scholarly journals Abstract LB231: Somatic evolution in normal colon of patients with and without cancer

2021 ◽  
Author(s):  
Júlia Matas Gironella ◽  
Brendan Kohrn ◽  
Jeanne Fredickson ◽  
Kelly Carter ◽  
Ting Wang ◽  
...  
Keyword(s):  
Normal Colon ◽  
Somatic Evolution

scholarly journals Somatic evolution in non-neoplastic IBD-affected colon

2019 ◽  
Author(s):  
Sigurgeir Olafsson ◽  
Rebecca E. McIntyre ◽  
Tim Coorens ◽  
Timothy Butler ◽  
Hyunchul Jung ◽  
...  
Keyword(s):  
Chronic Inflammatory Disease ◽  
Interleukin 17 ◽  
Normal Colon ◽  
Synonymous Mutations ◽  
Somatic Evolution ◽  
Colonic Crypts ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Selection Mechanisms ◽  
Mutational Processes

Summary paragraphInflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. Here, we whole-genome sequenced 447 colonic crypts from 46 IBD patients, and compared these to 412 crypts from 41 non-IBD controls. The average mutation rate of affected colonic epithelial cells is 2.4-fold that of healthy colon and this increase is mostly driven by acceleration of mutational processes ubiquitously observed in normal colon. In contrast to the normal colon, where clonal expansions outside the confines of the crypt are rare, we observed widespread millimeter-scale clonal expansions. We discovered non-synonymous mutations in ARID1A, FBXW7, PIGR and ZC3H12A, and genes in the interleukin 17 and Toll-like receptor pathways, under positive selection in IBD. These results suggest distinct selection mechanisms in the colitis-affected colon and that somatic mutations potentially play a causal role in IBD pathogenesis.

scholarly journals Racial Disparities in Epigenetic Aging of the Right vs Left Colon

2020 ◽  
Author(s):  
Matthew Devall ◽  
Xiangqing Sun ◽  
Fangcheng Yuan ◽  
Gregory S Cooper ◽  
Joseph Willis ◽  
...  
Keyword(s):  
Dna Methylation ◽  
African Americans ◽  
Racial Differences ◽  
Age Of Onset ◽  
Left Colon ◽  
Right Colon ◽  
Normal Colon ◽  
Epigenetic Aging ◽  
Epigenetic Age Acceleration ◽  
The Right

Abstract There are well-documented racial differences in age-of-onset and laterality of colorectal cancer. Epigenetic age acceleration is postulated to be an underlying factor. However, comparative studies of side-specific colonic tissue epigenetic aging are lacking. Here, we performed DNA methylation analysis of matched right and left biopsies of normal colon from 128 individuals. Among African Americans (n = 88), the right colon showed accelerated epigenetic aging as compared to individual-matched left colon (1.51 years; 95% CI = 0.62 to 2.40 years; two-sided P = .001). In contrast, among European Americans (n = 40), the right colon shows remarkable age deceleration (1.93 years; 95% CI = 0.65 to 3.21 years; two-sided P = .004). Further, epigenome-wide analysis of DNA methylation identifies a unique pattern of hypermethylation in African American right colon. Our study is the first to report such race and side-specific differences in epigenetic aging of normal colon, providing novel insight into the observed younger age-of-onset and relative preponderance of right-side colon neoplasia in African Americans.

Normal colon wall thickness on CT.

Radiology ◽  
1982 ◽  
Vol 145 (2) ◽  
pp. 415-418 ◽  
Author(s):  
J K Fisher
Keyword(s):  
Wall Thickness ◽  
Normal Colon ◽  
Colon Wall

scholarly journals Mast cells in adjacent normal colon mucosa rather than those in invasive margin are related to progression of colon cancer

2011 ◽  
Vol 23 (4) ◽  
pp. 276-282 ◽  
Author(s):  
Qing Xia ◽  
Ya Ding ◽  
Xiao-jun Wu ◽  
Rui-qing Peng ◽  
Qiang Zhou ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mast Cells ◽  
Colon Mucosa ◽  
Normal Colon ◽  
Invasive Margin ◽  
Normal Colon Mucosa

scholarly journals Stromal fibroblasts shape the myeloid phenotype in normal colon and colorectal cancer and induce CD163 and CCL2 expression in macrophages

2021 ◽  
Author(s):  
Mira Stadler ◽  
Karoline Pudelko ◽  
Alexander Biermeier ◽  
Natalie Walterskirchen ◽  
Anthoula Gaigneaux ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Normal Colon ◽  
Stromal Fibroblasts ◽  
Ccl2 Expression

Enterocytes are the primary source of the chemokine ENA-78 in normal colon and ulcerative colitis

1997 ◽  
Vol 273 (1) ◽  
pp. G75-G82 ◽  
Author(s):  
S. Keates ◽  
A. C. Keates ◽  
E. Mizoguchi ◽  
A. Bhan ◽  
C. P. Kelly
Keyword(s):  
Ulcerative Colitis ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Primary Source ◽  
Fold Increase ◽  
Human Colon ◽  
Neutrophil Recruitment ◽  
Normal Colon ◽  
Necrosis Factor Alpha ◽  
Cytokine Stimulation

Epithelial cell-derived neutrophil-activating protein-78 (ENA-78) is a neutrophil-directed C-X-C chemokine. We report that Caco-2 and T84 human intestinal epithelial cells produce ENA-78 after stimulation by interleukin (IL)-1 beta or tumor necrosis factor-alpha. Caco-2 cells show increased IL-8 production at 4-12 h and increased ENA-78 production at 8-24 h after cytokine stimulation. Immunohistochemical studies in normal human colon and in ulcerative colitis demonstrate ENA-78 immunoreactivity principally associated with crypt epithelial cells. Furthermore, human colonic tissues from patients with ulcerative colitis show elevated levels of ENA-78 mRNA (24-fold increase, P < 0.01) and protein (4-fold increase, P < 0.05) compared with normal controls. Thus ENA-78 is produced in normal colon and in ulcerative colitis and is predominantly of enterocyte origin. The kinetics of ENA-78 induction in human colon epithelial cell lines are delayed and prolonged compared with IL-8. We propose that ENA-78 and IL-8 serve complementary and sequential roles in neutrophil recruitment in ulcerative colitis. ENA-78 as an enterocyte-derived, neutrophil-activating chemokine may be especially important in neutrophil recruitment from the lamina propria into the epithelial layer.

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