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49(0.29, 0.81)). Further, people with moderately (HR=2.11(1.26, 3.55)) and poorly (HR=4.04(2.03, 8.03)) differentiated tumor grade had a higher short-term hazard of death compared to people with well-differentiated grade. Conclusion Predictive variables of colorectal cancer survival showed different effects in short- and long -terms. Site topography was a prognosis for both long-term and short-term survival; BMI and tumor grade were short-term predictors of survival while stage was a long-term predictor of survival. ©2019 RIGLD.Aim This study aimed to determine the link between Snail1 expression and CRC patients' survival as well as its significant association with EMAST status. Background Snail1 is an evolutionary preserved zinc-finger transcription protein which contributes to Epithelial-to-mesenchymal transition (EMT). EMT initiates invasion and proliferation in many tumors. Elevated microsatellite alteration at selected tetranucleotide repeats (EMAST) is a marker of poor prognosis in patients with colorectal cancer (CRC). We hypothesized that Snail1 overexpression is an important mediator of metastasis and decreased survival in CRCs that characteristically have EMAST phenotype. Methods Quantitative real-time polymerase chain reactions were carried out to analyze the expression levels of Snail1 in both normal and tumor specimens from a total of 122 paraffin-embedded tissues (FFPE) of CRC sample with known EMAST status. The correlation between Snail1 expression and clinicopathological characteristics, survival, and EMAST status were examined. Results Snail1 overexpression was detected in tumor tissues in 32% of all examined patients and its positive expression was related to metastasis (p=0.001) and EMAST+ phenotype (P=0.017). Further, positive Snail1 expression correlates with poor overall survival in CRC patients (P=0.01). Conclusion Our findings suggest that Snail1 overexpression is not only associated with EMAST but also with clinicopathological variables of poor prognosis. These results indicate that Snail1 expression levels may be useful for establishing novel therapeutic strategies and could help survival improvement in CRC patients. [https://www.selleckchem.com/products/vu661013.html VU661013] ©2019 RIGLD.Aim This study aimed to evaluate the distribution of PIK3CA E545K mutation in Iranian CRC patients and explored its roles in disease prognosis. Background Deregulation of the phosphoinositide 3-kinase (PI3K) pathway contributes to the progression of tumors. The p110a (PIK3CA), a catalytic subunit of PIK3, is mutated in many types of cancers. Exon 9 (E545K) is the most frequently mutated hotspot in PIK3CA in colorectal cancer (CRC). However, the prognostic role of PIK3CA E545K mutation needs to be elucidated. Methods Tumors from 187 CRC patients were retrospectively collected from the Taleghani and Shohada Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran, between 2010 and 2017. PIK3CA E545K status was detected in Formalin-fixed paraffin-embedded (FFPE) tissues using PCR-RFLP methods, and validated by pyrosequencing. Correlations between PIK3CA E545K mutation clinicopathological features were analyzed. Results The frequency of PIK3CA E545K gene mutations in CRC patients was 10.7%. Significant correlations were observed in PIK3CA E545K mutation with tumor differentiation and TNM stage (p less then 0.042 and p = 0.033, respectively). Kaplan-Meier analysis showed a worse prognosis in overall survival (OS) in patients with PIK3CA E545K mutation (p less then 0.001). Multivariate analysis indicated that PIK3CA E545K mutation was a detrimental factor for OS (HR = 6.497, 95% CI 2.859-14.768, p less then 0.021). Conclusion A high frequency of PIK3CA E545K mutation was detected in Iranian CRC patients. The results of the present study suggested that PIK3CA E545K mutation may be associated with poor prognosis. These findings require further confirmation via prospective studies with larger samples. ©2019 RIGLD.Colorectal cancer is the third most common cancer worldwide. New cancer treatment strategies such as monoclonal antibodies against growth factor and angiogenesis receptors have improved the overall survival (OS) and progression-free survival (PFS) in metastatic colorectal cancer (mCRC) patients. However, acquired resistance could happen after these therapies. Circulating tumor DNA (ctDNA) is the DNA fraction derived from tumor cells which could be applied as a non-invasive method for detecting tumor mutations before, during, and after therapies. Here, we reviewed most of the studies examining ctDNA as treatment monitoring in mCRC patients who receive different target therapies. Also, we compared ctDNA with other existing cancer-treatment monitoring methods. ©2019 RIGLD.Colorectal cancer is the third most common cancer worldwide. New cancer treatment strategies such as monoclonal antibodies against growth factor and angiogenesis receptors have improved the overall survival (OS) and progression-free survival (PFS) in metastatic colorectal cancer (mCRC) patients. However, acquired resistance could happen after these therapies. Circulating tumor DNA (ctDNA) is the DNA fraction derived from tumor cells which could be applied as a non-invasive method for detecting tumor mutations before, during, and after therapies. Here, we reviewed most of the studies examining ctDNA as treatment monitoring in mCRC patients who receive different target therapies. Also, we compared ctDNA with other existing cancer-treatment monitoring methods. ©2019 RIGLD.Gut microbiota play critical roles in maintaining the human health in several aspects. Bile acids (BAs) are endogenous cholesterol-derived molecules that can be modified by the gut microbiota and act as signaling molecules in the regulation of host metabolic and physiology processes. Gut microbiota release many enzymes that are capable to perform considerable modifications on BAs such as bile salt hydrolases (BSH), 7α-dehydroxylase (CYP7A), and hydroxysteroid dehydrogenase (HSDH). These enzymatic roles can change in the gut microbiota composition, cause alteration in BAs profile and metabolism and even gallstone formation. Patients with 15 years of asymptomatic gallstone have increased risk for colorectal cancer (CRC), which may be related to altered gut microbiota, changes in bile metabolism, as well as cellular and molecular effects in the proximal colon. In gallstone-associated CRC patients, the association between consensus molecular subtypes of CRC should be clarified to identify if specific pathways are related.