scholarly journals WNT-pathway components as predictive markers useful for diagnosis, prevention and therapy in inflammatory bowel disease and sporadic colorectal cancer

Oncotarget ◽  
2014 ◽  
Vol 5 (4) ◽  
pp. 978-992 ◽  
Author(s):  
Annalucia Serafino ◽  
Noemi Moroni ◽  
Manuela Zonfrillo ◽  
Federica Andreola ◽  
Luana Mercuri ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Wnt Pathway ◽  
Predictive Markers ◽  
Sporadic Colorectal Cancer ◽  
Inflammatory Bowel ◽  
Prevention And Therapy

Methylation Profiles of Tumor Suppressor Genes in Inflammatory Bowel Disease-Associated and Sporadic Colorectal Cancer: A Comparison

2011 ◽  
Vol 140 (5) ◽  
pp. S-349
Author(s):  
Marian M. Claessen ◽  
Frank P. Vleggaar ◽  
Marguerite E. Schipper ◽  
John W. Hinrichs ◽  
Remco D. Radersma ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Tumor Suppressor ◽  
Bowel Disease ◽  
Tumor Suppressor Genes ◽  
Sporadic Colorectal Cancer ◽  
Suppressor Genes ◽  
Inflammatory Bowel

scholarly journals A41 LOSS OF SATB2 EXPRESSION IN COLORECTAL CANCER IS ASSOCIATED WITH DURATION OF INFLAMMATORY BOWEL DISEASE

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 49-50
Author(s):  
J Atin ◽  
C Hernandez-Rocha ◽  
K Borowski ◽  
J Stempak ◽  
M Smith ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Clinical Data ◽  
Bowel Disease ◽  
Kidney Diseases ◽  
Smoking Status ◽  
Sporadic Colorectal Cancer ◽  
Neoplastic Tissue ◽  
Potential Biomarker ◽  
Inflammatory Bowel

Abstract Background Patients with inflammatory bowel disease (IBD) are at higher risk for developing colitis-associated colorectal cancer (CAC). Clinical and endoscopic features are used to stratify the risk of CAC, but new biomarkers are necessary to improve this stratification. Recent studies have shown that loss of expression of special AT-rich sequence binding protein 2 (SATB2) is frequent in CAC compared to sporadic colorectal cancer and this SATB2 status is found in pre-cancerous dysplastic lesions as well. However, the relationship of known clinical risk factors for CAC and loss of SATB2 has not been explored. Aims To assess the association of loss of SATB2 expression in CAC with clinical characteristics of IBD. Methods Patients with a known diagnosis of ileocolonic or colonic Crohn’s disease (CD), ulcerative colitis (UC), or IBD unclassified (IBDU) who underwent colectomy between October 2010 and December 2017 for CAC were included. SATB2 expression in neoplastic tissue was evaluated using immunohistochemistry (IHC), where less than 5% of tumor cells showing staining was considered loss of SATB2. Tumor grade, P53 and mismatch repair (MMR) status were assessed as well. Available clinical data such as sex, smoking status, IBD diagnosis (CD, UC or IBDU), age at IBD diagnosis, duration of IBD, extent of colitis and previous medications were collected. We used a generalized linear model to assess the association between these biomarkers and clinical data. Results A total of 58 patients with mean age at CAC diagnosis of 50.3 ±13 years, 27 (46%) females were analyzed. Mean IBD duration was 17.6 ±10 years and 22 (37.9%), 34 (58.6%) and 2 (3.4%) were CD, UC and IBDU, respectively. Thirty-two (55.2%) CACs had loss of SATB2 expression. There was no association between age at CAC diagnosis or grade of the tumor and loss of SATB2. However, longer duration of IBD (21.2 ± 9 years vs 13.7 ± 9 years, p = 0.01) was significantly associated with loss of SATB2. There was no association between SATB2 status and other explored clinical or endoscopic variables. Tumors with P53 mutation were associated with a younger age at diagnosis of CAC (47.2 ±13 vs 55.0 ±12 years, p = 0.03), but no other associations of this marker or MMR with clinical or endoscopic variables of IBD were found. Conclusions Loss of SATB2 expression is significantly associated with IBD duration, a well-known risk factor for CAC. This association with duration of IBD could denote an effect of longer chronic inflammation on SATB2 status. Given the previously reported association of loss of expression of SATB2 with pre-cancerous lesions in IBD patients, this could be a potential biomarker for risk of CAC. Funding Agencies National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

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 Age-Related Survival Differences in Patients With Inflammatory Bowel Disease–Associated Colorectal Cancer: A Population-Based Cohort Study

2019 ◽  
Vol 25 (12) ◽  
pp. 1957-1965 ◽  
Author(s):  
Jessica Bogach ◽  
Gregory Pond ◽  
Cagla Eskicioglu ◽  
Hsien Seow
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Population Based ◽  
Sporadic Colorectal Cancer ◽  
Age Related ◽  
Inflammatory Bowel ◽  
Survival Differences ◽  
Similar Stage ◽  
Related Survival

Despite similar stage at presentation and rates of cancer treatment, patients under 65 with inflammatory bowel disease associated colorectal cancer have worse survival outcomes than patients under 65 with sporadic colorectal cancer. This difference diminishes over age 65.

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