scholarly journals Proinflammatory cytokines and IL-10 in inflammatory bowel disease and colorectal cancer patients

2009 ◽  
Vol 57 (4) ◽  
pp. 291-294 ◽  
Author(s):  
Andrzej Szkaradkiewicz ◽  
Ryszard Marciniak ◽  
Izabela Chudzicka-Strugała ◽  
Agnieszka Wasilewska ◽  
Michał Drews ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Cancer Patients ◽  
Proinflammatory Cytokines ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Colorectal Cancer Patients

scholarly journals Su1602 Cancer-Associated Inflammation in a Cohort of Colorectal Cancer Patients With Inflammatory Bowel Disease

2013 ◽  
Vol 144 (5) ◽  
pp. S-1070
Author(s):  
Graeme J. Guthrie ◽  
Donald C. McMillan ◽  
Alan K. Foulis ◽  
Paul G. Horgan ◽  
Campbell S. Roxburgh
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Cancer Patients ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Colorectal Cancer Patients

Plasminogen Activators in the Intestine of Patients with Inflammatory Bowel Disease

1988 ◽  
Vol 60 (02) ◽  
pp. 262-266 ◽  
Author(s):  
P A F de Bruin ◽  
G Crama-Bohbouth ◽  
H W Verspaget ◽  
J H Verheijen ◽  
G Dooijewaard ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Plasminogen Activators ◽  
Intestinal Tissue ◽  
Colonic Adenomas ◽  
Tissue Plasminogen ◽  
Inflammatory Bowel ◽  
The Difference ◽  
Colorectal Cancer Patients

SummaryPlasminogen activators were determined in intestinal tissue, obtained after surgery from patients with Crohn’s disease and ulcerative colitis, and compared with normal intestinal tissue from colorectal cancer patients.The activity and quantity of tissue-plasminogen activator (t-PA) was found to decrease with the severity of inflammation in the patients with inflammatory bowel disease. Urokinase (u-PA) activity, however, was not changed compared with controls or in relation with severity of inflammation. In contrast, the level of u-PA antigen was found to be increased significantly in the inflammatory bowel disease tissues and was also related with severity of inflammation. The difference between u-PA activity and antigen in inflammatory bowel disease tissue could be attributed to an increase in inactive pro-u-PA and u-PA-inhibitor complexes.This increase in u-PA and the concomitant decrease in t-PA, are similar to those found in premalignant colonic adenomas, and might be related to the known increased cancer risk in inflammatory bowel disease.

scholarly journals Distinct pattern of epigenetic DNA modification in leukocytes from patients with colorectal carcinoma and individuals with precancerous conditions, benign adenoma and inflammatory bowel disease – a link to oxidative stress

2017 ◽  
Author(s):  
Marta Starczak ◽  
Ewelina Zarakowska ◽  
Martyna Modrzejewska ◽  
Tomasz Dziaman ◽  
Anna Szpila ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Distinct Pattern ◽  
Precancerous Conditions ◽  
Benign Adenoma ◽  
Colorectal Cancer Cells ◽  
Inflammatory Bowel ◽  
Tet Enzymes ◽  
Colorectal Cancer Patients

AbstractA characteristic feature of malignant cells, including colorectal cancer cells, is a profound decrease in level of 5-hydroxymethylcytosine, product of 5-methylcytosine oxidation by TET enzymes. This study included four groups of subjects: healthy controls, and patients with inflammatory bowel disease (IBD), benign polyps and colorectal cancer. Patients from all groups presented with significantly lower levels of 5-methylcytosine and 5-hydroxymethylcytosine than the controls. A similar tendency was also observed for 5-hydroxymethyluracil level. Patients with IBD showed the highest levels of 5-formylcytosine and 8-oxo-7,8-dihydro-2’-deoxyguanosine of all study subjects, and individuals with colorectal cancer presented with the lowest concentrations of vitamin C and A. Expressions of TET1 and TET2 turned out to be the highest in IBD group. To the best of our knowledge, this is the first study to show that healthy subjects, individuals with precancerous conditions and colorectal cancerpatients present with distinct specific patterns of epigenetic modifications in leukocyte DNA.

scholarly journals Profiling the lncRNA-miRNA-mRNA ceRNA network to reveal potential crosstalk between inflammatory bowel disease and colorectal cancer

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7451 ◽  
Author(s):  
Fangfang Sun ◽  
Weiwei Liang ◽  
Kejun Tang ◽  
Mengying Hong ◽  
Jing Qian
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Enrichment Analysis ◽  
Integrated Analysis ◽  
Cerna Network ◽  
Inflammatory Bowel ◽  
Differentially Expressed Mrna ◽  
Colorectal Cancer Patients ◽  
Functional Analyses

Background Because of the increasing dysplasia rate in the lifelong course of inflammatory bowel disease (IBD) patients, it is imperative to characterize the crosstalk between IBD and colorectal cancer (CRC). However, there have been no reports revealing the occurrence of the ceRNA network in IBD-related CRC. Methods In this study, we conducted gene expression profile studies of databases and performed an integrated analysis to detect the potential of lncRNA-miRNA-mRNA ceRNA in regulating disease transformation. R packages were used to screen differentially expressed mRNA, lncRNA and miRNA among CRC, IBD and normal tissue. The lncRNA-miRNA-mRNA network was constructed based on predicted miRNA-targeted lncRNAs and miRNA-targeted mRNAs. Functional analyses were then conducted to identify genes involved in the ceRNA network, and key lncRNAs were evaluated based on several clinical outcomes. Results A total of three lncRNAs, 15 miRNAs, and 138 mRNAs were identified as potential mediators in the pathophysiological processes of IBD-related CRC. Gene Ontology annotation enrichment analysis confirmed that the dysplasia process was strongly associated with immune response, response to lipopolysaccharide, and inflammatory response. Survival analysis showed that LINC01106 (HR = 1.7; p < 0.05) were strongly associated with overall survival of colorectal cancer patients. The current study identified a series of IBD-related mRNAs, miRNA, and lncRNAs, and highlighted the important role of ceRNAs in the pathogenesis of IBD-related CRC. Among them, the LINC01106-miRNA-mRNA axis was identified as vital targets for further research.

37 Monitoring the evolution of inflammatory bowel disease (IBD) in pediatric and adult cohorts of patients to identify biomarkers to predict cancer risk

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A38-A38
Author(s):  
Shilpa Ravindran ◽  
Heba Sidahmed ◽  
Harshitha Manjunath ◽  
Rebecca Mathew ◽  
Tanwir Habib ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Mesenchymal Transition ◽  
Increased Risk ◽  
Hamad Medical Corporation ◽  
Inflammatory Bowel ◽  
Left And Right

BackgroundPatients with inflammatory bowel disease (IBD) have increased risk of developing colorectal cancer (CRC), depending on the duration and severity of the disease. The evolutionary process in IBD is driven by chronic inflammation leading to epithelial-to-mesenchymal transition (EMT) events in colonic fibrotic areas. EMT plays a determinant role in tumor formation and progression, through the acquisition of ‘stemness’ properties and the generation of neoplastic cells. The aim of this study is to monitor EMT/cancer initiating tracts in IBD in association with the deep characterization of inflammation in order to assess the mechanisms of IBD severity and progression towards malignancy.Methods10 pediatric and 20 adult IBD patients, admitted at Sidra Medicine (SM) and Hamad Medical Corporation (HMC) respectively, have been enrolled in this study, from whom gut tissue biopsies (from both left and right side) were collected. Retrospectively collected tissues (N=10) from patients with malignancy and history of IBD were included in the study. DNA and RNA were extracted from fresh small size (2–4 mm in diameter) gut tissues using the BioMasher II (Kimble) and All Prep DNA/RNA kits (Qiagen). MicroRNA (miRNA; N=700) and gene expression (N=800) profiling have been performed (cCounter platform; Nanostring) as well as the methylation profiling microarray (Infinium Methylation Epic Bead Chip kit, Illumina) to interrogate up to 850,000 methylation sites across the genome.ResultsDifferential miRNA profile (N=27 miRNA; p<0.05) was found by the comparison of tissues from pediatric and adult patients. These miRNAs regulate: i. oxidative stress damage (e.g., miR 99b), ii. hypoxia induced autophagy; iii. genes associated with the susceptibility to IBD (ATG16L1, NOD2, IRGM), iv. immune responses, such as TH17 T cell subset (miR 29). N=6 miRNAs (miR135b, 10a196b, 125b, let7c, 375) linked with the regulation of Wnt/b-catenin, EM-transaction, autophagy, oxidative stress and play role also in cell proliferation and mobilization and colorectal cancer development were differentially expressed (p<0.05) in tissues from left and right sides of gut. Gene expression signature, including genes associated with inflammation, stemness and fibrosis, has also been performed for the IBD tissues mentioned above. Methylation sites at single nucleotide resolution have been analyzed.ConclusionsAlthough the results warrant further investigation, differential genomic profiling suggestive of altered pathways involved in oxidative stress, EMT, and of the possible stemness signature was found. The integration of data from multiple platforms will provide insights of the overall molecular determinants in IBD patients along with the evolution of the disease.Ethics ApprovalThis study was approved by Sidra Medicine and Hamad Medical Corporation Ethics Boards; approval number 180402817 and MRC-02-18-096, respectively.

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