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 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.

scholarly journals Inflammatory potential of diet and risk of colorectal cancer: a case–control study from Italy

2015 ◽  
Vol 114 (1) ◽  
pp. 152-158 ◽  
Author(s):  
Nitin Shivappa ◽  
Antonella Zucchetto ◽  
Maurizio Montella ◽  
Diego Serraino ◽  
Susan E. Steck ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Rectal Cancer ◽  
Case Control Study ◽  
Continuous Variable ◽  
Case Control ◽  
Logistic Regression Models ◽  
Inflammatory Index ◽  
Colon And Rectal Cancer ◽  
Increased Risk ◽  
Control Study

Diet and inflammation have been suggested to be important risk factors for colorectal cancer (CRC). In the present study, we examined the association between the dietary inflammatory index (DII) and the risk of CRC in a multi-centre case–control study conducted between 1992 and 1996 in Italy. The study included 1225 incident colon cancer cases, 728 incident rectal cancer cases and 4154 controls hospitalised for acute non-neoplastic diseases. The DII was computed based on dietary intake assessed using a validated seventy-eight-item FFQ that included assessment of alcohol intake. Logistic regression models were used to estimate the OR adjusted for age, sex, study centre, education, BMI, alcohol drinking, physical activity and family history of CRC. Energy intake was adjusted using the residual method. Subjects with higher DII scores (i.e. with a more pro-inflammatory diet) had a higher risk of CRC, with the DII being used both as a continuous variable (ORcontinuous 1·13, 95 % CI 1·09, 1·18) and as a categorical variable (ORquintile 5 v. 1 1·55, 95 % CI 1·29, 1·85; P for trend < 0·0001). Similar results were observed when the analyses were carried out separately for colon and rectal cancer cases. These results indicate that a pro-inflammatory diet is associated with an increased risk of CRC.

Risk and predictors of suicide in colorectal cancer patients: A SEER analysis.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 9596-9596
Author(s):  
Haider Samawi ◽  
Abdel Aziz Shaheen ◽  
Patricia Tang ◽  
Daniel Yick Chin Heng ◽  
Winson Y. Cheung ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Rectal Cancer ◽  
Colon Cancer ◽  
Cancer Patients ◽  
Primary Tumor ◽  
Univariate Analysis ◽  
Male Gender ◽  
White Race ◽  
Colon And Rectal Cancer ◽  
Increased Risk

9596 Background: Colorectal cancer (CRC) patients have a higher risk of suicide as compared with the general population. Due to differences in the sites/morbidity of recurrences as well as ostomy rates, we sought to evaluate the distribution and predictors of suicide among patients with colon and rectal cancer. Methods: A retrospective analysis was undertaken using the Surveillance, Epidemiology, and End Results (SEER) database from 1973-2009. Patients included were >18yrs and had confirmed adenocarcinoma of the colon or rectum. Results: Included in this analysis were 187,996 rectal cancer and 443,368 colon cancer patients. Colon cancer patients were older (median age 71 vs. 67 yrs, p <0.001) and included more females (51 vs. 43%, p <0.001) as compared to rectal cancer patients. Suicide rates were similar (611 [0.14%] vs. 337 [0.18%], p <0.001), as was the median time to suicide for colon vs. rectal cancer patients respectively (37 vs.32 months, p = 0.13). On univariate analysis, having rectal cancer was a predictor of suicide (HR 1.26; 95% CI: 1.10-1.43). However after adjustment for age, sex, race, marital, primary site surgery, stage and one primary, rectal cancer was not a predictor of suicide (HR 1.05; CI: 0.83- 1.33). In the combined CRC cohort, independent predictors of suicide included age >70 (HR 1.55; CI: 1.23-1.94), male gender (HR 7.56; CI: 5.34-10.70), being single (HR 1.56; CI: 1.14- 2.13), distant metastases at diagnosis (HR 1.58; CI: 1.13- 2.21), and white race (HR 3.21; CI: 1.75- 5.88). Also, lack of resection of primary tumor was associated with increased risk of suicide (HR 2.83; CI: 1.97- 4.05). Among colon cancer cohort, older age, male gender, and white race as well as lack of primary resection were independent predictors of suicide. Similarly, the aforementioned predictors as well as metastatic disease on presentation were the independent predictors of suicide in the rectal cohort. Conclusions: The suicide risk in CRC patients is low (< 0.2%) and no difference was found based on location of primary tumor. Gender, age, distant spread of disease, intact primary tumour and race are the main predictors of suicide among colorectal patients. Future studies and interventions are needed to target these high risk groups.

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

scholarly journals On the definition of the healthiest body weight for children and adults

2014 ◽  
pp. 103-112
Author(s):  
Antonello Lorenzini
Keyword(s):  
Body Weight ◽  
Life Span ◽  
Basic Research ◽  
Epidemiological Data ◽  
Laboratory Animals ◽  
Public Health Issue ◽  
Important Public Health ◽  
Increased Risk ◽  
Correct Weight ◽  
Definition Of

Ongoing changes in societies are driving an expanding fraction of the world’s population towards a sedentary and overfed lifestyle. An overwhelming amount of data has linked increased body weight with an increased risk of acquiring a number of major diseases. Gerontologists, in order to extend the life span of laboratory animals, have used caloric restriction successfully for decades. This basic research on animals along with epidemiological data taken from vast human cohorts is cumulatively indicating that reducing one’s body weight should be part of the strategy to increase health and life span while reducing pathologies. What is not a trivial matter is defining the correct weight for each individual. This mini review raises some discussion points regarding this important public health issue.

scholarly journals Association analysis of miRNA-related genetic polymorphisms in miR-143/145 and KRAS with colorectal cancer susceptibility and survival

2019 ◽  
Author(s):  
Danyang Wang ◽  
Qingmin Liu ◽  
Yanjun Ren ◽  
Yan Zhang ◽  
Xin Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Rectal Cancer ◽  
Genetic Polymorphisms ◽  
Target Gene ◽  
Cancer Registration ◽  
Cancer Tissue ◽  
Aberrant Expression ◽  
Registration System ◽  
Increased Risk ◽  
Genomic Regions

Abstract Background MicroRNAs have important roles in tumorigenesis. There is accumulating evidence of aberrant expression of miR-143 and miR-145 and their target gene KRAS has been described in colorectal cancer (CRC). We hypothesize that single nucleotide polymorphisms (SNPs) within or near mRNA-miRNA binding sites may affect miRNA/target gene interaction, resulting in differential mRNA/protein expression and promoting the development and progression of CRC.Methods We conducted a case-control study of 507 CRC cases recruited from a tertiary hospital and 497 population-based controls to assess the association of genetic polymorphisms in miR-143/145 and the KRAS 3′ untranslated region (3′ UTR) with CRC susceptibility and survival. Deaths and causes of death among the CRC cases were identified using the Hangzhou Cancer Registration System and Death Surveillance System. Genetic variations of genomic regions located from 500 bp upstream to 500 bp downstream of the miR-143/miR-145 gene and the 3′ UTR of KRAS were selected using the Haploview and HaploReg software. Results Using publicly available expression profiling data, we found that miR-143/145 and KRAS expression were all reduced in rectal cancer tissue compared with adjacent normal mucosa. The Rs74693964 C/T variant located 65 bp downstream of miR-145 genomic regions was observed to be associated with CRC susceptibility (adjusted odds ratio 2.414, 95% CI: 1.385–4.206). Among non-smokers, the miR-143 rs41291957 GA genotype and miR-145 rs74693964 CT genotype were borderline significantly associated with an increased risk of rectal cancer. However, there was no interaction effect between selected SNPs and smoking status. Cumulative effects of miR-143 and miR-145 on CRC risk were observed (Ptrend=0.03). CRC cases carrying variant genotype TT of KRAS rs712 had poorer survival (log-rank P=0.044, adjusted hazard ratio 4.328, 95% CI: 1.236–15.147). Conclusions Our results indicate that miRNA-related polymorphisms in miR-143/145 and KRAS are likely to be deleterious and represent potential biomarkers for CRC susceptibility and survival.

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