7%, 1-year survival 29.2%, no severe toxicity) [40]. The effect of sunitinib as second-line treatment in patients with GC has been assessed in a German phase II trial [41]. The overall response rate was 3.9% with a PFS of 1.28 months, an OS of 5.81 months, and a 1-year survival rate of 23.7%. These results do not support the application of sunitinib in this setting. Efforts are made to use the rapidly developing biostatistical approaches of gene-coexpression network profiling for the

identification of novel target genes or promising candidate compounds for the treatment of advanced GC [42]. Several studies have suggested that chronic infection with H. pylori may moderately increase the risk for colorectal cancer [43-45]. The background for this hypothesis is that infection with H. pylori leads to an increase of plasma gastrin levels. Hypergastrinemia stimulates mucosal cell proliferation. Chronic H. pylori PLX3397 molecular weight Silmitasertib manufacturer infection results in gastric atrophy, cell

mutation, and transformation of gastric mucosal cells into gastrin-producing cells, which also express gastrin receptors serving to stimulate cell proliferation and tumor growth [46-48]. Two meta-analysis reported that there is a modest increase in the risk of colorectal cancer owing to H. pylori infection [49, 50]. However, the studies had several weaknesses as thus included a small sample size of studies with high heterogeneity and made note or confounding controls. Recently, a large population-based case control study was conducted in Germany to investigate the association between H. pylori and colorectal cancer [51]. Serum anti-H. pylori antibodies and anti-CagA antibodies were measured in 1712 patients with colorectal cancer and 1669 controls. There was a high 上海皓元 H. pylori seroprevalence in the study population (mean age 69 years) with more than 40% in both arms. Overall, H. pylori infection

was more prevalent in colorectal cancer cases (46.1%) than in controls (40.1%). The authors performed a stratified analysis which showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio (OR) of 1.22 (95% CI: 1.02–1.45). The results of this large population-based study suggest that H. pylori infection may be associated with an increased risk for the selected group after the neoplasia of the left colorectum. Colorectal cancer development is based on the adenoma-carcinoma sequence. Thus, a study investigated correlation between H. pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma [52]. In this study, H. pylori infection was a risk factor for adenoma as a whole. The analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection when chronic atrophic gastritis was present. In a large cross-sectional study from Korea, 2195 eligible subjects undergoing screening colonoscopy have been evaluated for the prevalence of H.