Conventional hemorrhoidectomy is the mainstay of treatment for symptomatic haemorrhoids, but reported postoperative complications remains the main concern. On the contrary, with its minimally invasive nature, laser hemorrhoidoplasty showed the potential to reduce postoperative complications and discomfort. Therefore, we performed a systemic review and meta-analysis to evaluate the postoperative outcome of laser hemorrhoidoplasty compared to conventional hemorrhoidectomies, including Milligan-Morgan and Ferguson techniques. Of all studies from PubMed, EMBASE, Cochrane database, and Google Scholar, we included 17 trials with 1196 patients, of whom 596 (49.8 %) underwent laser hemorrhoidoplasty and 600 (50.2 %) underwent conventional hemorrhoidectomy. The primary outcomes were operative blood loss and postoperative haemorrhage, and the secondary outcomes were the operative time, postoperative pain score, complications, and haemorrhoid recurrence. In this study, we found that laser hemorrhoidoplasty showed benefits in operative blood loss (weighted mean difference [WMD]: -16.43 ml, 95 % confidence interval [CI]: -23.82 to -9.04), postoperative hemorrhage/bleeding (odds ratio [OR]: 0.16, 95 % CI: 0.10 to 0.28), operative time (WMD: -12.42 min, 95 % CI: -14.56 to -10.28), postoperative pain score on day 1 (WMD: -2.50, 95 % CI: -3.13 to -1.88), and anal stenosis (OR: 0.14, 95 % CI: 0.03 to 0.65) in comparison with conventional hemorrhoidectomy. However, incidence of fecal/flatus incontinence, urinary retention and hemorrhoid recurrence were not significantly different between the 2 groups. Consistent results were found in 5 subgroup analyses, including studies with low risk of bias, studies using 1470 nm laser, and studies using 980 nm laser, studies conducted in Asia, and studies conducted in Europe and America.

Approximately 25% of colorectal cancer (CRC) patients will develop metastatic (m)CRC despite treatment interventions. In this setting, tumor cells are attracted to the epidermal growth factor receptor (EGFR) oncogene. Kirsten rat sarcoma (RAS) 2 viral oncogene homolog (KRAS) mutations were reported to drive CRC by promoting cancer progression in activating Wnt/β-catenin and RAS/extracellular signal-regulated kinase (ERK) pathways. In addition, KRAS is associated with almost 40% of patients who acquire resistance to EGFR inhibitors in mCRC. Multiple studies have demonstrated that cancer stem cells (CSCs) promote tumorigenesis, tumor growth, and resistance to therapy. One of the most common CSC prognostic markers widely reported in CRC is a cluster of differentiation 44 (CD44), which regulates matrix metalloproteinases 7/9 (MMP7/9) to promote tumor progression and metastasis; however, the molecular role of CD44 in CRC is still unclear. In invasive CRC, overexpression of MMP7 was reported in tumor cells compared to normal cells and plays a crucial function in CRC cetuximab and oxaliplatin resistance and distant metastasis. Here, we utilized a bioinformatics analysis and identified overexpression of KRAS/MMP7/CD44 oncogenic signatures in CRC tumor tissues compared to normal tissues. In addition, a high incidence of mutations in KRAS and CD44 were associated with some of the top tumorigenic oncogene’s overexpression, which ultimately promoted a poor response to chemotherapy and resistance to some FDA-approved drugs. Based on these findings, we explored a computational approach to drug repurposing of the drug, sulfasalazine, and our in silico molecular docking revealed unique interactions of sulfasalazine with the KRAS/MMP7/CD44 oncogenes, resulting in high binding affinities compared to those of standard inhibitors. Our in vitro analysis demonstrated that sulfasalazine combined with cisplatin reduced cell viability, colony, and sphere formation in CRC cell lines. In addition, sulfasalazine alone and combined with cisplatin suppressed the expression of KRAS/MMP7/CD44 in DLD-1 and HCT116 cell lines. Thus, sulfasalazine is worthy of further investigation as an adjuvant agent for improving chemotherapeutic responses in CRC patients.

Immunotherapy targeting the immune functions of the tumor microenvironment (TME) is beneficial for colorectal cancer; however, the response rate is poor. Ciprofloxacin is a fluoroquinolone-class antibiotic that is used to treat bacterial infections. The purpose of this study is to assess the mechanism of ciprofloxacin that enhances anti-PD1 in colorectal cancer. We found that ciprofloxacin induced cytosolic DNA, including single-stranded and double-stranded DNA, formation in mouse CT26 colorectal adenocarcinoma cells. Molecules in DNA-sensing signaling such as cGAS, STING, and IFNβ mRNA and protein expression were elicited after ciprofloxacin treatment in CT26 cells. STING siRNA abrogated the cGAS-STING pathway activation by ciprofloxacin. In vivo, ciprofloxacin exhibited a synergistic effect with anti-PD1 to suppress tumor growth in a CT26 syngeneic animal model without biological toxicity. The examination of TME revealed that ciprofloxacin, alone and in combination therapy, induced M1 and red pulp macrophage production in the spleen. In tumors, M1 and M2 macrophage levels were increased by ciprofloxacin, and CD8⁺ T cell granzyme B expression was increased after combination therapy. STING showed the highest expression in tumor specimens after combination treatment. Ciprofloxacin may enhance the anti-PD1 efficacy and modulate the TME through the cGAS-STING pathway.

Colorectal cancer (CRC) remains a leading cause of cancer-related death worldwide, with resistance to targeted therapies presenting a significant clinical challenge. This study combines computational and experimental methods to identify and validate Antrocin, a natural sesquiterpene lactone, as a potential multi-target inhibitor of the BRAF/MEK/PI3K oncogenic pathway in CRC. Differential gene expression and mutational analyses were performed using public datasets (TCGA, TNMplot, GEPIA2, GSCA, PANDA, and cBioPortal) to assess the prevalence and clinical significance of BRAF, MEK, and PI3K alterations in CRC. In silico molecular docking, using AutoDock Vina, predicted strong binding affinities of Antrocin to BRAF (ΔG = −8.5 kcal/mol), MEK (ΔG = −7.3 kcal/mol), and PI3K (ΔG = −6.9 kcal/mol), comparable to those of FDA-approved inhibitors for BRAF (Dabrafenib), MEK (Trametinib), and PI3K (Alpelisib). Drug-likeness and ADME properties were evaluated via SwissADME and ADMETlab, supporting Antrocin’s potential as a drug candidate. In vitro assays using HCT116 and RKO CRC cell lines validated that Antrocin treatment suppressed cell viability, spheroid formation, and migration, accompanied by reduced expression levels of the oncogenic BRAF/MEK/PI3K signaling pathway. Antrocin-treated tumor-conditioned medium experiments demonstrated Antrocin’s ability to reduce the differentiation of cancer-associated fibroblasts and the polarization of M2 macrophages. Preclinical mouse xenograft experiments demonstrated a delay in tumor growth following treatment with Antrocin. These results suggest that Antrocin, identified through computational screening and validated experimentally, could be a promising multi-target agent to overcome therapy resistance in CRC.

Bowel perforation is a potential complication of colonoscopy, and colonoscopic polypectomy has a higher risk. Perforation may be responsible for abdominal compartment syndrome (ACS), which causes multiple organ dysfunction. Here, we have described the case of a woman who underwent colonoscopic polypectomy. Subsequent to the procedure, she developed progressive abdominal distension, dyspnea, drowsy consciousness, and hypotension. Her physical examination revealed increased abdominal circumference, coldness, and paleness of the lower limbs. ACS were accordingly diagnosed, most likely to have resulted from bowel perforation. Thus, decompression with a large-bore intravenous catheter and emergent laparotomy were performed. A 0.5-cm lesion over the cecum was discovered and repaired. The patient tolerated the procedure well and underwent intensive care. She was discharged on day 7 after operation, and she had completely recovered. ACS is a rare complication followed by perforation after colonoscopy. Multiple organ dysfunction may occur from ACS, affecting the cardiovascular, pulmonary, and gastro-intestinal system. In our case, we used a small-sized catheter for decompression but in vain due to the kinking of the catheter. ACS was eventually resolved via surgical intervention. Thus, when ACS occurred, emergent decompression with an appropriate size of catheter and surgical intervention are recommended. Colonoscopy perforation must be considered as a contributing factor to ACS; accordingly, early recognition and intervention may avoid deterioration of ACS.