Background The incidence of right-sided colon cancers has been increasing in recent years. It is unclear whether patient prognosis varies by tumor location. In this study, we have compared the survival of right-and left-sided colon cancers in a longitudinal population-based database. Methods A retrospective survival analysis was performed using the Surveillance, Epidemiology, and End Results Program (SEER) database between 1988 and 2003 on subjects who underwent surgical resection for the a primary diagnosis of pathologically confirmed invasive colon adenocarcinoma. Cox proportional hazard regression analysis was used to assess long-term survival outcomes comparing right-sided (cecum to transverse colon, excluding appendix) versus left-sided (splenic flexure to sigmoid, excluding rectum) colon cancers. Results A total of 77,978 subjects were identified with adenocarcinoma of the colon. Overall median survival was 83 months. Median survival for right-sided cancers was 78 vs. 89 months for left-sided cancers (P<.001). By Cox proportional hazard regression analysis, controlling for statistically significant confounders, including age, sex, race, marital status, tumor stage, tumor size, histologic grade, number of lymph nodes examined, and year of diagnosis, right-sided colon cancers were associated with a 5% increased mortality risk compared with left-sided colon cancers (hazard ratio, 1.04; 95% confidence interval, 1.02–1.07). These findings were consistent across subsets of subjects. Conclusion On the basis of analysis of information from the SEER database, we found that right-sided colon cancers have a worse prognosis than left-sided colon cancers. The reason for this remains unclear but may be due to biological and/or environmental factors and may have particular bearing, given the rising incidence of right-sided colon cancers.

Pancreatic ductal adenocarcinoma (PDAC) is believed to arise through a multistep model comprised of putative precursor lesions known as pancreatic intraepithelial neoplasia (PanIN). Recent genetically engineered mouse models of PDAC demonstrate a comparable morphologic spectrum of murine PanIN (mPanIN) lesions. The histogenesis of PanIN and PDAC in both mice and men remains controversial. The most faithful genetic models activate an oncogenic Kras G12D knockin allele within the pdx1-or ptf1a/p48-expression domain of the entire pancreatic anlage during development, thus obscuring the putative cell(s)-of-origin from which subsequent mPanIN lesions arise. In our study, activation of this knockin Kras G12D allele in the Elastase-and Mist1-expressing mature acinar compartment of adult mice resulted in the spontaneous induction of mPanIN lesions of all histological grades, although invasive carcinomas per se were not seen. We observed no requirement for concomitant chronic exocrine injury in the induction of mPanIN lesions from the mature acinar cell compartment. The acinar cell derivation of the mPanINs was established through lineage tracing in reporter mice, and by microdissection of lesional tissue demonstrating Cre-mediated recombination events. In contrast to the uniformly penetrant mPanIN phenotype observed following developmental activation of Kras G12D in the Pdx1-expressing progenitor cells, the Pdx1-expressing population in the mature pancreas (predominantly islet ␤ cells) appears to be relatively resistant to the effects of oncogenic Kras. We conclude that in the appropriate genetic context, the differentiated acinar cell compartment in adult mice retains its susceptibility for spontaneous transformation into mPanIN lesions, a finding with potential relevance vis-à -vis the origins of PDAC.lineage tracing ͉ transdifferentiation ͉ precursor lesions ͉ pancreatic cancer

Intraoperative hypotension, but not hypertension, is associated with increased 30-day operative mortality.