Tumori 2000, 86: 465–469.PubMed 24. Grothey A: Oxaliplatin-safety profile: Neurotoxicity. Oncol 2003, 30: 5–13. 25. Tournigrand C, Cervantes A, Figer A, Lledo G, Flesch M, Buyse M, Mineuer L, Calola E, Etienne PL, Rivera F, Chirivella I, Perez-Staub N, Louvet C, André T, Taban-Fisch I, de Gramont A: OPTIMOX 1: a randomized study of FOLFOX4 or FOLFOX7 with Oxaliplatin in a stop-and-go fashion in advanced colorectal cancer-a GERCOR study. J Clin Oncol 2006, 24: 394–400.CrossRef 26. Figer A, Perez-Staub Neratinib N, Carola E, Tournigrand C, Lledo G, Flesch

M, Barcelo R, Cervantes A, André T, Colin P, Louvet C, de Gramont A: FOLFOX in patients aged between 76 and 80 years with metastatic colorectal cancer: an exploratory cohort of the OPTIMOX 1 study. Cancer 2007, 110: 2666–2671.CrossRefPubMed Competing Vemurafenib order interests The authors declare that they have no competing interests. Authors’ contributions AK, KK, HY, and MI conceived and designed the study, SS, AK, KK, HY, and HT collected and assembled the data, SS performed the statistical analysis, and SS wrote the manuscript. All authors have read and approved the final manuscript.”
“Background In the homeobox gene family, the caudal-related CDX2 gene encodes

for an intestine-specific transcription factor involved in both cell turnover and intestinal differentiation [1]. Nuclear immunostain for Cdx2 is restricted to the native intestinal epithelia and its de novo expression is considered as suitable marker of a newly achieved intestinal commitment [2, 3]. Barrett’s esophagus (BE) is defined as replacement of the native esophageal squamous epithelium by columnar (intestinalized) mucosa [4–6]. Longstanding exposure of the squamous esophageal epithelium

learn more to gastric reflux is a primary risk factor for columnar metaplasia, which is consistently considered as precursor of esophageal adenocarcinoma (Ac) [7, 8]. Esophageal Ac is the final step in a sequence of phenotypic changes that include long-standing esophagitis, columnar cell metaplasia, and non-invasive neoplasia (NiN). The molecular derangements occurring in each of these phenotypic changes are largely unknown and they involve both genetic and chromosomal instability [9, 10]. More information on such molecular changes is crucial in any strategy of primary prevention of Barrett’s Ac [11–14]. In humans, both practical and ethical limitations prevent any sequential exploration of the cascade of Barrett’s Ac, so experimental models are used to characterize the biological alterations leading to neoplastic transformation [15–31]. In this experimental study, the expression of Cdx2 protein was tested over the whole spectrum of phenotypic lesions detected in a surgical murine model of esophago-gastroduodenal anastomosis (EGDA) resulting in longstanding esophageal reflux of gastro-duodenal contents [19, 21–24, 29].