have been specifically related to PDAC. Among others, these latter genes consisted of gained genes such as the PSCA gene, a plausible PDAC tumor marker associated with pancreatic cancer progression , the TNFRSF6B gene which is amplificated in many tumors and whose overexpression blocks growth inhibition signals in PDAC , and the NTSR1 and OGFR genes, involved in cancer progression , modulation of angiogenesis and regulation of cell proliferation . In turn, frequently deleted genes of interest were the RPH3AL gene, a potential tumor suppressor gene related with insulin exocytosis , the SERPINF1 gene which has been detected to be involved in many epithelium derived tumors , and the MAPRE2 gene, previously found to be lost in leukemic cells , pancreatic cancer and esophageal squamous cell carcinoma ; interestingly, deletion of other cancer associated genes which have not been previously associated to pancreatic malignances were found at higher frequencies than other genes shown to be recurrently altered/deleted in PDAC. These results underline the potential role of several previously unexplored tumor suppressor genes in the pathogenesis of PDAC. In turn, genes which have been previously found to be amplified in PDAC patients by SNP-arrays , such as the SACP2 gene, were also altered in our series but at a lower frequency . Such variability could be partially related to the lower number of patients analyzed and the effect of studying paired tumoral/ LY2157299 normal DNA samples in the resolution of the SNP-array for detection of CN alterations. Most interestingly, is the observation that based on the overall genetic profile of PDAC tumors detected by SNP-arrays two well defined groups of PDAC tumors emerge which are differentially characterized by gains of the chromosomal regions and by gains at 1q21.1 with coexisting losses of the chromosomal regions , respectively. From the clinical and histopathologicall point of view, while group 1 PDAC mostly corresponded to smaller well/moderately differentiated grade I/II cases, group 2 mainly consisted of larger and poorly-differentiated PDAC. Among the few well/moderately differentiated carcinomas included in this latter group, 2/3 cases showed intermediate cytogenetic features with coexistence of gains of chromosomes 1q21.1 together with gains of chromosomes 10q, 22q and 11q.