Colorectal Adenomatous Polyps Research Articles

POLIPOSE ADENOMATOSA FAMILIAR: UMA ABORDAGEM ABRANGENTE SOBRE A MANIFESTAÇÃO CLÍNICA, RASTREAMENTO, ABORDAGEM CIRÚRGICA E QUIMIOPREVENÇÃO

Familial Adenomatous Polyposis (FAP) is an autosomal dominant hereditary disease caused by pathogenic variants in the Adenomatous Polyposis Coli (APC) gene. The clinical picture manifests with 100 or more adenomatous colorectal polyps and is 100% associated with the risk of developing colorectal cancer (CRC). Patients with this pathology also have an increased risk of extra-colonic manifestations, such as desmoid tumors, osteomas, duodenal adenomas, including gastric cancer, and thyroid cancer. The treatment to prevent RCC is prophylactic colectomy, which has many complications and interferes with the patient's quality of life. This disease can take two forms: the classic form and the attenuated form. The classic form is represented by the presence of hundreds to thousands of adenomatous polyps in the colon and rectum, which appear in adolescence at small sizes and progressively increase in size. On the other hand, the attenuated form of familial adenomatous polyposis (FAP) manifests itself with few adenomas in the colon, starting later in life and presenting an 80% risk of malignant transformation, as well as an increased risk of extra-colonic manifestations. For this reason, the aim of this work is to discuss FAP so that it is possible to disseminate its knowledge and conduct according to the latest literature. For this reason, the aim of this work is to discuss FAP so that it is possible to disseminate its knowledge and conduct in accordance with the latest literature. An integrative literature review was therefore carried out, using a quantitative, qualitative and descriptive approach and searching the PubMed, Scielo and BVSdatabases with the descriptors: “familial adenomatous polyposis”, “Chemoprevention”, “treatment”. As a result, she was able to understand the basic concept of the disease and how it should be treated and managed on a daily basis.

The microbiota comparative analysis of the characteristics between colorectal adenomatous polyps and normal mucosal intestinal.

The aim of this study is to systematically examine and compare the characteristics distinguishing colorectal adenomatous polyps from normal mucosal intestinal microbiota. A total of 30 specimens were obtained from patients diagnosed with colorectal adenomatous polyps (adenoma group) who underwent endoscopic removal at Wenzhou People's Hospital between September 2021 and November 2021. Concurrently, 30 normal mucosal specimens were collected from patients without adenomatous polyps (control group). Subsequently, microbiome total DNA extraction was carried out, followed by PCR amplification targeting the V3-V4 region of the 16S rDNA. High-throughput sequencing was conducted using the Illumina MiSeq platform. Subsequent to sequencing, bioinformatics analysis was used to assess the diversity, composition, and functional aspects of the intestinal microbiota in both study groups. A notable dissimilarity in the microbiota structure was identified, specifically within the transverse colon, between these two groups ( P < 0.05). Species composition analysis revealed that Escherichia , Fusobacterium , and Bacteroides were predominant bacteria in both groups, with Escherichia and Enterobacter displaying significant differences at the genera level between the control group and the adenoma group ( P < 0.05). Correlation analysis and functional prediction demonstrated substantial disparities in interactions among dominant intestinal microbial genera within patients from both groups. Additionally, it was discovered that the intestinal microbiomes in patients in the adenoma group exhibited a significantly higher pathogenic potential. Upon conducting a comprehensive analysis, it was discerned that the microbiota present in the transverse colon of the control group exhibited distinctive characteristics that may contribute to the maintenance of intestinal health.

GUCA2A dysregulation as a promising biomarker for accurate diagnosis and prognosis of colorectal cancer

Colorectal cancer is a leading cause of global mortality and presents a significant barrier to improving life expectancy. The primary objective of this study was to discern a unique differentially expressed gene (DEG) that exhibits a strong association with colorectal cancer. By achieving this goal, the research aims to contribute valuable insights to the field of translational medicine. We performed analysis of colorectal cancer microarray and the TCGA colon adenoma carcinoma (COAD) datasets to identify DEGs associated with COAD and common DEGs were selected. Furthermore, a pan-cancer analysis encompassing 33 different cancer types was performed to identify differential genes significantly expressed only in COAD. Then, comprehensively in-silico analysis including gene set enrichment analysis, constructing Protein–Protein interaction, co-expression, and competing endogenous RNA (ceRNA) networks, investigating the correlation between tumor-immune signatures in distinct tumor microenvironment and also the potential interactions between the identified gene and various drugs was executed. Further, the candidate gene was experimentally validated in tumoral colorectal tissues and colorectal adenomatous polyps by qRael-Time PCR. GUCA2A emerged as a significant DEG specific to colorectal cancer (|log2FC|> 1 and adjusted q-value < 0.05). Importantly, GUCA2A exhibited excellent diagnostic performance for COAD, with a 99.6% and 78% area under the curve (AUC) based on TCGA-COAD and colon cancer patients. In addition, GUCA2A expression in adenomatous polyps equal to or larger than 5 mm was significantly lower compared to smaller than 5 mm. Moreover, low expression of GUCA2A significantly impacted overall patient survival. Significant correlations were observed between tumor-immune signatures and GUCA2A expression. The ceRNA constructed included GUCA2A, 8 shared miRNAs, and 61 circRNAs. This study identifies GUCA2A as a promising prognostic and diagnostic biomarker for colorectal cancer. Further investigations are warranted to explore the potential of GUCA2A as a therapeutic biomarker.

Diagnosis of Colorectal Cancer and Adenomatous Polyps of the Colon Based on the Level of MicroRNA Expression in the Mucous Membrane (Pilot Clinical Study)

Diagnosis of Colorectal Cancer and Adenomatous Polyps of the Colon Based on the Level of MicroRNA Expression in the Mucous Membrane (Pilot Clinical Study)

Age Matters: Adenoma Detection Rates in Average-risk Screening Patients Aged 45 to 49 Compared With Those Aged 50 to 54.

This study aims to address gaps in medical knowledge by determining whether adenoma detection rate (ADR) in average-risk screening patients aged 45 to 49 is equivalent to screening patients aged 50 to 54. Current guidelines recommend initiating colon cancer screening at age 45, yet our understanding of the effects of ADR in average-risk individuals among 45- to 49-year-olds is still limited. A retrospective analysis was conducted on records of average-risk screening colonoscopies performed on patients aged 45 to 54 from January 2018 to August 2022. Exclusions were prior diagnoses of colorectal cancer or adenomatous polyps, inflammatory bowel disease, personal or family history of genetic cancer syndromes, incomplete colonoscopy, and inadequate bowel preparation. The primary outcome was ADR in the age 45 to 49 group compared with the age 50 to 54 group. Of the 3199 average-risk screening colonoscopies performed, 879 and 2116 patients were included in the age 45 to 49 and 50 to 54 groups, respectively. Both groups were predominantly female, White ethnicity, never smokers, and obese. ADR was found to be 27% in the age 45 to 49 group compared with 34% in the age 50 to 54 group (odds ratio 0.70, 90% CI: 0.60-0.83, P -value for equivalence=0.81 w/ margin 0.77 to 1.30). The study did not demonstrate equivalent ADR between the 2 age groups, with ADR being substantially lower in the age 45 to 49 group (27% vs. 34%). Despite this, the ADR in the 45 to 49 age range surpasses the established benchmark of 25%, supporting the decision to lower the screening age to 45 years. Ongoing national monitoring is essential to comprehensively evaluate the impact of these updated guidelines.

Pseudoinvasion and squamous metaplasia/morules in colorectal adenomatous polyp: a case report and literature review

BackgroundSubmucosal pseudoinvasion and squamous metaplasia (SM) are incidental and special morphological findings in colorectal adenomas, and both can mimic invasive carcinoma. The coexistence of these two findings further increases the risk of misdiagnosis, posing a great diagnostic challenge to pathologists. From 1979 to 2022, only 8 cases have been reported, which was extremely rare. In this report, we presented a case of sigmoid colon adenoma accompanied by pseudoinvasion and SM. Additionally, relevant literature was analyzed to summarize the clinical and pathological characteristics.Case presentationA 51-year-old Chinese male patient presented with fresh blood after defecation. Electronic colonoscopy revealed multiple polyps, which were removed using a snare and subjected to high-frequency electrocoagulation resection. The largest polyp, located in the sigmoid colon, was a thick pedunculated and lobulated polyp with a maximum diameter of 2.8 cm. The surface of the polyp showed slight ruggedness and redness, and it was sent for pathological examination. Grossly, the polyp had a lobulated and slightly rough surface. Microscopically, it showed a tubulovillous adenoma with focal high-grade dysplasia and mucosal muscle hyperplasia. Glandular elements were observed in the submucosal layer, forming a well-defined lobular structure. Some of the glands displayed cystic change, and focal SM could be seen within the adenoma. SM could manifest as discrete solid cell nests of varying sizes or cribriform-morular-like structures. Immunohistochemical staining showed that SM cells were diffusely positive for cytokeratin 5/6 (CK5/6); p40, p63, and cytokeratin 20 (CK20) were negative; while caudal type homeobox 2 (CDX2) was weakly positive. β-catenin showed abnormal nuclear expression, and an extremely low Ki67 proliferation index was observed.ConclusionsCoexistence of SM and pseudoinvasion in colorectal adenomas is highly rare. It is more commonly observed in males and tends to occur in the sigmoid colon. It primarily manifests in tubulovillous adenoma and tubular adenoma, with a majority of cases exhibiting a pedicle. Histologically, it is similar to invasive lesions. The cystic dilation of the submucosal glands, hemosiderin deposition, and the presence of a lamina propria around the submucosal glands without adjacent desmoplastic reaction, suggest pseudoinvasion rather than cancer. The bland cytological morphology and Immunohistochemical markers play a crucial role in distinguishing SM from true invasive lesions.

Familial adenomatous polyposis: a case report

BackgroundFamilial adenomatous polyposis is characterized by the presence of multiple colorectal adenomatous polyps and caused by germline mutations in the tumor suppressor gene and adenomatous polyposis coli, located on chromosome 5q21–q22. Familial adenomatous polyposis occurs in approximately 1/10,000 to 1/30,000 live births, and accounts for less than 1% of all colorectal cancers in the USA. It affects both sexes equally and has a worldwide distribution. The incidence of colon cancer in low- and middle-income countries is rising. In addition to the increasing incidence, lack of early detection and impeded access to optimal multidisciplinary treatment may worsen survival outcomes. Developing quality diagnostic services in the proper health context is crucial for early diagnosis and successful therapy of patients with colorectal cancer, and applying a resource-sensitive approach to prioritize essential treatments on the basis of effectiveness and cost-effectiveness is key to overcoming barriers in low- and middle-income countries. We report a case of familial adenomatous polyposis presenting as adenocarcinoma with multiple colorectal adenomatous polyps. The diagnosis of familial adenomatous polyposis was made by the presence of numerous colorectal adenomatous polyps and family history of colonic adenocarcinoma. Due to its rarity, we decided to report it.Case presentationA 22-year-old Ethiopian female patient presented to Addis Ababa University College of Health science, Addis Ababa, Ethiopia with rectal bleeding. Abdominopelvic computed tomography scan was done and showed distal rectal asymmetric anterior wall thickening in keeping with rectal tumor. Colonoscopy was done and she was diagnosed to have familial adenomatous polyposis with severe dysplasia. In the meantime, colonoscopy guided biopsy was taken and the diagnosis of adenocarcinoma with familial adenomatous polyposis was rendered. For this, total proctocolectomy was carried out. On laparotomy there was also incidental finding of left ovarian deposition for which left salpingo-oophorectomy was done, and 4 weeks after surgical resection, the patient was started on oxaliplatin, leucovorin, fluorouracil chemotherapy regimen.ConclusionIn the clinical evaluation of a patient with rectal bleeding, familial adenomatous polyposis must be considered as a differential diagnosis in subjects having family history of colonic adenocarcinoma for early diagnostic workup, management, family genetic counseling, and testing.

The relationship between the expression of fibroblast growth factor 19 and insulin-like growth factor 1 in colorectal polyp tissues and the occurrence of colorectal adenomas

Objective: This investigation sought to delineate the associations among colorectal adenomatous polyps, diabetes, and biomolecules involved in glucose metabolism. Method: Data were collected from 40 patients who underwent endoscopic polypectomy at the Endoscopy Department of Shandong Cancer Hospital between June 2019 and September 2021. This cohort included 27 patients with inflammatory polyps and 13 with adenomatous polyps. We assessed fasting insulin (Fins), fasting blood glucose (FBG), and the mRNA expressions of fibroblast growth factor 19 (FGF-19) and insulin-like growth factor 1 (IGF-1) in the polyp tissues. Both univariate and multivariate logistic regression analyses were employed to ascertain the determinants influencing the emergence of adenomatous polyps. From these analyses, a predictive nomogram was constructed to forecast the occurrence of adenomatous polyps, and evaluations on the discriminative capacity, calibration, and clinical utility of the model were conducted. Results: The adenomatous polyp group exhibited markedly elevated levels of glucose, insulin, FGF-19, and IGF-1, with respective concentrations of (8.67±2.70) mmol/L, (12.72±7.69) μU/L, 2.20±1.88, and 1.36±0.69. These figures were significantly higher compared to the inflammatory polyp group, which showed levels of (5.51±0.72) mmol/L, (5.49±2.68) μU/L, 0.53±0.97, and 0.41±0.46, respectively, P=0.001. Multivariate logistic regression revealed that the relative expression of IGF-1 served as an independent risk factor for the development of colorectal adenomatous polyps (OR=5.622, 95% CI:1.085-29.126). The nomogram displayed a C-index of 0.849, indicating substantial discriminative capability. The calibration curve affirmed the model's accuracy in aligning predicted probabilities with actual outcomes, and the clinical decision curve demonstrated thepractical clinical applicability of the model. Conclusions: There was a significant correlation between the occurrence of colorectal adenomatous polyps and glucose metabolic pathways. Individuals with diabetes showed a higher propensity to develop such polyps.

Helicobacter pylori infection is associated with the development of sporadic colorectal carcinoma and colorectal adenomatous polyps

Helicobacter pylori (H. pylori) infection is a well-established carcinogen that has been extensively studied in the context of gastric diseases. Recent studies suggested a potential association between H. pylori and the risk of colorectal carcinoma (CRC). However, available data remains insufficient to definitively establish a causal relationship between H. pylori infection and the development of CRC and its precursor lesions. In our study, we reviewed all patients diagnosed with CRC in 2020 at our institution. H. pylori assessment was performed in all 92 CRC specimens by immunohistochemistry. Notably, two of the three patients detected with H. pylori infection are under the age of 50. Subsequently, we reviewed a total of 52 patients under the age of 50 diagnosed with CRC at our institution from 2015 to 2022. Among these patients, H. pylori infection was detected in 7 CRC specimens (13.46 %). All seven patients had adenocarcinoma on the left side of the colon. In exploring the link between H. pylori infection and the risk of developing CRC precursor lesions, we analyzed 242 patients who underwent colonoscopy guided polypectomy and also had stomach biopsies from 2015 to 2022. Of these patients, 21 were proved to be positive for H. pylori infection in the stomach, while the remaining 221 were negative. Among the H. pylori-positive group, 76.19 % (16 patients) exhibited adenomatous polyps, compared to 33.48 % (74 patients) in the H. pylori-negative patients (p=0.0001). However, no H. pylori was detected in any colonic adenomatous polyps. Our findings contribute additional evidence supporting the association between H. pylori infection and the development of sporadic CRC, probably a particular association with early-onset ones. Furthermore, gastric H. pylori infection appears to be linked to the higher prevalence of colonic adenomatous polyps, suggesting that individuals with gastric H. pylori infection may benefit from closer and earlier monitoring through colonoscopy.

Construction and Identification of a Human Colorectal Adenoma Epithelial Cell Line by SV40 Large T-Antigen Transfection.

Colorectal adenoma represents the critical step in the development of colorectal cancer. The establishment of an immortalized epithelial cell line of colorectal adenoma of human origin would provide a tool for studying the mechanism of precancerous lesions, screening the efficacy of novel drugs, and constructing in vivo disease models. Currently, there is no commercially available stable supply of epithelial cells from precancerous lesions. This study aimed to establish a natural LHPP low-expressing precancerous epithelial cell line by SV40-LT antigen gene transfection. Simian vacuolating virus 40(SV40), SV40-LT overexpressed lentivirus vector, was transfected into primary human colorectal adenomatous polyp epithelial cells. The transfected cells were screened, and the screened cells were amplified to obtain the epithelial cell line: IHCRA- CELL. The cells were identified by morphological observation, cell proliferation, Quantitative real-time PCR (qPCR), and Short Tandem Repeats (STR) experiments. Morphologically, the cells showed epithelial-like characteristics, such as polygon shape, desmosomes mitochondria, and strong positive keratin staining. There was no significant difference between the transfected cells and the primary cells. Through the STR identification experiment, no matching cell lines were found in the cell lines retrieval. We successfully established a natural LHPP low-expressing precancerous epithelial cell line by SV40-LT antigen gene transfection, which has been patented and is now preserved in the Chinese Typical Culture Preservation Center. It was verified that the transformed cells maintained the phenotype and biological characteristics of epithelial cells. This cell line can be used to study the mechanism of precancerous lesions, screen the efficacy of novel drugs, and construct in vivo disease models.

High risk features in colorectal adenomatous polyps: A multi-institutional study

High risk features in colorectal adenomatous polyps include size >1 cm and advanced histology: high-grade dysplasia and villous architecture. We investigated whether the diagnostic rates of advanced histology in colorectal adenomatous polyps were similar among institutions across the United States, and if not, could differences be explained by patient age, polyp size, and/or CRC rate. Nine academic institutions contributed data from three pathologists who had signed out at least 100 colorectal adenomatous polyps each from 2018 to 2019 taken from patients undergoing screening colonoscopy. For each case, we recorded patient age and sex, polyp size and location, concurrent CRC, and presence or absence of HGD and villous features. A total of 2700 polyps from 1886 patients (mean age: 61 years) were collected. One hundred twenty-four (5 %) of the 2700 polyps had advanced histology, including 35 (1 %) with HGD and 101 (4 %) with villous features. The diagnostic rate of advanced histology varied by institution from 1.7 % to 9.3 % (median: 4.3 %, standard deviation [SD]: 2.5 %). The rate of HGD ranged from 0 % to 3.3 % (median: 1 %, SD: 1.2 %), while the rate of villous architecture varied from 1 % to 8 % (median: 3.7 %, SD: 2.5 %). In a multivariate analysis, the factor most strongly associated with advanced histology was polyp size >1 cm with an odds ratio (OR) of 31.82 (95 % confidence interval [CI]: 20.52–50.25, p < 0.05). Inter-institutional differences in the rate of polyps >1 cm likely explain some of the diagnostic variance, but pathologic subjectivity may be another contributing factor.

Methylation of NRIP3 Is a Synthetic Lethal Marker for Combined PI3K and ATR/ATM Inhibitors in Colorectal Cancer.

The aim of this study was to investigate the epigenetic regulation and underlying mechanism of NRIP3 in colorectal cancer (CRC). Eight cell lines (SW480, SW620, DKO, LOVO, HT29, HCT116, DLD1, and RKO), 187 resected margin samples from colorectal cancer tissue, 146 cases with colorectal adenomatous polyps, and 308 colorectal cancer samples were used. Methylation-specific PCR, Western blotting, RNA interference assay, and a xenograft mouse model were used. NRIP3 exhibited methylation in 2.7% (5/187) of resected margin samples from colorectal cancer tissue, 32.2% (47/146) of colorectal adenomatous polyps, and 50.6% (156/308) of CRC samples, and the expression of NRIP3 was regulated by promoter region methylation. The methylation of NRIP3 was found to be significantly associated with late onset (at age 50 years or older), poor tumor differentiation, lymph node metastasis, and poor 5-year overall survival in CRC (all P < 0.05). In addition, NRIP3 methylation was an independent poor prognostic marker ( P < 0.05). NRIP3 inhibited cell proliferation, colony formation, invasion, and migration, while induced G1/S arrest. NRIP3 suppressed CRC growth by inhibiting PI3K-AKT signaling both in vitro and in vivo . Methylation of NRIP3 sensitized CRC cells to combined PI3K and ATR/ATM inhibitors. NRIP3 was frequently methylated in both colorectal adenomatous polyps and CRC. The methylation of NRIP3 may potentially serve as an early detection, late-onset, and poor prognostic marker in CRC. NRIP3 is a potential tumor suppressor. NRIP3 methylation is a potential synthetic lethal marker for combined PI3K and ATR/ATM inhibitors.

Modifiable factors of development and recurrence of adenomatous colorectal polyps (literature review)

Relevance. Adenomatous colorectal polyps are associated with a high risk of developing a malignant tumor. They are considered precancerous conditions and can lead to the development of colorectal cancer. To date, colorectal cancer ranks third in the world in frequency of occurrence among all malignant neoplasms.Objective. Improving the results of diagnosis and surgical treatment of patients with colorectal adenomatous neoplasms by identifying development factors and identifying risk groups for this nosology.Materials and methods. Analysis of literary data.Results. Among the factors leading to the development of colorectal polyps, it is worth noting a genetic predisposition, so by immunoblotting, PCR sequencing of the entire exome in cases of patients with familial dentate polyposis, rare variants of the germ line in the WNK2 gene were identified. Functional studies have shown that variants of the WINK2 germ line affect protein function in the context of the MAPK pathway, a molecular trait of this disease. Also, in the course of many domestic and foreign randomized clinical trials, the following modifiable factors for the development of adenomatous colorectal polyps were identified.Conclusion. The study revealed the factors of development and recurrence of colorectal neoplasms and identified risk groups for this nosology. The study revealed low compliance of patients with respect to changes in certain living conditions (the use of ethyl alcohol and products containing it, tobacco smoking, both active and passive, the fight against obesity and inactivity), which leads to recurrence and increases the risks of malignancy of colorectal polyps.

Familial Adenomatous Polyposis within the Pediatric Hereditary Polyposis Registry

Background/Objective: &#x0D; Familial Adenomatous Polyposis (FAP) is a condition characterized by values exceeding hundreds of colorectal adenomatous polyps. FAP has a prevalence of 1 in 8,300 people, demonstrating an autosomal dominant inheritance pattern. This condition follows a pathogenic variation of the Adenomatous Polyposis Coli (APC) gene, located on chromosome 5q21-22. These mutations are heavily correlated with the incidence of colorectal carcinoma, requiring prophylactic colectomy. The management and treatment of FAP requires routine surveillance to reduce gastrointestinal polyp burden. The objective for this study is to characterize the current patient population at Riley with polyposis syndromes and assess clinical surveillance in patients diagnosed with FAP. &#x0D; Methods: &#x0D; Historical data from 2020-2022 GI clinical visits were reviewed using the diagnostic codes Family history of colonic polyps, Benign neoplasm of colon unspecified, and Other phakomatoses not elsewhere classified. These criteria identified 93 patients of which 64 patients were diagnosed with a hereditary polyposis syndrome for inclusion within the registry. Of the 64 patients, 42 had a diagnosis of FAP. Clinical data reviewed included the patient’s age of diagnosis, completion of genetic testing and follow-up, surgical treatment, routine endoscopic surveillance, and modes of imaging. &#x0D; Results: &#x0D; Results indicated a median age of diagnosis of 10 years, lower than previously reported national averages of 13.5-17 years. Evaluation of routine follow-up indicated a rate of endoscopy at 0.822 scopes per year and demonstrated that abdominal CT scans as well as abdominal X-rays were the most common supplemental modes of imaging. &#x0D; Conclusion/ Future Directions: &#x0D; The data from this registry will help direct care of patients with FAP, ensuring they receive treatment in accordance with national guidelines for routine surveillance and prophylactic colectomy. Moving forward, the intention is to expand the registry's date range to incorporate more patients and elaborate further on endoscopic findings for the specific subtypes of FAP.

Diagnostic significance of CD10 marker to differentiate colorectal adenocarcinoma from adenomatous polyp: A pathological correlation.

Colorectal cancer could be developed from adenomatous polyp. The study aimed to evaluate the diagnostic significance of stromal and epithelial CD10 (Neprilysin) expression in patients with colorectal adenocarcinoma and adenomatous polyps. This cross-sectional study was conducted on 141 patients with colorectal adenocarcinoma and adenomatous polyps referred to Ayatollah Rouhani Hospital from March 2020 to March 2021. Differential diagnoses of colorectal adenocarcinoma and adenomatous polyps were made colonoscopically, and then samples were taken from the lesions. The pathologists confirmed the final diagnosis as colorectal adenocarcinoma, high-grade or low-grade adenomatous polyps. The stromal and epithelial CD10 expression was evaluated by immunohistochemistry. The data was analyzed by SPSS 22 software (p<0.05). Sixty-five (46.1%) of the cases were low-grade polyps that were included positive (4 cases; 6.20%) and negative (61 cases; 93.80%) CD10 expression (P=0.001), also 76 (53.9%) of them were either high-grade polyps (21 cases) or adenocarcinomas (21 cases). Also, epithelial CD10 expression was significantly higher in the well-differentiated adenocarcinoma (38 cases) group than moderate (13 cases) and poor (4 cases) groups (P =0.001). Moreover, the CD10 expression level in the adenomatous polyps (10 positive cases and 76 negative cases) was correlated with the degree of dysplasia (P = 0.001) and the presence of tumor invasion (8 positive cases and 133 negative cases) (P = 0.001). The CD10 expression is associated with an increased degree of dysplasia and the presence of tumor invasion in patients with pre-neoplastic lesions and colorectal adenocarcinoma.

Evaluating Cytokines and Antimicrobial Peptides as Diagnostic Biomarkers in Colorectal Cancer and Adenomatous Polyps

Evaluating Cytokines and Antimicrobial Peptides as Diagnostic Biomarkers in Colorectal Cancer and Adenomatous Polyps

Polymorphisms in Cyclooxygenase, Lipoxygenase and TP53 genes predict colorectal polyp risk reduction by aspirin in the seAFOod polyp prevention trial.

Aspirin and eicosapentaenoic acid (EPA) reduce colorectal adenomatous polyp risk and affect synthesis of oxylipins including prostaglandin E2. We investigated whether 35 single nucleotide polymorphisms (SNPs) in oxylipin metabolism genes such as cyclooxygenase [PTGS] and lipoxygenase [ALOX], as well as 7 SNPs already associated with colorectal cancer (CRC) risk reduction by aspirin (eg. TP53; rs104522), modified the effects of aspirin and EPA on colorectal polyp recurrence in the randomised 2x2 factorial seAFOod trial. Treatment effects were reported as the incidence rate ratio (IRR) and 95% confidence interval (CI) by stratifying negative binomial and Poisson regression analyses of colorectal polyp risk on SNP genotype. Statistical significance was reported with adjustment for the false discovery rate as the P and q value. Five hundred and forty-two (of 707) trial participants had both genotype and colonoscopy outcome data. Reduction in colorectal polyp risk in aspirin users compared with non-aspirin users was restricted to rs4837960 (PTGS1) common homozygotes (IRR 0.69 [95%CI 0.53,0.90]; q=0.06), rs2745557 (PTGS2) compound heterozygote-rare homozygotes (IRR 0.60 [0.41,0.88]; q=0.06), rs7090328 (ALOX5) rare homozygotes (IRR 0.27 [0.11,0.64]; q=0.05), rs2073438 (ALOX12) common homozygotes (IRR 0.57 [0.41,0.80]; q=0.05), and rs104522 (TP53) rare homozygotes (IRR 0.37 [0.17,0.79]; q=0.06). No modification of colorectal polyp risk in EPA users was observed. In conclusion, genetic variants relevant to the proposed mechanism of action on oxylipins are associated with differential colorectal polyp risk reduction by aspirin in individuals who develop multiple colorectal polyps. SNP genotypes should be considered during development of personalised, predictive models of CRC chemoprevention by aspirin.

Dietary Inflammatory Potential and the Risk of Serrated and Adenomatous Colorectal Polyps

Studies of dietary inflammation potential and risks of colorectal cancer precursors are limited, particularly for sessile serrated lesions (SSLs). This study examines the association using the energy-adjusted dietary inflammatory index (E-DIITM), a measure of anti- and/or pro-inflammatory diet, in a large US colonoscopy-based case-control study of 3246 controls, 1530 adenoma cases, 472 hyperplastic polyp cases, and 180 SSL cases. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived from logistic regression models. Analyses were stratified by participant characteristics, and urinary prostaglandin E2 metabolite (PGE-M) and high-sensitivity plasma C-reactive protein (hs-CRP) levels, inflammation biomarkers. Highest E-DII™ intake was associated with significantly increased risks of colorectal adenomas (OR 1.36, 95% CI 1.11, 1.67), and hyperplastic polyps (OR 1.43, 95% CI 1.06, 1.98), compared with participants consuming the lowest E-DII™ quartile. A similar, but non-significant, increased risk was also observed for SSLs (OR 1.41, 95% CI 0.82, 2.41). The positive association was stronger in females (pinteraction <0.001), normal weight individuals (ptrend 0.01), and in individuals with lower inflammatory biomarkers (ptrend 0.02 and 0.01 for PGE-M and hs-CRP, respectively). A high E-DII™ is associated with colorectal polyp risk, therefore promoting an anti-inflammatory diet may aid in preventing colorectal polyps.

Association between Dietary Inflammatory Index and Risk of Colorectal Adenomatous Polyps in Kashgar Prefecture of Xinjiang, China.

Malignant colorectal tumors and precancerous lesions are closely associated with chronic inflammation. Specific dietary patterns can increase chronic inflammation in the body, thereby promoting the occurrence of tumors and precancerous lesions. We have conducted a case-control study in Kashgar Prefecture, Xinjiang, China, to explore the association between the energy-adjusted dietary inflammatory index (E-DII) and the risk of colorectal adenomatous polyps (CAP). A total of 52 newly diagnosed patients with CAP and 192 controls at the First People's Hospital of Kashgar Prefecture were enrolled in this study. Dietary information was collected using a food frequency questionnaire. The E-DII was calculated based on dietary data, reflecting an individual's dietary inflammatory potential. Logistic regression models were used to evaluate the relationship between the E-DII and the risk of CAP, with adjustments for potential confounding factors. The results showed that the maximum anti- and pro-inflammatory values of E-DII were -4.33 and +3.48, respectively. Higher E-DII scores were associated with an increased risk of CAP, and this association remained statistically significant after adjusting for age, sex, body mass index, smoking status, and other relevant variables. Notably, a more pro-inflammatory dietary pattern may be related to an increased risk of developing CAP in Kashgar Prefecture.

The siRNA-mediated knockdown of SNHG4 efficiently induced pro-apoptotic signaling and suppressed metastasis in SW1116 colorectal cancer cell line.

Long non-coding RNAs are broadly dysregulated in disease conditions, especially cancer, and are associated with tumor initiation, invasion, and overall survival. This study aimed to elucidate the expression level of Small Nucleolar RNA Host Gene 4 (SNHG4) lncRNA in colorectal cancer (CRC) and its effect on cell cycle progression, invasion, and death. We evaluated the expression level of SNHG4 in clinical samples, including CRC tissues, adenomatous colorectal polyps (ACP), and their marginals. SNHG4-silenced SW1116 cells were used to evaluate the cell viability, cycle arrest, invasion, and apoptosis using MTT assay, scratching, flow cytometry, and immunoblotting. We also predicted molecular networks related to the SNHG4 involvement in CRC development. Results showed that SNHG4 expresses in cancerous tissues significantly higher than in polyps and marginals. This overexpression discriminated CRC from marginals and ACP with a suitable prognostic potential. Silencing of SNHG4 arrested the cell cycle at S and G2 phases and promoted early apoptosis in SW1116. It affected the active form of MMP2 and prevented cell invasion. Sponging of miRNAs which promotes the choline metabolism is the probable mechanism of SNHG4 involvement in CRC. In conclusion, SNHG4 promotes CRC by dysregulating apoptosis and cell migration, and shows significant prognostic potential for CRC.