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Background: While adherence to cancer prevention recommendations is linked to lower risk of colorectal cancer (CRC), few have studied associations across the entire spectrum of colorectal carcinogenesis. Here, we studied the relationship of the standardized 2018 World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) Score for cancer prevention recommendations with detection of colorectal lesions in a screening setting. As a secondary objective, we examined to what extent the recommendations were being followed in an external cohort of CRC patients. Methods: Adherence to the seven‐point 2018 WCRF/AICR Score was measured in screening participants receiving a positive fecal immunochemical test and in CRC patients participating in an intervention study. Dietary intake, body fatness and physical activity were assessed using self‐administered questionnaires. Multinomial logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for screen‐detected lesions. Results: Of 1486 screening participants, 548 were free from adenomas, 524 had non‐advanced adenomas, 349 had advanced lesions and 65 had CRC. Adherence to the 2018 WCRF/AICR Score was inversely associated with advanced lesions; OR 0.82 (95% CI 0.71, 0.94) per score point, but not with CRC. Of the seven individual components included in the score, alcohol, and BMI seemed to be the most influential. Of the 430 CRC patients included in the external cohort, the greatest potential for lifestyle improvement was seen for the recommendations concerning alcohol and red and processed meat, where 10% and 2% fully adhered, respectively. Conclusions: Adherence to the 2018 WCRF/AICR Score was associated with lower probability of screen‐detected advanced precancerous lesions, but not CRC. Although some components of the score seemed to be more influential than others (i.e., alcohol and BMI), taking a holistic approach to cancer prevention is likely the best way to prevent the occurrence of precancerous colorectal lesions. [ABSTRACT FROM AUTHOR]

Background: Colorectal cancer survivors are not only at risk for recurrent disease but also at increased risk of comorbidities such as other cancers, cardiovascular disease, diabetes, hypertension and functional decline. In this trial, we aim at investigating whether a diet in accordance with the Norwegian food-based dietary guidelines and focusing at dampening inflammation and oxidative stress will improve long-term disease outcomes and survival in colorectal cancer patients.Methods/design: This paper presents the study protocol of the Norwegian Dietary Guidelines and Colorectal Cancer Survival study. Men and women aged 50-80 years diagnosed with primary invasive colorectal cancer (Stage I-III) are invited to this randomized controlled, parallel two-arm trial 2-9 months after curative surgery. The intervention group (n = 250) receives an intensive dietary intervention lasting for 12 months and a subsequent maintenance intervention for 14 years. The control group (n = 250) receives no dietary intervention other than standard clinical care. Both groups are offered equal general advice of physical activity. Patients are followed-up at 6 months and 1, 3, 5, 7, 10 and 15 years after baseline. The study center is located at the Department of Nutrition, University of Oslo, and patients are recruited from two hospitals within the South-Eastern Norway Regional Health Authority. Primary outcomes are disease-free survival and overall survival. Secondary outcomes are time to recurrence, cardiovascular disease-free survival, compliance to the dietary recommendations and the effects of the intervention on new comorbidities, intermediate biomarkers, nutrition status, physical activity, physical function and quality of life.Discussion: The current study is designed to gain a better understanding of the role of a healthy diet aimed at dampening inflammation and oxidative stress on long-term disease outcomes and survival in colorectal cancer patients. Since previous research on the role of diet for colorectal cancer survivors is limited, the study may be of great importance for this cancer population.Trial Registration: ClinicalTrials.gov Identifier: NCT01570010 . [ABSTRACT FROM AUTHOR]

DNA damage caused by oxidative reactions plays a crucial role in the pathogenesis of colorectal cancer (CRC). In a previous cross-sectional study, CRC patients diagnosed with regional disease (stage III) exhibited a higher level of DNA base oxidation in peripheral blood mononuclear cells (PBMCs) 2–9 months post-surgery compared to those with localized disease (stage I-II). To further explore this observation over time, the present study aimed to investigate DNA base oxidation in CRC patients with localized versus regional disease 6 and 12 months after the initial measurements. The present study included patients enrolled in the randomized controlled trial Norwegian Dietary Guidelines and Colorectal Cancer Survival (CRC-NORDIET). The standard comet assay, modified with the lesion-specific enzyme formamidopyrimidine DNA glycosylase (Fpg), was applied to measure DNA base oxidation in PBMCs at the 6- and 12-month follow-ups. Of the 255 patients assessed at baseline, 156 were included at the 6-month follow-up, with 89 of these patients included in the 12-month follow-up. In contrast to our observation at baseline, there were no significant differences in the levels of DNA base oxidation between patients diagnosed with localized disease and those with regional involvement at the 6- and 12-month follow-up visits (P = 0.81 and P = 0.09, respectively). Patients with stage III disease exhibited a significant decrease in the levels of DNA base oxidation from baseline to 6 months (P < 0.01) and baseline to 12 months (P = 0.03), but no significant difference from 6 to 12 months (P = 0.80). In conclusion, the initially elevated levels of DNA base oxidation in PBMCs, observed 2–9 months post-surgery in patients diagnosed with regional disease (stage III), subsequently decreased to levels comparable to patients with localized disease (stage I-II) at the 6- and 12-month follow-ups. [Display omitted] • Elevated DNA base oxidation in colorectal stage III patients 2–9 months post-surgery. • DNA base oxidation levels comparable to stage I-II during a one-year follow-up. • Enzyme-modified comet assay serve as a valuable biomarker for DNA base oxidation. [ABSTRACT FROM AUTHOR]

DNA repair is essential to maintain genomic integrity and may affect colorectal cancer (CRC) patients' risk of secondary cancers, treatment efficiency, and susceptibility to various comorbidities. Bioactive compounds identified in plant foods have the potential to modulate DNA repair mechanisms, but there is limited evidence of how dietary factors may affect DNA repair activity in CRC patients in remission after surgery. The aim of this study was to investigate the effect of a 6-month personalized intensive dietary intervention on DNA repair activity in post-surgery CRC patients (stage I-III). The present study included patients from the randomized controlled trial CRC-NORDIET, enrolled 2–9 months after surgery. The intervention group received an intensive dietary intervention emphasizing a prudent diet with specific plant-based foods suggested to dampen inflammation and oxidative stress, while the control group received only standard care advice. The comet-based in vitro repair assay was applied to assess DNA repair activity, specifically base excision repair (BER), in peripheral blood mononuclear cells (PBMCs). Statistical analyses were conducted using gamma generalized linear mixed models (Gamma GLMM). A total of 138 CRC patients were included, 72 from the intervention group and 66 from the control group. The BER activity in the intervention group did not change significantly compared to the control group. Our findings revealed a substantial range in both inter- and intra-individual levels of BER. In conclusion, the results do not support an effect of dietary intervention on BER activity in post-surgery CRC patients during a 6-month intervention period. [Display omitted] • DNA repair is essential to maintain genomic integrity. • Prudent diet does not moderate base excision repair in colorectal cancer patients. • Base excision repair activity varies in non-metastatic colorectal cancer remission. • Comet-based in vitro repair assay serve as a valuable biomarker for DNA repair. [ABSTRACT FROM AUTHOR]

Accumulation of DNA damage is a critical feature of genomic instability, which is a hallmark of various cancers. The enzyme-modified comet assay is a recognized method to detect specific DNA lesions at the level of individual cells. In this cross-sectional investigation, we explore possible links between clinicopathological and treatment related factors, nutritional status, physical activity and function, and DNA damage in a cohort of colorectal cancer (CRC) patients with non-metastatic disease. Levels of DNA damage in peripheral mononuclear blood cells (PBMCs) assessed 2–9 months post-surgery, were compared across tumour stage (localized (stage I-II) vs. regional (stage III) disease), localization (colon vs. rectosigmoid/rectum cancer), and adjuvant chemotherapy usage, with the last dosage administrated 2–191 days prior to sampling. Associations between DNA damage and indicators of nutritional status, physical activity and function were also explored. In PBMCs, DNA base oxidation was higher in patients diagnosed with regional compared with localized tumours (P = 0.03), but no difference was seen for DNA strand breaks (P > 0.05). Number of days since last chemotherapy dosage was negatively associated with DNA base oxidation (P < 0.01), and patients recently receiving chemotherapy (<15 days before blood collection) had higher levels of DNA base oxidation than those not receiving chemotherapy (P = 0.03). In the chemotherapy group, higher fat mass (in kg and %) as well as lower physical activity were associated with greater DNA base oxidation (P < 0.05). In conclusion, DNA base oxidation measured with the enzyme-modified comet assay varies according to tumour and lifestyle related factors in CRC patients treated for non-metastatic disease. [Display omitted] • DNA base oxidation varies in non-metastatic colorectal cancer remission. • High levels potentially affect prognosis and the risk of long-term side effects. • Enzyme-modified comet assay serve as a valuable biomarker for DNA base oxidation. [ABSTRACT FROM AUTHOR]

DNA damage can be considered as a biomarker for toxicity and response to chemotherapy. It is not known whether the chemotherapy-induced genotoxicity is associated with malnutrition. In this pilot study, we assess genotoxicity by means of DNA damage in patients with lymph-node positive colorectal cancer (CRC) and explore associations with chemotherapy treatment and nutritional status. DNA damage was compared between patients receiving chemotherapy (n = 24) and those not receiving chemotherapy (n = 20). DNA damage was measured in frozen whole blood by the comet assay. Associations between DNA damage and various indicators of malnutrition were also explored, including Patient-Generated Subjective Global Assessment (PG-SGA), bioelectrical impedance analysis (BIA) and anthropometric measurements, using multiple linear regression models. Patients on chemotherapy have higher levels of DNA damage in blood cells than patients not receiving chemotherapy (median of 16.9 and 7.9% tail DNA respectively, p  = 0.001). The moderately malnourished patients (PG-SGA category B), representing 41% of the patients, have higher levels of cellular DNA damage than patients with good nutritional status (mean difference of 7.5% tail DNA, p  = 0.033). In conclusion, adjuvant chemotherapy and malnutrition are both associated with increased levels of DNA damage in blood cells of CRC patients. Carefully controlled longitudinal studies or randomized controlled trials should be performed to determine whether good nutritional status may protect against chemotherapy-induced genotoxicity and enhance compliance to therapy in CRC patients. [ABSTRACT FROM AUTHOR]