scholarly journals Pathophysiological Roles of PPARγin Gastrointestinal Epithelial Cells

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Brian M. Necela ◽  
E. Aubrey Thompson
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Epithelial Cells ◽  
Bowel Disease ◽  
The Body ◽  
Published Data ◽  
Physiological Functions ◽  
Considerable Controversy ◽  
Inflammatory Bowel ◽  
Gastrointestinal Epithelium

Although the highest levels of PPARγexpression in the body have been reported in the gastrointestinal epithelium, little is known about the physiological functions of that receptor in the gut. Moreover, there is considerable controversy concerning the effects of thiazolidinedione PPARγagonists on the two major diseases of the gastrointestinal track: colorectal cancer and inflammatory bowel disease. We will undertake to review both historical and recently published data with a view toward summarizing what is presently known about the roles of PPARγin both physiological and pathological processes in the gastrointestinal epithelium.

Dysbiosis in Microbiome Leading to Colitis-Associated Cancer

2021 ◽  
pp. 142-169
Author(s):  
Priyamvada Priyamvada
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Risk Factor ◽  
Bowel Disease ◽  
Gut Microbiome ◽  
The Body ◽  
Physiological Processes ◽  
Microbiome Diversity ◽  
The World ◽  
Inflammatory Bowel

Colitis-associated cancers are a metastatic form of inflammatory bowel disease considered a vital health associated risk factor causing the death of approximately five lacs people every year throughout the world. There are trillions of bacteria that are associated with our gut as a part of our healthy microbiome. The microbiota plays a plethora of important role in determining the normal physiological processes of the cells and, subsequently, the body. The imbalance in microbiome diversity (dysbiosis) due to abnormal dietary habitats, hectic lifestyle, and other factors thus alters the normal physiological processes of the body, thereby causing several chronic diseases. Therefore, it is essential to maintain the homeostasis between the host and their gut microbiome. So, based on the facts mentioned above, this chapter is entirely devoted to providing an overview of colitis-associated cancer and their relation with the dysbiosis of a healthy microbiome. Moreover, the mechanism involved in the development of colorectal cancer and its preventive insights has also been addressed.

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.

scholarly journals Identification of a common variant with potential pleiotropic effect on risk of inflammatory bowel disease and colorectal cancer

2015 ◽  
Vol 36 (9) ◽  
pp. 999-1007 ◽  
Author(s):  
Hamed Khalili ◽  
Jian Gong ◽  
Hermann Brenner ◽  
Thomas R. Austin ◽  
Carolyn M. Hutter ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Pleiotropic Effect ◽  
Common Variant ◽  
Inflammatory Bowel
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