The Role of Prophylactic Colectomy in Patients at Increased Risk of Colorectal Cancer: Do the Benefits Outweigh the Costs?

2014 ◽  
Vol 186 (2) ◽  
pp. 500
Author(s):  
N.H. Poulsen ◽  
L. Sparber ◽  
R.S. Chamberlain
Keyword(s):  
Colorectal Cancer ◽  
Prophylactic Colectomy ◽  
Increased Risk

scholarly journals Comprehensive Assessment of Diet Quality and Risk of Precursors of Early-Onset Colorectal Cancer

2020 ◽  
Author(s):  
Xiaobin Zheng ◽  
Jinhee Hur ◽  
Long H Nguyen ◽  
Jie Liu ◽  
Mingyang Song ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
High Risk ◽  
Diet Quality ◽  
Early Onset ◽  
Strong Support ◽  
Healthy Eating Index ◽  
Malignant Potential ◽  
Poor Diet ◽  
Increased Risk

Abstract Background The role of poor diet quality in the rising incidence of colorectal cancer (CRC) diagnosed under age 50 has not been explored. Based on molecular features of early-onset CRC, early-onset adenomas are emerging surrogate endpoints. Methods In a prospective cohort study (Nurses’ Health Study II), we evaluated two empirical dietary patterns (Western and prudent) and three recommendation-based indexes (Dietary Approaches to Stop Hypertension [DASH], Alternative Mediterranean Diet [AMED], and Alternative Healthy Eating Index [AHEI]-2010) with risk of early-onset adenoma overall and by malignant potential (high-risk: ≥1 cm, tubulovillous/villous histology, high-grade dysplasia, or ≥ 3 adenomas), among 29474 women with ≥1 lower endoscopy before age 50 (1991-2011). Multivariable logistic regressions were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results We documented 1157 early-onset adenomas with 375 of high-risk. Western diet was positively, whereas prudent diet, DASH, AMED, and AHEI-2010 were inversely associated with risk of early-onset adenoma. The associations were largely confined to high-risk adenomas (OR [95% CI] for the highest versus lowest quintile: Western = 1.67 [1.18 to 2.37]; prudent = 0.69 [0.48 to 0.98]; DASH = 0.65 [0.45 to 0.93]; AMED = 0.55 [0.38 to 0.79]; AHEI-2010 = 0.71 [0.51 to 1.01]; all P  trend≤.03), driven by those identified in the distal colon and rectum (all P  trend≤.04 except AMED: Ptrend=.14). Conclusion Poor diet quality was associated with an increased risk of early-onset distal and rectal adenomas of high malignant potential. These findings provide preliminary but strong support to the role of diet in early-onset CRC.

Inflammation and Cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation

2004 ◽  
Vol 287 (1) ◽  
pp. G7-G17 ◽  
Author(s):  
Steven H. Itzkowitz ◽  
Xianyang Yio
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Normal Colonic Mucosa ◽  
Sporadic Colorectal Cancer ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Repair Genes

Patients with ulcerative colitis and Crohn's disease are at increased risk for developing colorectal cancer. To date, no known genetic basis has been identified to explain colorectal cancer predisposition in these inflammatory bowel diseases. Instead, it is assumed that chronic inflammation is what causes cancer. This is supported by the fact that colon cancer risk increases with longer duration of colitis, greater anatomic extent of colitis, the concomitant presence of other inflammatory manifestations such as primary sclerosing cholangitis, and the fact that certain drugs used to treat inflammation, such as 5-aminosalicylates and steroids, may prevent the development of colorectal cancer. The major carcinogenic pathways that lead to sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also occur in colitis-associated colorectal cancers. Unlike normal colonic mucosa, however, inflamed colonic mucosa demonstrates abnormalities in these molecular pathways even before any histological evidence of dysplasia or cancer. Whereas the reasons for this are unknown, oxidative stress likely plays a role. Reactive oxygen and nitrogen species produced by inflammatory cells can interact with key genes involved in carcinogenic pathways such as p53, DNA mismatch repair genes, and even DNA base excision-repair genes. Other factors such as NF-κB and cyclooxygenases may also contribute. Administering agents that cause colitis in healthy rodents or genetically engineered cancer-prone mice accelerates the development of colorectal cancer. Mice genetically prone to inflammatory bowel disease also develop colorectal cancer especially in the presence of bacterial colonization. These observations offer compelling support for the role of inflammation in colon carcinogenesis.

scholarly journals The Role of Proinflammatory Pathways in the Pathogenesis of Colitis-Associated Colorectal Cancer

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Chengxin Luo ◽  
Hu Zhang
Keyword(s):  
Colorectal Cancer ◽  
Nuclear Factor Kappa B ◽  
Disease Duration ◽  
Evidence Based ◽  
Nuclear Factor ◽  
Predisposing Factor ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Underlying Mechanisms

Patients with inflammatory bowel disease (IBD) are at an increased risk of developing colorectal cancer (CRC). The risk factors of CRC in IBD patients include long disease duration, extensive colitis, severe histological inflammation, and coexistence with primary sclerosing cholangitis (PSC). Several molecular pathways that contribute to sporadic CRC are also involved in the pathogenesis of colitis-associated CRC. It is well established that long-standing chronic inflammation is a key predisposing factor of CRC in IBD. Proinflammatory pathways, including nuclear factor kappa B (NF-κB), IL-6/STAT3, cyclooxygenase-2 (COX-2)/PGE2, and IL-23/Th17, promote tumorigenesis by inducing the production of inflammatory mediators, upregulating the expression of antiapoptotic genes, and stimulating cell proliferation as well as angiogenesis. Better understanding of the underlying mechanisms may provide some promising targets for prevention and therapy. This review aims to elucidate the role of these signaling pathways in the pathogenesis of colitis-associated CRC using evidence-based approaches.

scholarly journals Inflammatory Bowel Disease and Risk of Colorectal Cancer: An Overview From Pathophysiology to Pharmacological Prevention

2021 ◽  
Vol 12 ◽  
Author(s):  
Marianna Lucafò ◽  
Debora Curci ◽  
Martina Franzin ◽  
Giuliana Decorti ◽  
Gabriele Stocco
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Current Knowledge ◽  
Genetic Alterations ◽  
Pharmacological Prevention ◽  
Increased Risk ◽  
Inflammatory Bowel

Increased risk of colorectal cancer (CRC) in inflammatory bowel disease (IBD) patients has been attributed to long-standing chronic inflammation, with the contribution of genetic alterations and environmental factors such as the microbiota. Moreover, accumulating data indicate that IBD-associated CRC (IBD-CRC) may initiate and develop through a pathway of tumorigenesis distinct from that of sporadic CRC. This mini-review summarizes the current knowledge of IBD-CRC, focusing on the main mechanisms underlying its pathogenesis, and on the important role of immunomodulators and biologics used to treat IBD patients in interfering with the inflammatory process involved in carcinogenesis.

The Role of the XPF Gene Polymorphism (Xrcc4) Ser835ser in the Risk of Malignant Transformation of Cells in the Colorectal Cancer

2015 ◽  
Vol 87 (2) ◽  
Author(s):  
Jacek Kabziński ◽  
Ireneusz Majsterek ◽  
Adam Dziki ◽  
Michał Mik
Keyword(s):  
Colorectal Cancer ◽  
Dna Repair ◽  
Gene Polymorphism ◽  
Risk Groups ◽  
Control Group ◽  
Preventive Program ◽  
Increased Risk ◽  
Long Time ◽  
Repair Systems

AbstractParticipation of DNA repair systems in the pathogenesis of cancer has been a suspected phenomenon for a long time. Decreased efficiency in DNA repair translates to their ability to fix and consequently leads to mutations and the process of carcinogenesis. Linking individual polymorphisms of DNA repair systems with an increased risk of colorectal cancer will allow the classification of patients to high-risk groups and their placement under preventive program.The aim of the study was to determine the effect of XPF gene polymorphism Ser835Ser on increasing the risk of colorectal cancer in the Polish population.Material and methods. as the material blood collected from 146 patients diagnosed with colon cancer was used. The control group consisted of 149 healthy subjects. Genotyping was performed by Taq- Man method.Results. The results indicate that genotype TCC/TCT is associated with an decreased risk of colorectal cancer (OR 0.574; CI 95% 0.335-0.984; p=0.043).Conclusions. Based on these results, we conclude that the XPF gene polymorphism Ser835Ser may be associated with a decreased risk of colorectal cancer

Mo1152 The Role of Cancer Stem Cells in the Increased Risk of Colorectal Cancer in African-Americans

2014 ◽  
Vol 146 (5) ◽  
pp. S-571
Author(s):  
Fadi Antaki ◽  
Lulu Farhana ◽  
Lawrence A. Miller ◽  
Mohammad R. Anees ◽  
Yingjie Yu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
African Americans ◽  
Cancer Stem Cells ◽  
Increased Risk

scholarly journals The Role of Colorectal Cancer Risk Chromosomal Regions in Colombian Admixed Populations

2018 ◽  
Vol 4 (Supplement 2) ◽  
pp. 207s-207s
Author(s):  
A. Criollo-Rayo ◽  
M. Bohórquez ◽  
P. Lott ◽  
A. Carracedo ◽  
I. Tomlinson ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Susceptibility ◽  
Association Studies ◽  
Demographic History ◽  
Recessive Model ◽  
Genome Wide Association Studies ◽  
Increased Risk ◽  
Risk Snps ◽  
Population Demographic

Background: Several colorectal cancer susceptibility disease loci have been discovered through genome-wide association studies. However most of the variants were originally identified in Caucasian populations. Aim: To analyze the role of 20 known risk SNPs for colorectal cancer. Methods: Given that linkage disequilibrium is highly dependent on population demographic history and admixture background, we studied 20 risk SNPs in a pooled sample of 955 cases and 968 controls from admixed populations in Colombia. Results: The replication was reached for 11 out of 20 nominally associated SNPs; with allelic odds ratios (OR) ranging from 1.14 to 1.41, indicating a minimal increase in risk individually, however coinheritance of those SNPs resulted in an overall OR = 5.4 (95% CI: 3.052-9.731, P = 1.16E−08). Most of the variants followed a recessive model consistent with significant homozygous ORs distributed between 1.3 and 1.65. Among the most associated markers we found: rs4939827 (18q21.1, P = 7.35E−6), rs10411210 (19q13.11, P = 0.001), rs10795668 (10p14, P = 0.0024), rs4444235 (14q.2.2, P = 0.005), rs961253 (20p12.3, P = 0.006), rs16892766 (8q23.3, P = 0.011) and rs1050547 (8q24.21, P = 0.017). Conclusion: Our findings in Colombia have addressed the admixture and how this has influenced the risk associated with the known/unknown colorectal cancer regions, providing a comprehensive vision about several CRC-susceptibility SNPs identified in European populations, which also resulted, associated with an increased risk to CRC in the Colombian population, even though frequency and genetic structure differences accounted for those nonreplicated SNPs.

scholarly journals The Role of Smoking in the Development of Colorectal Cancer

2016 ◽  
Vol 62 (4) ◽  
pp. 400-402 ◽  
Author(s):  
Márton István Dénes ◽  
Cristian Borz ◽  
Árpád Török ◽  
Tibor Kántor ◽  
Valentin Nădășan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Rectal Cancer ◽  
Heavy Smoker ◽  
Public Health Issue ◽  
Important Public Health ◽  
Increased Risk ◽  
Carcinogenic Substances ◽  
Former Smokers ◽  
Heavy Smokers

AbstractIntroduction. Smoking is an important public health issue nowadays. It causes a lot of diseases and represents also a source of carcinogenic substances. Recent studies showed an increased incidence of colorectal cancer in smokers. The aim of our study is to assess the association between smoking and colorectal cancer and to establish the prevalence of heavy smokers among the patients operated on for colorectal cancer.Methodology. We run a retrospective study of the charts belonging to the patients diagnosed with colorectal cancer and operated on in our department between 2004 and 2013. The patients were classified in smokers, former smokers and nonsmokers. The amount of tobacco was evaluated according to the number of smoked cigarettes per day, the smoking period, respectively the pack-years. The data were corroborated with the location of the tumor and analyzed using the online version of Graphpad.Results. From 982 patients diagnosed with colorectal cancer, we found 297 smokers (30.24%). Among these, 106 patients (35.69%) have smoked for over 30 years, at least 20 cigarettes per day, more than 30 pack-years. The number of heavy smokers was significantly greater (p=0.0001) in the group with rectal cancer compared to the group with colon cancer. The association of smoking with rectal cancer was also important (p=0.0015) among the former smokers.Conclusions. Smoking is related to higher incidence of colorectal cancer. Our data sustain the hypothesis of increased risk of developing rectal cancer in heavy smokers. We recommend the screening for colorectal cancer among the heavy smoker population.

scholarly journals Dietary Factors in the Control of Gut Homeostasis, Intestinal Stem Cells, and Colorectal Cancer

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2936 ◽  
Author(s):  
Federica Francescangeli ◽  
Maria Laura De Angelis ◽  
Ann Zeuner
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Low Income ◽  
Dietary Factors ◽  
Intestinal Stem Cells ◽  
Intestinal Homeostasis ◽  
Increased Risk ◽  
Incidence And Mortality

Colorectal cancer (CRC) is the third commonly diagnosed cancer and the second leading cause of cancer-related deaths worldwide. Global CRC burden is expected to increase by 60% in the next decade, with low-income countries experiencing an escalation of CRC incidence and mortality in parallel to the adoption of western lifestyles. CRC incidence is also sharply increasing in individuals younger than 50 years, often presenting at advanced stages and with aggressive features. Both genetic and environmental factors have been recognized as major contributors for the development of CRC, the latter including diet-related conditions such as chronic inflammation and obesity. In particular, a diet rich in fat and sugars (Western-style diet, WSD) has been shown to induce multiple pathophysiological changes in the intestine linked to an increased risk of CRC. In this scenario, dietary factors have been recently shown to play novel unexpected roles in the regulation of intestinal stem cells (ISCs) and of the gut microbiota, which represent the two main biological systems responsible for intestinal homeostasis. Furthermore, diet is increasingly recognized to play a key role in the neoplastic transformation of ISCs and in the metabolic regulation of colorectal cancer stem cells. This review illustrates novel discoveries on the role of dietary components in regulating intestinal homeostasis and colorectal tumorigenesis. Particular focus is dedicated to new areas of research with potential clinical relevance including the effect of food components on ISCs and cancer stem cells (CSCs), the existence of CRC-specific microbial signatures and the alterations of intestinal homeostasis potentially involved in early-onset CRC. New insights on the role of dietary factors in intestinal regulation will provide new tools not only for the prevention and early diagnosis of CRC but also for improving the effectiveness of current CRC therapies.

scholarly journals Gut Microbial Signatures in Sporadic and Hereditary Colorectal Cancer

2021 ◽  
Vol 22 (3) ◽  
pp. 1312
Author(s):  
Giorgia Mori ◽  
Maria Rosalia Pasca
Keyword(s):  
Colorectal Cancer ◽  
Gut Microbiota ◽  
Test Results ◽  
Hereditary Cancers ◽  
Increased Risk ◽  
Genetic Test Results ◽  
Gut Microorganisms ◽  
Very High

Colorectal cancer (CRC) is the fourth most common cause of cancer-related death and the third most common cancer in the world. Depending on the origin of the mutation, colorectal carcinomas are classified as sporadic or hereditary. Cancers derived from mutations appearing during life, affecting individual cells and their descendants, are called sporadic and account for almost 95% of the CRCs. Less than 5% of CRC cases result from constitutional mutations conferring a very high risk of developing cancer. Screening for hereditary-related cancers is offered to individuals at risk for hereditary CRC, who have either not undergone genetic evaluation or have uncertain genetic test results. In this review, we briefly summarize the main findings on the correlation between sporadic CRC and the gut microbiota, and we specifically focus on the few evidences about the role that gut microorganisms have on the development of CRC hereditary syndromes. The characterization of a gut microbiota associated with an increased risk of developing CRC could have a profound impact for prevention purposes. We also discuss the potential role of the gut microbiota as therapeutic treatment.

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