Cancer Chemother Pharmacol 2006, 58: 776–784.PubMedCrossRef 30. Comerford KM, Wallace TJ, Karhausen J, Louis NA, Montalto MC, Colgan SP: Hypoxia-inducible factor-1-dependent regulation of the multidrug resistance (MDR1) gene. Cancer Res 2002, 62: 3387–3394.PubMed 31. Thottassery JV, Zambetti GP, Arimori K, Schuetz EG, Schuetz JD: p53-dependent regulation of MDR1 gene expression causes

selective resistance to chemotherapeutic agents. Proc Natl Acad Sci USA 1997, 94: 11037–11042.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions ZJ and HL conceived of the study, and participated in its design and coordination and helped to draft the manuscript. YH, XQ and XC carried out the molecular AZD6244 supplier genetic studies. ZL and DF participated in its design and coordination. BM and QF participated in the conception

and the design of the analysis. All authors read and approved the final manuscript.”
“Background Oesophageal cancer remains an important public health concern worldwide with an estimated burden of 500, 000 new cases in 2005 [1]. The two major histological types of oesophageal cancers, squamous cell carcinoma (SCC) and adenocarcinoma (ADC) differ substantially in their underlying patterns of incidence and key etiologic factors. Alcoholism and smoking are the major established risk factors for SCC, whereas Barrett’s oesophagus or gastro-oesophageal JNJ-64619178 research buy reflux disease (GORD) are consistently associated with an increased risk of ADC. Oxidative stress and reactive oxygen species (ROS) are thought to play a role in oesophageal carcinogenesis. ROS may result from external factors such as smoking, and alcohol

metabolism, or may be produced endogenously via inflammatory conditions such as oesophagitis or GORD or may also be due to precancerous lesions (Barrett’s oesophagus), as has been shown experimentally Bumetanide in rats [2, 3]. Diet influences incidence of oesophageal cancers. An adequate diet of fruits and vegetables is associated with a decreased incidence [4], presumably due to a better supply of antioxidants. Among the various markers of oxidative stress, 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) is particularly popular. It is generated by the oxidation of DNA under physiopathological conditions or environmental stress, but is also a by-product of normal cellular metabolism. It is a premutagenic oxidized-DNA lesion as it is able to mispair with adenine, thus generating G:C to T:A Avapritinib datasheet transversion mutations, unless the lesion is repaired prior to DNA replication [5]. Moreover, affordable analytical methods are available for its quantification.