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Background Colorectal cancer (CRC) is a common malignant gastrointestinal tumor. In China, CRC is the 5th most commonly diagnosed cancer. The vast majority of CRC cases are sporadic and evolve with the adenoma-carcinoma sequence. There is mounting evidence indicating that gut microbiota and inflammation play important roles in the development of CRC although study results are not entirely consistent. In the current study, we investigated the changes in the CRC-associated bacteria and plasma inflammatory factors and their relationships based on data from a case-control study of Han Chinese. We included 130 initially diagnosed CRC patients, 88 advanced colorectal adenoma patients (A-CRA), 62 patients with benign intestinal polyps and 130 controls. Results Fecal microbiota composition was obtained using 16S ribosomal DNA (16S rDNA) sequencing. PCOA analysis showed structural differences in microbiota among the four study groups ( P =  0.001, Unweighted Unifrac). Twenty-four CRC-associated bacteria were selected by a two-step statistical method and significant correlations were observed within these microbes. CRC-associated bacteria were found to change with the degree of malignancy. Plasma C-reactive protein (CRP) and soluble tumor necrosis factor II (sTNFR-II) displayed significant differences among the four study groups and increased with adenoma-carcinoma sequence. The correlations of CRP and sTNFR-II with several CRC-associated microbes were also explored. Conclusions CRC-associated species and plasma inflammatory factors tended to change along the adenoma-carcinoma sequence. Several CRC-associated bacteria were correlated with CRP and sTNFR-II. It is likely that gut microbiome and inflammation gradually form a microenvironment that is associated with CRC development.

Colorectal cancer (CRC) remains a major global cause of cancer-related mortality, lacking effective biomarkers and therapeutic targets. Revealing the critical pathogenic factors of CRC and the underlying mechanisms would offer potential therapeutic strategies for clinical application. G protein signaling (RGS) protein family modulators play essential role within regulating downstream signaling of GPCR receptors, with function in cancers unclear. Our study focused on the expression patterns of RGS proteins in CRC, identifying Regulator of G protein signaling 16 (RGS16) as a prospective diagnostic and therapeutic target. Analyzing 899 CRC tissues revealed elevated RGS16 levels, correlating with clinicopathological features and CRC prognosis by immunohistochemistry (IHC) combined with microarray. We confirmed the elevated RGS16 protein level in CRC, and found that patients with RGS16-high tumors exhibited decreased disease-specific survival (DSS) and disease-free survival (DFS) compared to those with low RGS16 expression. Functional assays demonstrated that RGS16 promoted the CRC progression, knockdown of RGS16 led to significantly increased apoptosis rates of CRC in vitro and in vivo. Notably, we also confirmed these phenotypes of RGS16 in organoids originated from resected primary human CRC tissues. Mechanistically, RGS16 restrained JNK/P38-mediated apoptosis in CRC cells through disrupting the recruitment of TAB2/TAK1 to TRAF6. This study provides insights into addressing the challenges posed by CRC, offering avenues for clinical translation.

To comprehensively summarize the association between dietary intake of vitamins A, C, and E and the risk of colorectal adenoma (CRA), the precursor of colorectal cancer, relevant studies were identified in MEDLINE and EMBASE up to 31 October 2012. Summary relative risks (SRRs) with 95 % confidence intervals (CIs) were pooled with a random-effects model. Between-study heterogeneity was assessed using Cochran’s Q and l² statistics. A total of 13 studies with 3832 CRA cases were included in this meta-analysis. On the basis of the highest versus lowest analysis, dietary intake of vitamin C reduced the risk of CRA by 22% (SRRs 0.78, 95% CIs: 0.62–0.98). Subgroup analyses showed that this relation was not modified by BMI, smoking status, and dietary energy intake. Further, dietary intake of β-carotene was also inversely associated with the risk of CRA. However, dietary intake of vitamins A and E was not associated with the risk of CRA in overall and subgroup analyses (vitamin A: SRRs 0.87, 95% CIs: 0.67–1.14; vitamin E: SRRs 0.87, 95% CIs: 0.69–1.10). Our results indicate that dietary intake of vitamin C and β-carotene, but not vitamins A and E, could reduce the risk of CRA. However, these associations seem to be limited. Further investigation using large samples and a rigorous methodology is warranted.

Colorectal cancer (CRC) is one of the most commonly diagnosed malignant tumors of the digestive tract. H2-calponin (CNN2), an actin cytoskeleton-binding protein, is an isoform of the calponin protein family whose role in CRC is still unknown. Research based on clinical samples showed the up-regulation of CNN2 in CRC and its association with tumor development, metastasis, and poor prognosis of patients. Both in vitro loss-of-function and gain-of-function experiments showed that CNN2 participates in CRC development through influencing malignant cell phenotypes. In vivo, xenografts formed by CNN2 knockdown cells also showed a slower growth rate and smaller final tumors. Furthermore, EGR1 was identified as a downstream of CNN2, forming a complex with CNN2 and YAP1 and playing an essential role in the CNN2-induced regulation of CRC development. Mechanistically, CNN2 knockdown down-regulated EGR1 expression through enhancing its ubiquitination, thus decreasing its protein stability in a YAP1-dependent manner. In summary, CNN2 plays an EGR1-dependent promotion role in the development and progression of CRC, which may be a promising therapeutic target for CRC treatment.

Mechanism of radioresistance in rectal carcinoma remains largely unknown. We aimed to evaluate the predictive role of ATP-binding cassette subfamily C member 4 (ABCC4) in locally advanced rectal carcinoma and explore possible molecular mechanisms by which ABCC4 confers the resistance to neoadjuvant radiotherapy. The expression of ABCC4 and P53 mutant in biopsy tissue specimens from 121 locally advanced rectal carcinoma patients was examined using immunohistochemistry. The factors contributing to 3-year overall survival and disease-free survival were evaluated using the Kaplan-Meier method and Cox proportional hazard model. Lentivirus-mediated small hairpin RNA was applied to inhibit ABCC4 expression in colorectal carcinoma cell line RKO, and investigate the radiosensitivity in xenograft model. Intracellular cyclic adenosine monophosphate concentration and cell cycle distribution following irradiation were detected. High expression of ABCC4 and p53 mutant in pretreated tumors, poor pathological response, and high final tumor staging were significant factors independently predicted an unfavorable prognosis of locally advanced rectal carcinoma patients after neoadjuvant radiotherapy. Down-regulation of ABCC4 expression significantly enhanced irradiation-induced suppression of tumor growth in xenograft model. Furthermore, down-regulation of ABCC4 expression enhanced intracellular cyclic adenosine monophosphate production and noticeable deficiency of G1-S phase checkpoint in cell cycle following irradiation. Our study suggests that ABCC4 serves as a novel predictive biomarker that is responsible for the radioresistance and predicts a poor prognosis for locally advanced rectal carcinoma after neoadjuvant radiotherapy.

Purpose Local excision is an effective approach for managing rectal cancer exhibiting substantial regression after neoadjuvant chemoradiotherapy. The purpose of this study is to compare the outcomes between local excision and total mesorectal excision in rectal cancer patients achieving clinical complete or near-complete response after neoadjuvant chemoradiotherapy. Methods This is a retrospective cohort study that includes a consecutive series of rectal cancer patients who responded well to neoadjuvant chemoradiotherapy followed by surgery. A total of 180 rectal cancer patients at a single institution during a 12-year period are included. The main outcomes include short-term outcomes, oncological outcomes, and functional outcomes between the two groups. Results A total of 180 patients were included in the study. Sixty-one (33.9%) received local excision and 119 (66.1%) received total mesorectal excision. The baseline characteristics were generally balanced between the two groups. The local excision group demonstrated a significantly shorter operative time, less blood loss, and shorter hospital stay ( p  < 0.001). 3-year overall survival rates were 97.5% (95% CI, 0.93–1.00) and 95.5% (95% CI, 0.91–1.00) between the two groups ( p  = 0.38). The local excision group exhibited significantly higher 3-year local recurrence rates 15.7% (95% CI, 0.74–0.97) vs 4.2% (95% CI, 0.92–1.00) ( p  = 0.017), yet lower 3-year distant metastasis rates 9.6% (95% CI, 0.82–1.00) vs 12.6% (95% CI, 0.81–0.94) ( p  = 0.33) and lower 3-year disease-free survival rates 76.8% (95% CI, 0.64–0.92) vs 84.7% (95% CI, 0.78–0.92) ( p  = 0.56) comparing with the total mesorectal excision group. The local excision group demonstrated significantly better functional outcomes compared with the total mesorectal excision group ( p  < 0.001). Conclusion Patients who achieve either clinical complete or near-complete response after neoadjuvant chemoradiotherapy are suitable candidates for local excision. The local excision group demonstrated superior short-term and functional outcomes, and the oncological outcomes were not compromised.

Background Colorectal cancer (CRC) is one of the most prevalent gastrointestinal tumors worldwide. Complex interactions between tumor microenvironment (TME) and host inflammatory response influence CRC progression and recurrence. The current study provides a comprehensive bibliometric visualization of the current state and frontier trends of inflammatory TME in CRC. Materials and methods Scientific publications on the inflammatory TME in CRC from 2000 to 2024 were retrieved from the Web of Science Core Collection (WoSCC) database. Biblioshiny software was mainly applied for visualization and analysis of literature. CiteSpace software and VOSviewer software were used to validate the results. Results A total of 1593 articles related to CRC inflammatory TME have been retrieved since the 21st century. Cancers and Frontiers in Immunology were the two most popular journals, and Cancer Research is the most cited journal. Mcmillan DC, Park JH and Mantovani A were the most academic influential authors in inflammatory TME in CRC. Conclusions This study preliminary visualize the association of inflammatory TME with CRC through bibliometric analysis. The immunomodulatory mechanisms in IBD-associated carcinogenesis, NF-κB-mediated TME remodeling in tumor progression, and CRC patient stratification and precision therapeutics were three hotspots for future research endeavors on the inflammatory TME in CRC research.

Background Anastomotic bleeding is rare but is one of the dangerous complications, with associated morbidity and mortality, at the early stage of rectal cancer surgery. The aim of this study was to report our experiences in the treatment of this emergency condition. Methods We retrospectively analyzed the general characteristics, treatment and outcome of patients with severe anastomotic bleeding after undergoing rectal cancer resection with stapled anastomosis at the Department of Colorectal Surgery of Changhai Hospital (China) between January 2011 and December 2013. Results Anastomotic bleeding occurred in six out of 2,181 patients (0.3%) who underwent anterior resection with stapled anastomosis due to rectal cancer. All patients’ bleeding was stopped with colonoscopic techniques. There were no anastomotic leakages or strictures in these six patients. Conclusions Anastomotic bleeding was a very rare complication after rectal cancer resection with stapled anastomosis. Colonoscopic treatment, including electrocoagulation and clipping, were both safely and effectively used in the early postoperative period to cease persistent anastomotic bleeding.

The role of the novel oncogene, mitochondrial transcription termination factor (MTERFD1), in human colorectal cancer (CRC) is unclear. Here, we report the role MTERFD1 in CRC. We conducted plasmid construction and transfection analyses, cell proliferation assays, apoptosis detection assays, ELISA, western blotting, and qRT-PCR using cell culture applications. MTERFD1 was upregulated in human and chemically induced mouse CRC tissues. functional assays showed that MTERFD1 overexpression promoted human CRC cell proliferation, whereas knockdown of endogenous MTERFD1 significantly enhanced apoptosis in these cells. MTERFD1 expression was positively linked to irradiation resistance in CRC cells. Furthermore, interleukin (IL)-6 and IL-11 were identified as the effector molecules of MTERFD1 in its oncogenic role and irradiation resistance in CRC cells. Our results demonstrated that MTERFD1 played an oncogenic role in CRC development and enhanced irradiation resistance by regulating IL-6 and IL-11 in CRC cells. MTERFD1 may serve as a potential prognostic and therapeutic marker for radiotherapy in CRC.

Background Colonoscopic perforation (CP) has a low incidence rate. However, with the extensive use of colonoscopy, even low incidence rates should be evaluated to identify and address risks. Information on CP is quite limited in China. Objective Our study aimed to determine the frequency of CP in colonoscopies performed by surgeons at a large teaching hospital in China over a 12-year period. Methods A retrospective review of medical records was performed for all patients who had CPs from 1 January 2000 to 31 December 2012. Iatrogenic perforations were identified mainly by abdominal X-ray or computed tomography scan. Follow-up information of adverse events post-colonoscopy was identified from the colorectal surgery database of our hospital. Patients’ demographic data, colonoscopy procedure information, location of perforation, treatment, and outcome were recorded. Results A total of 110,785 diagnostic and therapeutic colonoscopy procedures were performed (86,800 diagnostic cases and 23,985 therapeutic cases) within the 12-year study period. A total of 14 incidents (0.012 %) of CP were reported (seven males and seven females), of which nine cases occurred during diagnostic colonoscopy (0.01 %) and five after therapeutic colonoscopy (three polypectomy cases, one endoscopic mucosal resection, and one endoscopic mucosal dissection). Mean patient age was 67.14 years. One case of CP (7.14 %) after colonoscopy polypectomy was treated using curative colonoscopy endoclips. Other patients underwent operations: six cases (46.15 %) of primary repair, four cases (28.57 %) of resection with anastomosis, and two cases (15.38 %) of resection without anastomosis. No obvious perforation was found in one patient (7.69 %). Surgeons attempted to treat one case laparoscopically but eventually resorted to open surgery. The postoperative course was uncomplicated in eight cases (57.14 %) and complicated in six cases (42.86 %) but without mortality. Conclusion CP is a serious but rare complication of colonoscopy. A perforation risk of 0.012 % was found in our study. The optimal management of CP remains controversial. Treatment for CP should be individualized according to the patient’s condition, related devices, and surgical skills of endoscopists or surgeons. Selective measures such as colonoscopy without intravenous sedation and decrease of loop formation can effectively reduce rates of perforation.