scholarly journals Vitamins as Possible Cancer Biomarkers: Significance and Limitations

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3914
Author(s):  
Sascha Venturelli ◽  
Christian Leischner ◽  
Thomas Helling ◽  
Markus Burkard ◽  
Luigi Marongiu
Keyword(s):  
Cancer Risk ◽  
Large Body ◽  
Developed Countries ◽  
Cellular Damage ◽  
Tissue Concentrations ◽  
Blood Concentrations ◽  
Vitamin Intake ◽  
Hidden Hunger ◽  
Daily Allowance ◽  
Risk Of Cancer

The Western-style diet, which is common in developed countries and spreading into developing countries, is unbalanced in many respects. For instance, micronutrients (vitamins A, B complex, C, D, E, and K plus iron, zinc, selenium, and iodine) are generally depleted in Western food (causing what is known as ‘hidden hunger’), whereas some others (such as phosphorus) are added beyond the daily allowance. This imbalance in micronutrients can induce cellular damage that can increase the risk of cancer. Interestingly, there is a large body of evidence suggesting a strong correlation between vitamin intake as well as vitamin blood concentrations with the occurrence of certain types of cancer. The direction of association between the concentration of a given vitamin and cancer risk is tumor specific. The present review summarized the literature regarding vitamins and cancer risk to assess whether these could be used as diagnostic or prognostic markers, thus confirming their potential as biomarkers. Despite many studies that highlight the importance of monitoring vitamin blood or tissue concentrations in cancer patients and demonstrate the link between vitamin intake and cancer risk, there is still an urgent need for more data to assess the effectiveness of vitamins as biomarkers in the context of cancer. Therefore, this review aims to provide a solid basis to support further studies on this promising topic.

scholarly journals The Association between Ranitidine Use and Gastrointestinal Cancers

Cancers ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 24
Author(s):  
Gerald McGwin
Keyword(s):  
Adverse Event ◽  
Adverse Events ◽  
Reporting System ◽  
Large Body ◽  
Science Research ◽  
Gastrointestinal System ◽  
Gastrointestinal Cancers ◽  
H2 Antagonists ◽  
Study Results ◽  
Risk Of Cancer

N-nitrosodimethylamine (NDMA) is a carcinogen in experimental animals. It has been classified a probable human carcinogen and has been found in ranitidine. This study sought to evaluate the association between ranitidine use and cancer of the gastrointestinal system. Events reported to the FDA Adverse Events Reporting System that were associated with the use of proton pump inhibitors (PPIs) and H2 antagonists were selected. Proportionate reporting ratios (PRRs) and associated 95% confidence intervals (CIs) were calculated to compare the proportion of all reported adverse events that were for gastrointestinal system cancers among adverse event reports for ranitidine to adverse event reports for other H2 antagonists. The proportion of adverse events for any gastrointestinal system cancer relative to all other events was elevated for ranitidine compared to PPIs and other H2 antagonists (PRR 3.66, 95% CI 3.19–4.20). Elevated and significant PRRs were observed for pharyngeal (PRR 9.24), esophageal (PRR 3.56), stomach (PRR 1.48), colorectal (PRR 16.31), liver (PRR 2.64), and pancreatic (PRR 2.18) cancers. The PRRs for anal (PRR 4.62) and gallbladder (PRR 4.62) cancer were also elevated though not statistically significant. In conjunction with a large body of epidemiologic and human and animal basic science research, the study results support the hypothesis that NDMA-contaminated ranitidine increases the risk of cancer and supports the withdrawal of these medications from the market.

scholarly journals Family history assessment significantly enhances delivery of precision medicine in the genomics era

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Yasmin Bylstra ◽  
Weng Khong Lim ◽  
Sylvia Kam ◽  
Koei Wan Tham ◽  
R. Ryanne Wu ◽  
...  
Keyword(s):  
Family History ◽  
Cancer Risk ◽  
Clinical Care ◽  
Genomic Analysis ◽  
Population Level ◽  
Cancer Genes ◽  
Family History Information ◽  
Screening Programs ◽  
Family History Assessment ◽  
Risk Of Cancer

Abstract Background Family history has traditionally been an essential part of clinical care to assess health risks. However, declining sequencing costs have precipitated a shift towards genomics-first approaches in population screening programs rendering the value of family history unknown. We evaluated the utility of incorporating family history information for genomic sequencing selection. Methods To ascertain the relationship between family histories on such population-level initiatives, we analysed whole genome sequences of 1750 research participants with no known pre-existing conditions, of which half received comprehensive family history assessment of up to four generations, focusing on 95 cancer genes. Results Amongst the 1750 participants, 866 (49.5%) had high-quality standardised family history available. Within this group, 73 (8.4%) participants had an increased family history risk of cancer (increased FH risk cohort) and 1 in 7 participants (n = 10/73) carried a clinically actionable variant inferring a sixfold increase compared with 1 in 47 participants (n = 17/793) assessed at average family history cancer risk (average FH risk cohort) (p = 0.00001) and a sevenfold increase compared to 1 in 52 participants (n = 17/884) where family history was not available (FH not available cohort) (p = 0.00001). The enrichment was further pronounced (up to 18-fold) when assessing only the 25 cancer genes in the American College of Medical Genetics (ACMG) Secondary Findings (SF) genes. Furthermore, 63 (7.3%) participants had an increased family history cancer risk in the absence of an apparent clinically actionable variant. Conclusions These findings demonstrate that the collection and analysis of comprehensive family history and genomic data are complementary and in combination can prioritise individuals for genomic analysis. Thus, family history remains a critical component of health risk assessment, providing important actionable data when implementing genomics screening programs. Trial registration ClinicalTrials.gov NCT02791152. Retrospectively registered on May 31, 2016.

scholarly journals Risk of Cancer Following the Use of N-Nitrosodimethylamine (NDMA) Contaminated Ranitidine Products: A Nationwide Cohort Study in South Korea

2021 ◽  
Vol 10 (1) ◽  
pp. 153
Author(s):  
Hong Jin Yoon ◽  
Jie-Hyun Kim ◽  
Gi Hyeon Seo ◽  
Hyojin Park
Keyword(s):  
Cohort Study ◽  
Cancer Risk ◽  
South Korea ◽  
Primary Study ◽  
Study Cohort ◽  
Matched Cohort ◽  
Cancer Outcomes ◽  
H2 Receptor Antagonist ◽  
Carcinogenic Agent ◽  
Risk Of Cancer

N-nitrosodimethylamine (NDMA), a known carcinogenic agent, was recently detected in some products of ranitidine. Several studies have investigated the detectability of NDMA, in drugs and their risks. However, only a few epidemiological studies have evaluated cancer risk from the use of such individual drugs. This study investigates the risk of cancer in ranitidine users. We conducted an observational population-based cohort study using the Health Insurance Review and Assessment databases, which contain information about the use of medicines in South Korea. The primary study cohort consisted of ranitidine users (n = 88,416). For controls, we enrolled users of famotidine, another H2-receptor antagonist in which no NDMA has been detected. A 4:1 matched cohort was constructed to compare cancer outcomes of the two groups. Our matched cohort comprised of 40,488 ranitidine users and 10,122 famotidine users. There was no statistical difference in the overall cancer risk between the ranitidine and famotidine groups (7.45% vs. 7.56%, HR 0.99, 95% CI 0.91–1.07, p = 0.716). Additionally, no significant differences were observed in the analysis of 11 single cancer outcomes. We found no evidence that exposure to NDMA through ranitidine increases the risk of cancer.

Prediction of 10-year and lifetime risk of cancer in individual patients with established cardiovascular disease, results from UCC-SMART and CANTOS

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.C Van 't Klooster ◽  
P.M Ridker ◽  
N.R Cook ◽  
J.G.J.V Aerts ◽  
J Westerink ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Risk Factors ◽  
Lung Cancer ◽  
Cancer Risk ◽  
Prediction Models ◽  
Funding Source ◽  
Cancer Models ◽  
Total Cancer ◽  
The Cantos ◽  
Risk Of Cancer

Abstract Background As treatment for cardiovascular disease (CVD) has improved substantially over the last decades, more patients survive acute CVD manifestations and are at risk for developing cancer as well as recurrent CVD. Due to similar risk factors, including smoking and obesity, patients with established CVD are at higher risk for cancer. Objectives The aim of this study was to develop and externally validate prediction models for the estimation of 10-year and lifetime risk for total, colorectal, and lung cancer in patients with established CVD. Methods Data from patients with established CVD from the UCC-SMART prospective cohort study (N=7,280) were used for model development, and data from the CANTOS trial (N=9,322) were used for model validation. Predictors were selected based on previously published cancer risk prediction models or cancer risk factors, easy clinical availability, and availability in the derivation dataset (UCC-SMART cohort). A Fine and Gray competing risk-adjusted lifetime model was developed for total, colorectal, and lung cancer. Results Selected predictors were age, sex, smoking status, weight, height, alcohol use, antiplatelet use, diabetes mellitus, and C-reactive protein. External calibration for 4-year risks of the total cancer, colorectal cancer, and lung cancer models was good (Figure 1), and C-statistics were 0.63–0.74 in the CANTOS trial population. Median predicted lifetime risks in CANTOS were 26% (range 1%-52%) for total cancer, 4% (range 0%-13%) for colorectal cancer, and 5% (range 0%-37%) for lung cancer. Conclusions Lifetime and 10-year risk of cancer can be estimated with easy to measure variables in patients with established CVD, showing a wide distribution of predicted lifetime risks for total cancer and lung cancer. Using these lifetime models in clinical practice could increase understanding of cancer risk and aid in emphasizing healthy lifestyle changes. Figure 1. Calibration plots of cancer models Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): University Medical Center; Additional funding: CANTOS trial was funded by Novartis Pharmaceuticals.

scholarly journals The Association of Nighttime Fasting Duration and Prostate Cancer Risk: Results from the Multicase-Control (MCC) Study in Spain

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2662
Author(s):  
Anna Palomar-Cros ◽  
Ana Espinosa ◽  
Kurt Straif ◽  
Beatriz Pérez-Gómez ◽  
Kyriaki Papantoniou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Lower Risk ◽  
Night Shift ◽  
Prostate Cancer Risk ◽  
Meal Timing ◽  
Risk Of Cancer ◽  
Fasting Duration ◽  
Population Controls ◽  
Reduced Risk

Nighttime fasting has been inconclusively associated with a reduced risk of cancer. The purpose of this study was to investigate this association in relation to prostate cancer risk. We examined data from 607 prostate cancer cases and 848 population controls who had never worked in night shift work from the Spanish multicase-control (MCC) study, 2008–2013. Through an interview, we collected circadian information on meal timing at mid-age. We estimated odds ratios (OR) and 95% confidence intervals (CI) with unconditional logistic regression. After controlling for time of breakfast, fasting for more than 11 h overnight (the median duration among controls) was associated with a reduced risk of prostate cancer compared to those fasting for 11 h or less (OR = 0.77, 95% 0.54–1.07). Combining a long nighttime fasting and an early breakfast was associated with a lower risk of prostate cancer compared to a short nighttime fasting and a late breakfast (OR = 0.54, 95% CI 0.27–1.04). This study suggests that a prolonged nighttime fasting duration and an early breakfast may be associated with a lower risk of prostate cancer. Findings should be interpreted cautiously and add to growing evidence on the importance of chrononutrition in relation to cancer risk.

scholarly journals Diabetes, Antidiabetic Medications and Cancer Risk in Type 2 Diabetes: Focus on SGLT-2 Inhibitors

2021 ◽  
Vol 22 (4) ◽  
pp. 1680
Author(s):  
Mariusz Dąbrowski
Keyword(s):  
Type 2 Diabetes ◽  
Cancer Risk ◽  
The European Union ◽  
Sodium Glucose Cotransporter ◽  
Incidence And Mortality ◽  
Increasing Risk ◽  
Risk Of Cancer ◽  
Diabetes And Obesity ◽  
Increased Activity

In the last decade, cancer became the leading cause of death in the population under 65 in the European Union. Diabetes is also considered as a factor increasing risk of cancer incidence and mortality. Type 2 diabetes is frequently associated with being overweight and obese, which also plays a role in malignancy. Among biological mechanisms linking diabetes and obesity with cancer hyperglycemia, hyperinsulinemia, insulin resistance, increased levels of growth factors, steroid and peptide hormones, oxidative stress and increased activity of pro-inflammatory cytokines are listed. Antidiabetic medications can modulate cancer risk through directly impacting metabolism of cancer cells as well as indirectly through impact on risk factors of malignancy. Some of them are considered beneficial (metformin and thiazolidinedions—with the exception of bladder cancer); on the other hand, excess of exogenous insulin may be potentially harmful, while other medications seem to have neutral impact on cancer risk. Inhibitors of the sodium-glucose cotransporter-2 (SGLT-2) are increasingly used in the treatment of type 2 diabetes. However, their association with cancer risk is unclear. The aim of this review was to analyze the anticancer potential of this class of drugs, as well as risks of site-specific malignancies associated with their use.

scholarly journals The association between XRCC3 rs1799794 polymorphism and cancer risk: a meta-analysis of 34 case–control studies

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Weiqing Liu ◽  
Shumin Ma ◽  
Lei Liang ◽  
Zhiyong Kou ◽  
Hongbin Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ovarian Cancer ◽  
Thyroid Cancer ◽  
Cancer Risk ◽  
Large Scale ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Cancer Type ◽  
Increased Risk ◽  
Risk Of Cancer

Abstract Background Studies on the XRCC3 rs1799794 polymorphism show that this polymorphism is involved in a variety of cancers, but its specific relationships or effects are not consistent. The purpose of this meta-analysis was to investigate the association between rs1799794 polymorphism and susceptibility to cancer. Methods PubMed, Embase, the Cochrane Library, Web of Science, and Scopus were searched for eligible studies through June 11, 2019. All analyses were performed with Stata 14.0. Subgroup analyses were performed by cancer type, ethnicity, source of control, and detection method. A total of 37 studies with 23,537 cases and 30,649 controls were included in this meta-analysis. Results XRCC3 rs1799794 increased cancer risk in the dominant model and heterozygous model (GG + AG vs. AA: odds ratio [OR] = 1.04, 95% confidence interval [CI] = 1.00–1.08, P = 0.051; AG vs. AA: OR = 1.05, 95% CI = 1.00–1.01, P = 0.015). The existence of rs1799794 increased the risk of breast cancer and thyroid cancer, but reduced the risk of ovarian cancer. In addition, rs1799794 increased the risk of cancer in the Caucasian population. Conclusion This meta-analysis confirms that XRCC3 rs1799794 is related to cancer risk, especially increased risk for breast cancer and thyroid cancer and reduced risk for ovarian cancer. However, well-designed large-scale studies are required to further evaluate the results.

scholarly journals Risk of cancer development in patients with keloids

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ying-Yi Lu ◽  
Hung-Pin Tu ◽  
Chieh-Hsin Wu ◽  
Chien-Hui Hong ◽  
Kuo-Chia Yang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Relative Risk ◽  
Skin Cancer ◽  
Cancer Risk ◽  
Population Based ◽  
Abdominal Ultrasonography ◽  
Cancer Risk Factors ◽  
Oral Cancers ◽  
Cox Proportional Hazard Regression ◽  
Risk Of Cancer

AbstractKeloid is a skin disease characterized by exaggerated scar formation, excessive fibroblast proliferation, and excessive collagen deposition. Cancers commonly arise from a fibrotic microenvironment; e.g., hepatoma arises from liver cirrhosis, and oral cancers arise from submucosal fibrosis. As keloids are a prototypic fibroproliferative disease, this study investigated whether patients with keloids have an increased cancer risk. In a matched, population-based study, first 17,401 patients treated for keloids during 1998–2010 with 69,604 controls without keloids at a ratio of 1:4 were evaluated. The association between keloids and risk of cancer was estimated by logistic regression or Cox proportional hazard regression models after adjustment of covariates. In total, 893 first-time cases of cancer were identified in the 17,401 patients with keloids. The overall cancer risk was 1.49-fold higher in the keloids group compared to controls. Regarding specific cancers, the keloids group, had a significantly higher risk of skin cancer compared to controls (Relative risk = 1.73). The relative risk for skin cancer was even higher for males with keloids (Relative risk = 2.16). Further stratified analyses also revealed a significantly higher risk of developing pancreatic cancer in female patients with keloids compared to controls (Relative risk = 2.19) after adjustment for known pancreatic cancer risk factors. This study indicates that patients with keloids have a higher than normal risk for several cancer types, especially skin cancers (both genders) and pancreatic cancer (females). Therefore, patients with keloids should undergo regular skin examinations, and females with keloids should regularly undergo abdominal ultrasonography.

scholarly journals Anti-seizure medication is not associated with an increased risk to develop cancer in epilepsy patients

2021 ◽  
Author(s):  
Jenny Stritzelberger ◽  
Johannes D. Lang ◽  
Tamara M. Mueller ◽  
Caroline Reindl ◽  
Vivien Westermayer ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Cancer Diagnosis ◽  
Index Date ◽  
Control Group ◽  
Protective Effects ◽  
Promoting Effect ◽  
Increased Risk ◽  
Comorbidity Index ◽  
Preclinical And Clinical Studies ◽  
Risk Of Cancer

Abstract Objective Whether anti-seizure medication (ASM) increases the risk for cancer has been debated for decades. While for some ASM, a carcinoma-promoting effect has been suspected, carcinoma-protective effects have been shown for other ASM. However, the issue remains unresolved as data from preclinical and clinical studies have been inconsistent and contradictory. Methods We collected anonymous patient data from practice neurologists throughout Germany between 2009 and 2018 using the IMS Disease Analyzer database (QuintilesIMS, Frankfurt, Germany). People with epilepsy (PWE) with an initial cancer diagnosis and antiepileptic therapy prior to the index date were 1:1 matched with a control group of PWE without cancer according to age, gender, index year, Charlson Comorbidity Index, and treating physician. For both groups, the risk to develop cancer under treatment with different ASMs was analyzed using three different models (ever use vs. never use (I), effect per one (II) and per five therapy years (III). Results A total of 3152 PWE were included (each group, n = 1,576; age = 67.3 ± 14.0 years). The risk to develop cancer was not significantly elevated for any ASM. Carbamazepine was associated with a decreased cancer risk (OR Model I: 0.699, p < .0001, OR Model II: 0.952, p = .4878, OR Model III: 0.758, p < .0004). Significance Our findings suggest that ASM use does not increase the risk of cancer in epilepsy patients.

scholarly journals Tea Drinking and Risk of Cancer Incidence: A Meta-Analysis of Prospective Cohort Studies and Evidence Evaluation

2020 ◽  
Author(s):  
Long-Gang Zhao ◽  
Zhuo-Ying Li ◽  
Guo-Shan Feng ◽  
Xiao-Wei Ji ◽  
Yu-Ting Tan ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Green Tea ◽  
Dose Response ◽  
Prospective Studies ◽  
Prediction Interval ◽  
Meta Analysis ◽  
Black Tea ◽  
Current Evidence ◽  
Tea Drinking ◽  
Risk Of Cancer

ABSTRACT Here we provide a comprehensive meta-analysis to summarize and appraise the quality of the current evidence on the associations of tea drinking in relation to cancer risk. PubMed, Embase, and the Cochrane Database of Systematic Reviews were searched up to June 2020. We reanalyzed the individual prospective studies focused on associations between tea drinking and cancer risk in humans. We conducted a meta-analysis of prospective studies and provided the highest- versus lowest-category analyses, dose-response analyses, and test of nonlinearity of each association by modeling restricted cubic spline regression for each type of tea. We graded the evidence based on the summary effect size, its 95% confidence interval, 95% prediction interval, the extent of heterogeneity, evidence of small-study effects, and excess significance bias. We identified 113 individual studies investigating the associations between tea drinking and 26 cancer sites including 153,598 cancer cases. We assessed 12 associations for the intake of black tea with cancer risk and 26 associations each for the intake of green tea and total tea with cancer risk. Except for an association between lymphoid neoplasms with green tea, we did not find consistent associations for the highest versus lowest categories and dose-response analyses for any cancer. When grading current evidence for each association (number of studies ≥2), weak evidence was detected for lymphoid neoplasm (green tea), glioma (total tea, per 1 cup), bladder cancer (total tea, per 1 cup), and gastric and esophageal cancer (tea, per 1 cup). This review of prospective studies provides little evidence to support the hypothesis that tea drinking is associated with cancer risk. More well-designed studies are still needed to identify associations between tea intake and rare cancers.

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