Surgical Symposia during the 14th UEGW, Berlin, Germany, 2006

markers are found, such as CA 19-9, DUPAN-2, SPan1, and CEA. In parallel with other tumours, it was recently discovered that also the invasive pancreatic ductal adenocarcinoma is most probably the result of a stepwise tumour progression from early dysplastic lesions to invasive carcinoma. Five years ago, a panel of specialized pathologists proposed a classification of precursor lesions of ductal adenocarcinoma [1] . The so-called PanIN classification includes four types of PanIN lesions: PanIN 1A, PanIN 1B, PanIN 2 and PanIN 3, which represent different degrees of structural dysplasia and cytological atypia finally leading to invasive ductal adenocarcinoma. Genetically, ductal adenocarcinoma shows both activation of oncogenes and inactivation of tumour suppressor genes. The well-known players were discussed which are mutated in pancreatic carcinogenesis: K-ras oncogene (80%), CDKN2A/p16 (60%), TP53/p53 (50%), SMAD4/DPC4 (50%) and telomerase activity (95%). Recently it was shown that the stepwise morphological changes in the precursor lesions are associated with these genetic alterations [2] . Several studies revealed that the rising incidence of loss of heterozygosity for p16, p53 and DPC4 is associated with an increasing PanIN grade. On the other hand mutated K-ras and telomerase activity, which are already seen in PanIN 1 lesions, represent most probably very early genetic events. Light will be shed on the time frame during which invasive ductal adenocarcinoma develops and answers will become available concerning the implications of the PanIN lesions for the patients’ prognosis. Helmut Friess discussed the impact of genomics on the management of patients with pancreatic cancer. He underlined that we still need to better understand the biology of pancreatic cancer and to find the mechanisms which make this tumour so aggressive. The clinical problems of local aggressiveness, early invasion and infiltration, early formation of distant metastasis and resistance to neoadjuvant treatment have to be solved. The molecular findings in the last 15 years were reviewed [3] . It was shown that by activation of growth factors and their receptors, the local tumour growth of pancreatic cancer is significantly stimulated. Furthermore, the deregulation of growth inhibitory mechanisms leads to a further increase of tumour growth. Moreover, other Pancreatic Cancer