RESUMO
Despite evidence of an increased prevalence of irritable bowel syndrome (IBS) in adults with inflammatory bowel disease (IBD) compared with the general population, the prevalence of IBS in children with IBD is unclear. In this review, we aimed to identify the reported prevalence of IBS or functional abdominal pain disorders (FAPDs) in children with IBD in remission. A search of three databases (MEDLINE, Embase, and PubMed) was performed to identify studies reporting the prevalence of IBS or FAPDs in pediatric patients with IBD in remission. A total of 60 studies were identified, with four eligible studies remaining following abstract screening. In children with IBD in remission, the overall prevalence of IBS ranged between 3.9 and 16.1%, and the overall prevalence of FAPDs ranged between 9.6 and 29.5%. The prevalence of FAPDs in patients in biomarker-based remission was generally higher than those in clinical remission (range 16-22.5% vs 9.6-16.7%, respectively). There is a paucity of literature reporting on the prevalence of IBS or FAPDs in children with IBD in remission. Despite the differences in criteria used to define IBD remission in the included articles, there seems to be an increased overall prevalence of IBS or FAPDs in children with IBD.
RESUMO
Pancreatic cancer is a leading cause of cancer-related deaths in Western societies. This poor prognosis is due to chemotherapeutic drug resistance and metastatic spread. Evidence suggests that microtubule proteins namely, ß-tubulins are dysregulated in tumor cells and are involved in regulating chemosensitivity. However, the role of ß-tubulins in pancreatic cancer are unknown. We measured the expression of different ß-tubulin isotypes in pancreatic adenocarcinoma tissue and pancreatic cancer cells. Next, we used RNAi to silence ßIII-tubulin expression in pancreatic cancer cells, and measured cell growth in the absence and presence of chemotherapeutic drugs. Finally, we assessed the role of ßIII-tubulin in regulating tumor growth and metastases using an orthotopic pancreatic cancer mouse model. We found that ßIII-tubulin is highly expressed in pancreatic adenocarcinoma tissue and pancreatic cancer cells. Further, we demonstrated that silencing ßIII-tubulin expression reduced pancreatic cancer cell growth and tumorigenic potential in the absence and presence of chemotherapeutic drugs. Finally, we demonstrated that suppression of ßIII-tubulin reduced tumor growth and metastases in vivo. Our novel data demonstrate that ßIII-tubulin is a key player in promoting pancreatic cancer growth and survival, and silencing its expression may be a potential therapeutic strategy to increase the long-term survival of pancreatic cancer patients.