Is genomic instability at both the base pair level and the chromosomal level detectable in earliest PanIN lesions in tissues of chronic pancreatitis?
Heterozygous mutations of p53- and p16 genes together with chromosomal instability occur early in CP and are clonally expanded, but final inactivation mostly by LOH happens later in pancreatic carcinogenesis. Determination of aneuploidy in pancreatic juice may be of value for early detection and risk assessment in patients with long-standing CP.
High levels of serum CRP and CEA, and N2 disease are independent prognostic indicators for the survival of patients with stage III-IV NSCLC.