DNA adducts in human pancreatic tissues and their potential role in carcinogenesis

摘要: Pancreas cancer is the fourth and fifth leading cause of death for men women, respectively, in United States. Although etiology this poorly understood, smoking dietary fat have been implicated by epidemiological studies. To test hypothesis that DNA damage derived from carcinogen exposure diet involved pancreatic carcinogenesis, aromatic lipid peroxidation-related adducts 13 normal tissues adjacent to tumor 20 tumors patients were analyzed 32P-postlabeling. Normal 5 nonpancreatic 19 healthy organ donors served as controls. correlate adduct level with patients' characteristics, information on age, sex, body mass index, status collected medical records. A significantly higher total was detected compared The mean adducts/10(8) nucleotides (A tissues) 102 +/- 21 39 6 1 (T controls (C tissues), respectively. Among observed, one single (spot 1) present 100, 90, 0% A, T, C tissues, Two novel clusters (spots 2 3) observed 11 13, 12 20, 24 presence these positively correlated status. In addition, previously defined smoking-related diagonal radioactive zone three samples only, although 50% (10 20) cancers study ever smokers. Putative all examined than T samples. Multiple regression analyses showed index levels spot tumors. Smoking also adducts. These observations are consistent previous findings support related peroxidation human carcinogenesis.