Assessing the role of anastomotic level in low anterior resection (LAR) surgery among rectal cancer patients in the development of LAR syndrome: a systematic review study.

BACKGROUND: The etiology of LARS has not been elaborated on clearly. Studies have reported neoadjuvant therapy, low-lying rectal cancers, adjuvant therapy and anastomotic leakage as risk factors for the development of LARS. Anastomotic level has also been proposed as a possible risk factor; However, there have been conflicting results. This study aims to evaluate the role of the level of anastomosis as a potential risk factor for the development of LARS. METHOD: A systematic literature search was conducted on Pubmed, Scopus, Embase, and Web of Science databases using Mesh terms and non-Mesh terms from 2012 to 2023. Original English studies conducted on rectal cancer patients reporting of anastomotic level and LARS status were included in this study. Eligible studies were assessed regarding quality control with Joanna-Briggs Institute (JBI) questionnaires. RESULTS: A total of 396 articles were found using the research queries, and after applying selection criteria 4 articles were selected. A sample population of 808 patients were included in this study with a mean age of 61.51 years with male patients consisting 59.28% of the cases. The Mean assessment time was 15.6 months which revealed a mean prevalence of 48.89% for LAR syndrome. Regression analysis revealed significantly increased risk of LAR syndrome development due to low anastomosis level in all 4 studies with odds ratios of 5.336 (95% CI:3.197-8.907), 3.76 (95% CI: 1.34-10.61), 1.145 (95% CI: 1.141-2.149) and 2.11 (95% CI: 1.05-4.27) for low anastomoses and 4.34 (95% CI: 1.05-18.04) for ultralow anastomoses. CONCLUSIONS: LARS is a long-term complication following surgery, leading to reduced quality of life. Low anastomosis level has been reported as a possible risk factor. All of the studies in this systematic review were associated with an increased risk of LARS development among patients with low anastomosis.

A comprehensive view on the apigenin impact on colorectal cancer: Focusing on cellular and molecular mechanisms.

Colon cancer (CC) is one of the most common and deadly cancers worldwide. Oncologists are facing challenges such as development of drug resistance and lack of suitable drug options for CC treatment. Flavonoids are a group of natural compounds found in fruits, vegetables, and other plant-based foods. According to research, they have a potential role in the prevention and treatment of cancer. Apigenin is a flavonoid that is present in many fruits and vegetables. It has been used as a natural antioxidant for a long time and has been considered due to its anticancer effects and low toxicity. The results of this review study show that apigenin has potential anticancer effects on CC cells through various mechanisms. In this comprehensive review, we present the cellular targets and signaling pathways of apigenin indicated to date in in vivo and in vitro CC models. Among the most important modulated pathways, Wnt/ß-catenin, PI3K/AKT/mTOR, MAPK/ERK, JNK, STAT3, Bcl-xL and Mcl-1, PKM2, and NF-kB have been described. Furthermore, apigenin suppresses the cell cycle in G2/M phase in CC cells. In CC cells, apigenin-induced apoptosis is increased by inhibiting the formation of autophagy. According to the results of this study, apigenin appears to have the potential to be a promising agent for CC therapy, but more research is required in the field of pharmacology and pharmacokinetics to establish the apigenin effects and its dosage for clinical studies.