Risk Of Colon Cancer Research Articles

Stage-specific risk of colon and rectal cancer in patients presenting with rectal bleeding or change in bowel habit in primary care: A population-based cohort study

IntroductionRectal bleeding and change in bowel habit are red-flag symptoms for colon and rectal cancer but how they relate to advanced stage disease is not adequately understood. MethodsWe analysed primary care electronic health records data on patients aged 30–99 years. Using logistic regression, we first examined the risk of colon and rectal cancer within 12 months in patients presenting with change in bowel habit and rectal bleeding, and then the risk of advanced stage at diagnosis within cancer cases. We combined the results to estimate risk of advanced stage colon and rectal cancers at diagnosis. ResultsFor both symptoms and sexes, risk of cancer (overall and by stage) increased with increasing age. We illustrate the findings for persons at the highest age-specific observed risk (typically aged around 80). In men, change in bowel habit (CIBH) and rectal bleeding were associated with different risk of advanced stage colon and rectal cancers (e.g., for colon, CIBH = 2.7% (95% CI 2.2–3.1) and rectal bleeding = 1.7% (95% CI 1.4–2.0)), but without evidence of risk difference between the two symptoms for non-advanced disease. The opposite pattern was apparent in women, with both symptoms associated with similar risk of advanced disease, but different risk of non-advanced colon and rectal cancers (e.g., for colon, CIBH = 1.0% (95% CI 0.8–1.3) and rectal bleeding = 1.3% (95% CI 1.1–1.6)). DiscussionChange in bowel habit and rectal bleeding have different age-specific associations with advanced stage disease, which vary by sex. A substantial proportion of cases is diagnosed at non-advanced stage, supporting the need for prompt diagnostic assessment of patients who present with those symptoms, taking into account the age-specific nature of risks.

Kinase Signaling in Colitis-Associated Colon Cancer and Inflammatory Bowel Disease.

Colorectal cancer is a known complication of chronic inflammation of the colon ("colitis-associated colon cancer"). Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Patients with IBD are at increased risk of colon cancer compared to the general population. Kinase signaling pathways play critical roles in both the inflammation and regulating cellular processes such as proliferation and survival that contribute to cancer development. Here we review the interplay of kinase signaling pathways (mitogen-activated protein kinases, cyclin-dependent kinases, autophagy-activated kinases, JAK-STAT, and other kinases) and their effects on colitis-associated colon cancer. We also discuss the role of JAK-STAT signaling in the pathogenesis of IBD and the therapeutic landscape of JAK inhibitors for the treatment of IBD.

The association of the healthy eating index with risk of colorectal cancers (overall and by subsite) among Canadians

BackgroundHealthy dietary patterns characterized by high intake of fruits and vegetables, grains/cereals, and lean meat/fish, and low intake of red/processed meats and refined carbohydrates, have been shown to be associated with reduced risk of colorectal cancer, but evidence regarding their association with colorectal cancer subsites is limited. Hence, this study was conducted to assess the association of a healthy dietary pattern, as reflected in the Healthy Eating Index (HEI) (a composite score based on consumption of various food groups), with risk of colorectal cancer, overall and by subsite. MethodsWe conducted a case-cohort study in the Canadian Study of Diet, Lifestyle and Health (CSDLH). The study included all cases of incident colorectal cancer in the entire cohort, and an age-stratified subcohort of 3185 women and 2622 men. Cox regression models were used to estimate hazard ratios (HR) for the association between the HEI and the risk of colorectal cancer, overall and by subsite. We also assessed the association by sex and by selected metabolic factors. ResultsFor both sexes combined, the highest quintile of the HEI score was inversely associated with risk of colorectal cancer, colon cancer and proximal colon cancer (HR: 0.65; 95% CI: 0. 49–0.85, HR: 0.60, 95% CI: 0.44–0.83 and HR: 0.54, 95% CI: 0.35–0.85, respectively). However, these associations were mostly observed among men (HR: 0.56; 95% CI: 0.38–0.81, HR: 0.44, 95% CI: 0.28–0.69 and HR: 0.26; 95% CI: 0.12–0.56, for colorectal cancer, colon cancer and proximal colon cancer, respectively; p-interactions=0.029, 0.032 and 0.063, respectively). An inverse association was also observed between the HEI and risk of colorectal cancer among normal weight participants, overweight/obese participants, non-smokers, non-alcohol drinkers and participants who were physically inactive. ConclusionA healthy dietary pattern may reduce risk of colorectal cancer, particularly among men.

The Mysterious Association Between Atrial Fibrillation and Cancer: A Literature Review.

Atrial fibrillation (AF) is a prevalent cardiac dysrhythmia, particularly affecting older adults, with its prevalence rising due to the aging population. AF is linked to several adverse outcomes, including embolic stroke, heart failure, and cancer. The association between AF and cancer is intricate and not yet fully understood. Studies suggest that the rise in cancer survivorship, along with cancer treatments, may contribute to an increased incidence of AF among cancer patients. This literature review was conducted using various databases to explore the relationship between AF and cancer. Studies from 2002 to 2022 were included, focusing on the adult population. Independent authors evaluated and validated the studies, ensuring rigorous methodology. The connection between AF and cancer appears multifaceted. There is evidence of increased cancer incidence within the first few months following an AF diagnosis, with potential shared risk factors like age, obesity, and smoking. Medications used to treat AF, notably amiodarone, were associated with increased cancer risk. Colon cancer risk might be linked to anticoagulation-induced gastrointestinal bleeding. It remains uncertain whether AF diagnosis leads to early cancer detection or if cancer itself contributes to AF development. The complex interplay between AF and cancer involves shared risk factors, potential medication-related influences, and unclear causal directions. The intricacies of this relationship warrant further research to clarify the underlying mechanisms and potential interactions. A comprehensive meta-analysis could provide more insights into this intriguing association and guide future clinical interventions.

Influence of MTHFR polymorphism, alone or in combination with smoking and alcohol consumption, on cancer susceptibility.

5,10-methylenetetrahydrofolate reductase (MTHFR) mutations play a significant role in various types of cancers, serving as crucial regulators of folate levels in this process. Several studies have examined the effects of smoking and drinking on MTHFR-related cancers, yielding inconsistent results. Therefore, the objective of this study was to evaluate the magnitude of the effects of gene-smoking or gene-drinking interactions on cancer development. We conducted a comprehensive literature search in PubMed, Web of Science, CNKI, and Wan Fang databases up until May 10th, 2022, to identify relevant articles that met our inclusion criteria. The extracted data from these studies were used to calculate the overall odds ratio (OR) and corresponding 95% confidence interval (95% CI) using either a fixed-effect or random-effect model in Stata version 11.2. Stratified analyses were performed based on ethnicity, control group origin, and cancer classification to assess the risk of cancers associated with gene-smoking or gene-drinking interactions. Sensitivity analyses were conducted to investigate potential sources of heterogeneity, and publication bias was assessed using the Begg's test and Egger's test. Additionally, regression analysis was employed to explore the influence of relevant variables on heterogeneity. To evaluate the statistical correlations, analytical methods such as the false-positive report probability and the Bayesian false discovery probability were applied to assess the reliability of the findings. In our meta-analysis, a total of 47 articles were included, comprising 13,701 cases and 21,995 controls for the C677T polymorphism and 5,149 cases and 8,450 controls for the A1298C polymorphism. The results indicated a significant association between C677T polymorphism and cancer risks when combined with smoking (CT + TT vs CC, OR [95% CI] = 1.225 [1.009-1.487], p = 0.041). Stratified analysis further revealed a significant increase in liver cancer risk for individuals with the C677T when combined with smoking (liver cancer: CT + TT vs CC, OR [95% CI] = 1.564 [1.014-2.413], p = 0.043), particularly among Asian smokers (CT + TT vs CC, OR [95% CI] = 1.292 [1.007-1.658], p = 0.044). Regarding the A1298C polymorphism, an elevated risk of cancer was observed in mixed populations alone (CC + AC vs AA, OR [95% CI] = 1.609 [1.087-2.381], p = 0.018), as well as when combined with smoking (CC + AC vs AA, OR [95% CI] = 1.531 [1.127-2.080], p = 0.006). In non-drinkers, C677T polymorphism was found to be associated with esophageal cancer risk (C677T: CT + TT vs CC, OR [95% CI] = 1.544 [1.011-2.359], p = 0.044) and colon cancer risk (CC + AC vs AA, OR [95% CI] = 1.877 [1.166-3.054], p = 0.010), but there was no clear link between this polymorphism and cancer risk among drinkers. The association between the C677T polymorphism and cancer risk among smokers was found to be significant, suggesting that the combination of tobacco and the C677T polymorphism may enhance the carcinogenic process, particularly in liver cancer. However, no similar relationship was observed for the A1298C polymorphism. Interestingly, significantly increased cancer risk was observed in individuals with C677T genetic variants who were nondrinkers, but not among drinkers. These findings highlight the potential role of the C677T polymorphism in modifying cancer risk in specific contexts, such as smoking and alcohol consumption.

Physical activity and cancer risk: a dose-response analysis for the Global Burden of Disease Study 2019.

Adopting a healthy lifestyle, including regular physical activity, is widely believed to decrease cancer risk. This study aimed to quantitatively establish the dose-response relationships between total physical activity and the risk of breast, colon, lung, gastric, and liver cancers. A systematic review and dose-response analysis were conducted using PubMed and Embase from January 1, 1980 to March 20, 2023. Prospective cohort studies that examined the association between physical activity and the risks of any of the 5 outcomes were included. The search was confined to publications in the English language with a specific focus on human studies. Physical activity is standardized by using the data from US National Health and Nutrition Examination Surveys (NHANES) and the Global Burden of Disease 2019 database. A total of 98 studies, involving a combined population of 16,418,361 individuals, were included in the analysis. Among the included studies, 57 focused on breast cancer, 17 on lung cancer, 23 on colon cancer, 5 on gastric cancer, and 7 on liver cancer. Overall, elevated levels of physical activity exhibited an inverse correlation with the risk of cancer. The dose-response curve for lung cancer exhibited a non-linear pattern, with the greatest benefit risk reduction observed at 13,200 MET-minutes/week of physical activity, resulting in a 14.7% reduction in risk (relative risk 0.853, uncertainty interval 0.798 to 0.912) compared to the inactive population. In contrast, the dose-response curves for colon, gastric, breast, and liver cancers showed linear associations, indicating that heightened levels of total physical activity were consistently associated with reduced cancer risks. However, the increase in physical activity yielded a smaller risk reduction for colon and gastric cancers compared to breast and liver cancers. Compared to individuals with insufficient activity (total activity level < 600 MET-minutes/week), individuals with high levels of activity (≥ 8,000 MET-minutes/week) experienced a 10.3% (0.897, 0.860 to 0.934) risk reduction for breast cancer; 5.9% (0.941, 0.884 to 1.001) for lung cancer; 7.1% (0.929, 0.909 to 0.949) for colon cancer; 5.1% (0.949, 0.908 to 0.992) for gastric cancer; 17.1% (0.829, 0.760 to 0.903) for liver cancer. This study demonstrated a significant inverse relationship between total physical activity and the risk of breast, gastric, liver, colon, and lung cancers.

A review on banana flower: Nutritional composition, processed products and health benefits

India is the world’s largest producer of banana with 13.90 million tons followed by Uganda (10.14 million tons). Banana blossom also known as a banana heart, is a fleshy purple - skinned flower shaped like tear, which grows at the end of banana fruit cluster. Now days researchers aimed to addressing dietary related diseases through promotion of food products enriched with high protein, vitamins, minerals and dietary fiber. Banana blossom is rich source of nutrients and antioxidants which have several health benefits. The juice from the male bud provides an apparent remedy for stomach problems in people of all ages. Banana blossom is a popular dish in Sri Lanka. It is consumed as a curry as well as a boiled or deep fried salad with rice and wheat bread. It is generally valued as a fiber-rich source. Dietary fiber has demonstrated its benefits in health and disease prevention in medical nutrition therapy. Consumption of dietary fiber is known to lower blood cholesterol level, normalize blood glucose and insulin level, promote normal laxation, avoid constipation, prevent diverticulosis and diverticukitis, lower the risk of colon cancer and breast cancer and prevent obesity. The flower has been used to treat bronchitis, constipation and peptic ulcer. The extract has anti-oxidant property that prevents free radicals and control cell and tissue damage. Based on the main components of banana flower extract and its anti-oxidant properties, we hypothesized that the banana flower extract may have anticancer activities against cancer cell lines.

Genetic Approaches to Increase Arabinoxylan and β-Glucan Content in Wheat.

Wheat is one of the three staple crops feeding the world. The demand for wheat is ever increasing as a relatively good source of protein, energy, nutrients, and dietary fiber (DF) when consumed as wholemeal. Arabinoxylan and β-glucan are the major hemicelluloses in the cell walls and dietary fiber in wheat grains. The amount and structure of DF varies between grain tissues. Reducing post-prandial glycemic response as well as intestinal transit time and contribution to increased fecal bulk are only a few benefits of DF consumption. Dietary fiber is fermented in the colon and stimulates growth of beneficial bacteria producing SCFA, considered responsible for a wide range of health benefits, including reducing the risk of heart disease and colon cancer. The recommended daily intake of 25-30 g is met by only few individuals. Cereals cover nearly 40% of fiber in the Western diet. Therefore, wheat is a good target for improving dietary fiber content, as it would increase the fiber intake and simultaneously impact the health of many people. This review reflects the current status of the research on genetics of the two major dietary fiber components, as well as breeding approaches used to improve their quantity and quality in wheat grain.

Association between tea consumption and colorectal cancer: a systematic review and meta-analysis of a population-based study

PurposeA meta-analysis study was performed to systematically assess the association between tea consumption and CRC risk.MethodsCochrane Library, Embase, PubMed, and Web of Science were retrieved to collect articles in English since 24 July 2023. Databases were searched and evaluated by two reviewers independently.We screened the literature based on inclusion and exclusion criteria. After determining the random effect model or fixed utility model based on a heterogeneity test, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated.ResultsWe included fourteen articles in this meta-analysis. We analyzed the data using a random effect model to explore the association between tea consumption and CRC because of apparent heterogeneity (P < 0.001, I2 = 99.5%). The combined results of all tests showed that there is no statistically significant association between tea consumption and CRC risk (OR = 0.756, 95%CI = 0.470–1.215, P = 0.247). Subsequently, subgroup analysis and sensitivity analysis were performed. Excluding any single study, the overall results ranged from 0.73 (95%CI = 0.44–1.20) to 0.86 (95%CI = 0.53–1.40). It was determined that there was no significant publication bias between tea consumption and CRC risk (P = 0.064) by Egger's tests.ConclusionsThe results indicated that tea consumption may not be significantly associated with the development of CRC.Implications of key findingsTea reduces colon cancer risk by 24%, but the estimate is uncertain. The actual effect on risk can range from a reduction of 51% to an increase of 18%, but regional and population differences may cause differences.

Increased risk of colon cancer after acute appendicitis: a nationwide, population-based study

Acute appendicitis is the most common digestive disease requiring emergency surgery. Colorectal cancer is the third most common cancer in France. An increased risk of colorectal cancer after acute appendicitis has been suggested. We aimed to assess the frequency of hospitalization for colon cancer after appendicitis in a nationwide analysis. Using the French Hospital Discharge Database (PMSI), we included all patients aged 18-59 years presenting with acute appendicitis between 2010 and 2015. Univariate and multivariate analyses were performed to compare colon cancer occurrence in these patients vs a control-matched population with a hospital stay for trauma in the same period. Patients presenting strong risk factors for colorectal cancer were excluded. A total of 230,349 patients with acute appendicitis (exposed group) were included. We used a propensity score to match each exposed patient with two unexposed patients (controls) to ensure the comparability of the groups, resulting in a control group of 460,698 patients. Univariate analysis found significantly more colon cancer in the appendicitis group, especially during the first year after appendicitis (5 per 10,000 vs 1 per 10,000, p<0.000, this corresponds to 111 patients in the appendicitis group), namely within the first 6 months. Survival analysis confirmed patients treated for appendicitis present a 4 times higher risk of being diagnosed with colon cancer than control patients during the first year of follow-up (sHR=4.67 (95% CI: 3.51-6.21), and 8 times higher during the first 6 months (sHR=8.39; 95% CI: 5.41-12.99). The association was even more marked for right-sided colon cancer (sHR=8.25; 95% CI: 5.03-13.54 during the 1st year). While the risk of diagnosis of colon cancer was also significant for patients over 40 years, it was even greater in patients under 40 years, who had between a 6-fold and 12-fold increase in risk. In this population-based study, we found that acute appendicitis seems to be a warning sign for colon cancer (reverse causality) in both middle-aged and younger adults. The risk of presenting with cancer colon was higher during the first six months after acute appendicitis. This raises the issue of routine diagnostic work-up in adults presenting with acute appendicitis. Regional Council of Burgundy.

Association of meat consumption with the risk of gastrointestinal cancers: a systematic review and meta-analysis

BackgroundThe association between gastrointestinal cancer and types of meat consumption, including red meat, processed meat, or a combination of both, remains disputable. Therefore, we performed a systematic review and meta-analysis of prospective cohort studies to estimate the association between meat consumption and gastrointestinal cancer risk.MethodsPubMed, EmBase, and the Cochrane library databases were searched systematically for eligible studies that investigated the relation between meat consumption and the risk of developing gastrointestinal cancers, including esophageal cancer (EC), gastric cancer (GC), colorectal cancer (CRC), colon cancer (CC), rectal cancer (RC), pancreatic cancer (PC), and hepatocellular carcinoma (HCC) throughout February, 2023. The pooled relative risk (RR) with 95% confidence interval (CI) was assigned as an effect estimate and calculated using a random-effects model with inverse variance weighting.ResultsForty cohorts comprising 3,780,590 individuals were selected for the final quantitative analysis. The summary results indicated that a higher red meat consumption was associated with an increased risk of CRC (RR: 1.09; 95% CI: 1.02–1.16; P = 0.007) and CC (RR: 1.13; 95% CI: 1.03–1.25; P = 0.011). Moreover, a higher processed meat consumption was associated with an increased risk of CRC (RR: 1.19; 95% CI: 1.13–1.26; P < 0.001), CC (RR: 1.24; 95% CI: 1.13–1.26; P < 0.001), and RC (RR: 1.24; 95% CI: 1.08–1.42; P = 0.002). Furthermore, a higher total consumption of red and processed meat was associated with an increased risk of CRC (RR: 1.13; 95% CI: 1.06–1.20; P < 0.001), CC (RR: 1.17; 95% CI: 1.04–1.33; P = 0.012), and RC (RR: 1.20; 95% CI: 1.04–1.39; P = 0.016). Finally, the strength of higher consumption of total red and processed meat with the risk of GC, and higher consumption of red meat with the risk of RC in subgroup of high adjusted level was lower than subgroup of moderate adjusted level, while the strength of higher consumption of processed meat with the risk of RC and HCC in subgroup of follow-up ≥ 10.0 years was higher than subgroup of follow-up < 10.0 years.ConclusionsThis study found that meat consumption was associated with an increased risk of CRC, CC, and RC, and dietary intervention could be considered an effective strategy in preventing CRC.

Anti-IFI16 Antibodies in Inflammatory Bowel Disease and Their Variation with Infliximab Therapy in Comparison to Other Modalities of Treatment

Abstract Background Amatory bowel diseases (IBDs) are remittent or progressive conditions that may affect the entire gastrointestinal tract and the colonic mucosa and are associated with an increased risk for colon cancer. Patients with mucosal lesions may not have clinical symptoms, or only present with mild symptoms. Objective measurements are required to assess and monitor IBD disease activity. Moreover responses to treatments must be closely monitored to determine effectiveness and avoid disease complications. Aim of the Work The aim of this study is to assess the utility of IFI16 antibodies as a predictor of infliximab-induced remission in IBD patients in comparison to other modalities of treatment. Patients and Methods A Comparative cross sectional study in internal medicine and gastroenterology outpatient clinic at Ain Shams University Hospital. With 60 IBD patients are included in this study divided into three groups. Results Patients with low levels of IgG antibodies against IFI16 at baseline had a higher probability of a clinical response or remission at the end of induction therapy with IFX (OR 1/4 0.143; 95% CI 0.027–0.761). The only statistically significant association found in patients with UC was that between anti-IFI16 IgG and extensive colitis (E3) (OR 1/4 7.255; 95% CI 2.452–21.463; P 1/4 0.0001) (data not shown). Conclusion Overall, the findings presented in this study deserve more investigation to verify the possibility of exploiting a patient’s reac- tivity against the IFI16 autoantigen as a predictive marker of response to IFX therapy. Anti-IFI16 IgG titers may be of great clinical relevance and provide guidance when tailoring therapeutic choices to individual patients.

Clinical plasma cells-related genes to aid therapy in colon cancer

The tumor immune microenvironment (TIME) of colon cancer (CC) has been associated with extensive immune cell infiltration (IMI). Increasing evidence demonstrated that plasma cells (PC) have an extremely important role in advance of antitumor immunity. Nonetheless, there is a lack of comprehensive analyses of PC infiltration in clinical prognosis and immunotherapy in CC. This study systematically addressed the gene expression model and clinical information of CC patients. Clinical samples were obtained from the TCGA (The Cancer Genome Atlas) databases. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), GSVA, and the MAlignant Tumors using Expression data (ESTIMATE) algorithm were employed to research the potential mechanism and pathways. Immunophenoscore (IPS) was obtained to evaluate the immunotherapeutic significance of risk score. Half maximal inhibitory concentration (IC50) of chemotherapeutic medicine was predicted by employing the pRRophetic algorithm. A total of 513 CC samples (including 472 tumor samples and 41 normal samples) were collected from the TCGA-GDC database. Significant black modules and 313 candidate genes were considered PC-related genes by accessing WGCNA. Five pivotal genes were established through multiple analyses, which revealed excellent prognostic. The underlying correlation between risk score with tumor mutation burden (TMB) was further explored. In addition, the risk score was obviously correlated with various tumor immune microenvironment (TIME). Also, risk CC samples showed various signaling pathways activity and different pivotal sensitivities to administering chemotherapy. Finally, the biological roles of the CD177 gene were uncovered in CC.

Animal models of inflammatory bowel disease: novel experiments for revealing pathogenesis of colitis, fibrosis, and colitis-associated colon cancer.

Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is a lifelong disease that manifests with chronic intestinal inflammation, sequential fibrosis, and an increased risk of colitis-associated colon cancer (CAC). The combined effects of genetic, immunological, environmental, and microbial factors render it difficult to determine the specific mechanism underlying the induction and perpetuation of IBD. Various animal models of IBD have contributed enormously to the understanding of IBD pathogenesis in terms of genomics, transcriptomics, proteomics, microbiome, and drug development of novel therapeutics. Although comprehensive research on IBD has been enabled by advanced technologies, such as genetically engineered models, there is a great need to develop relevant in vivo models of colitis and fibrosis. Here, we review 4 categories of animal models of acute and chronic intestinal inflammation, fibrosis, and CAC: chemically induced, genetically engineered, T cell transfer, and spontaneous gene mutation models.

Refined fiber inulin promotes inflammation-associated colon tumorigenesis by modulating microbial succinate production.

There is an increased risk of colon cancer associated with inflammatory bowel disease (IBD). Dietary fibers (DFs) naturally present in vegetables and whole grains offer numerous beneficial effects on intestinal health. However, the effects of refined DFs on intestinal health remain unclear. Therefore, we elucidated the impact of the refined DF inulin on colonic inflammation and tumorigenesis. Four-week-old wild-type (WT) mice were fed diets containing insoluble DF cellulose (control) or refined DF inulin for 4 weeks. A subgroup of mice was then switched to drinking water containing dextran sulfate sodium (DSS, 1.4% wt/vol) for colitis induction. In another subgroup of mice, colitis-associated colorectal cancer (CRC) was initiated with three 7-day alternate cycles of DSS following an initial dose of mutagenic substance azoxymethane (AOM; 7.5 mg/kg body weight; i.p.). Post 7 weeks of AOM treatment, mice were euthanized and examined for CRC development. Mice consuming inulin-containing diet exhibited severe colitis upon DSS administration, as evidenced by more body weight loss, rectal bleeding, and increased colonic inflammation than the DSS-treated control group. Correspondingly, histological analysis revealed extensive disruption of colon architecture and massive infiltration of immune cells in the inulin-fed group. We next examined the effect of inulin on CRC development. Surprisingly, significant mortality (~50%) was observed in the inulin-fed but not in the control group during the DSS cycle. Consequently, the remaining inulin-fed mice, which completed the study exhibited extensive colon tumorigenesis. Immunohistochemical characterization showed comparatively high expression of the cell proliferation marker Ki67 and activation of the Wnt signaling in tumor sections obtained from the inulin-fed group. Gut microbiota and metabolite analysis revealed expansion of succinate producers and elevated cecal succinate in inulin-fed mice. Human colorectal carcinoma cells (HCT116) proliferated more rapidly when supplemented with succinate in an inflamed environment, suggesting that elevated luminal succinate may contribute to tumorigenesis. Our study uncovers that supplementation of diet with refined inulin induces abnormal succinate accumulation in the intestinal lumen, which in part contributes to promoting colon inflammation and tumorigenesis.

Adherence to the Paleolithic diet and Paleolithic-like lifestyle reduce the risk of colorectal cancer in the United States: a prospective cohort study

BackgroundThe plant-based paleolithic diet (PD) and the paleolithic-like lifestyle (PLL) may reduce the risk of chronic diseases, including colorectal adenomas. These dietary and lifestyle approaches are proposed to exert their effects through mechanisms such as reducing inflammation, oxidative stress, and insulin levels. However, whether PD and PLL is associated with the risk of colorectal cancer (CRC) has not been determined.MethodsA cohort of 74,721 individuals who participated in the PLCO study were included in this analysis. Adherence to the PD and PLL was assessed using PD and PLL scores, where higher scores indicated greater adherence. Multivariable Cox models were utilized to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of CRC and its subsites (proximal colon cancer and distal CRC). Subgroup analyses were conducted to identify potential effect modifiers.ResultsDuring a mean follow-up of 9.2 years, a total of 694 CRC cases were identified. Participants in the highest compared with the lowest quartiles of PD score had a lower risk of CRC (Q4 vs Q1: HR 0.76, 95% CI 0.61–0.95, Ptrend = 0.009) and proximal colon cancer (Q4 vs Q1: HR 0.73, 95% CI 0.55–0.97, Ptrend = 0.02). A stronger inverse association was observed for PLL score with the risk of CRC (Q4 vs Q1: HR 0.64, 95% CI 0.51–0.81, Ptrend < 0.001), proximal colon (Q4 vs Q1: HR 0.62, 95% CI 0.46–0.83, Ptrend = 0.001) and distal CRC (Q4 vs Q1: HR 0.69, 95% CI 0.48–0.98, Ptrend = 0.03). Subgroup analyses revealed the inverse association of PD score with the risk of CRC was more pronounced in participants with BMI < 30 (Q4 vs Q1: HR 0.68, 95% CI 0.53–0.87) than in those with BMI ≥ 30 (Q4 vs Q1: HR 1.07, 95% CI 0.68–1.67) (Pinteraction = 0.02).ConclusionsOur findings suggest that adhering to the PD and PLL could be a new option to reduce CRC risk.

Exercise and diet in colorectal cancer prevention and therapy

Colorectal carcinoma is a leading cause of cancer diseases in Europe. Due to modern therapies survival rate is increasing. Nevertheless, cancer and its treatment is associated with significant morbidity. Physical activity appears as having a positive impact on cancer risk, as well as, reducing peri- and postoperative morbidity and mortality. We searched pubmed and googlescholar for English- and German-language studies from inception to September 2022. The search terms physical activity, colon cancer, colorectal cancer, diet, survivors. prehabilitation, postoperative morbidity, quality of life and outcome were used. Guidelines of national advisory commmittees and Cochrane reviews were included. There is considerable evidence that physical activity is associated with reduced risk of colon cancer, epigenetic mechanisms play a central role in connection. Different studies showed a risk reduction of 12 to 27 percent. A prehabilitation programme consisting of exercise, nutritional intervention, and psychosocial rehabilitation can reduce peri- and postoperative complications. Aerobic exercise and strength training can improve survival rates and overall mortality. However, a causal relationship between nutritional treatment and cancer related symptoms (e.g. fatigue) is missing. There is a wide range of scientific papers on the influence of physical activity and nutrition; nevertheless, its influence on the various stages of colorectal disease are not addressed adequately. Recommendations concerning prehabilitation and tertiary prevention can only be given on the basis of heterogeneous trial data.

Association Between Cardiorespiratory Fitness and Cancer Incidence and Cancer-Specific Mortality of Colon, Lung, and Prostate Cancer Among Swedish Men

Cardiorespiratory fitness (CRF) levels appear to be an important risk factor for cancer incidence and death. To examine CRF and prostate, colon, and lung cancer incidence and mortality in Swedish men, and to assess whether age moderated any associations between CRF and cancer. A prospective cohort study was conducted in a population of men who completed an occupational health profile assessment between October 1982 and December 2019 in Sweden. Data analysis was performed from June 22, 2022, to May 11, 2023. Cardiorespiratory fitness was assessed as maximal oxygen consumption, estimated using a submaximal cycle ergometer test. Data on prostate, colon, and lung cancer incidence and mortality were derived from national registers. Hazard ratios (HRs) and 95% CIs were calculated using Cox proportional hazards regression. Data on 177 709 men (age range, 18-75 years; mean [SD] age, 42 [11] years; mean [SD] body mass index, 26 [3.8]) were analyzed. During a mean (SD) follow-up time of 9.6 (5.5) years, a total of 499 incident cases of colon, 283 of lung, and 1918 of prostate cancer occurred, as well as 152 deaths due to colon cancer, 207 due to lung cancer, and 141 deaths due to prostate cancer. Higher levels of CRF (maximal oxygen consumption as milliliters per minute per kilogram) were associated with a significantly lower risk of colon (HR, 0.98, 95% CI, 0.96-0.98) and lung cancer (HR, 0.98; 95% CI, 0.96-0.99) incidence, and a higher risk of prostate cancer incidence (HR, 1.01; 95% CI, 1.00-1.01). Higher CRF was associated with a lower risk of death due to colon (HR, 0.98; 95% CI, 0.96-1.00), lung (HR, 0.97; 95% CI, 0.95-0.99), and prostate (HR, 0.95; 95% CI, 0.93-0.97) cancer. After stratification into 4 groups and in fully adjusted models, the associations remained for moderate (>35-45 mL/min/kg), 0.72 (0.53-0.96) and high (>45 mL/min/kg), 0.63 (0.41-0.98) levels of CRF, compared with very low (<25 mL/min/kg) CRF for colon cancer incidence. For prostate cancer mortality, associations remained for low (HR, 0.67; 95% CI, 0.45-1.00), moderate (HR, 0.57; 95% CI, 0.34-0.97), and high (HR, 0.29; 95% CI, 0.10-0.86) CRF. For lung cancer mortality, only high CRF (HR, 0.41; 95% CI, 0.17-0.99) was significant. Age modified the associations for lung (HR, 0.99; 95% CI, 0.99-0.99) and prostate (HR, 1.00; 95% CI, 1.00-1.00; P < .001) cancer incidence, and for death due to lung cancer (HR, 0.99; 95% CI, 0.99-0.99; P = .04). In this cohort of Swedish men, moderate and high CRF were associated with a lower risk of colon cancer. Low, moderate, and high CRF were associated with lower risk of death due to prostate cancer, while only high CRF was associated with lower risk of death due to lung cancer. If evidence for causality is established, interventions to improve CRF in individuals with low CRF should be prioritized.

No association between cholecystectomy and risk of colorectal cancer: a meta-analysis of cohort studies.

Cohort studies have reported an association between colorectal cancer and cholecystectomy. However, the conclusions are inconsistent. Thus, this meta-analysis will quantify the risk of colorectal cancer following cholecystectomy. PubMed, EMBASE and Cochrane Library databases were searched for relevant cohort studies. The quality of individual observational studies was assessed using the Newcastle-Ottawa Quality Assessment Scale. The relative risk of colorectal cancer after cholecystectomy was calculated using STATA 14.0 software. Subgroup and sensitivity analyses were used to examine the source of heterogeneity. Funnel plots and Egger's test were finally performed to assess the publication bias. This meta-analysis included 14 studies comprising 2,283,616 subjects. Pooled analysis indicated that cholecystectomy was not a risk factor for colorectal cancer (Colorectal: RR 1.06; 95% CI 0.75-1.51, p = 0.739 Colon: RR 1.30; 95% CI 0.88-1.93, p = 0.182 Rectal: RR 0.99; 95% CI 0.74-1.32, p = 0.932). Subgroup showed that patients are at an increased risk of sigmoid colon following cholecystectomy (RR 1.42; 95% CI 1.27-1.58, p = 0.000). Furthermore, it was shown that both females and males undergoing cholecystectomy may have higher risks of colon cancer (Female: RR = 1.47, 95% CI 1.01-2.14, P = 0.042 Male: RR = 1.32; 95% CI 1.07-1.63, P = 0.010), which is similarly observed in the right colon (Female: RR 1.99; 95% CI 1.31-3.03, p = 0.001, P = 0.017 Male: RR 1.68; 95% CI 0.81-3.49, p = 0.166). No clear evidence to support the association between cholecystectomy and an increased risk of colorectal cancer. For patients with valid indications, timely cholecystectomy could be performed without the risk of colorectal cancer.

CYP eicosanoid pathway mediates colon cancer-promoting effects of dietary linoleic acid.

Human and animal studies support that consuming a high level of linoleic acid (LA, 18:2ω-6), an essential fatty acid and key component of the human diet, increases the risk of colon cancer. However, results from human studies have been inconsistent, making it challenging to establish dietary recommendations for optimal LA intake. Given the importance of LA in the human diet, it is crucial to better understand the molecular mechanisms underlying its potential colon cancer-promoting effects. Using LC-MS/MS-based targeted lipidomics, we find that the cytochrome P450 (CYP) monooxygenase pathway is a major pathway for LA metabolism in vivo. Furthermore, CYP monooxygenase is required for the colon cancer-promoting effects of LA, since the LA-rich diet fails to exacerbate colon cancer in CYP monooxygenase-deficient mice. Finally, CYP monooxygenase mediates the pro-cancer effects of LA by converting LA to epoxy octadecenoic acids (EpOMEs), which have potent effects on promoting colon tumorigenesis via gut microbiota-dependent mechanisms. Overall, these results support that CYP monooxygenase-mediated conversion of LA to EpOMEs plays a crucial role in the health effects of LA, establishing a unique mechanistic link between dietary fatty acid intake and cancer risk. These results could help in developing more effective dietary guidelines for optimal LA intake and identifying subpopulations that may be especially vulnerable to LA's negative effects.