Growth in Epithelial Cell Proliferation and Apoptosis Correlates Specifically to the Inflammation Activity of Inflammatory Bowel Diseases: Ulcerative Colitis Shows Specific p53- and EGFR Expression Alterations

Sípos, Ferenc; Molnár, Béla; Zágoni, Tamás; Berczi, Lajos; Tulassay, Zsolt

doi:10.1007/s10350-004-0831-5

Cited by 54 publications

(36 citation statements)

References 30 publications

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“…This new model will allow a more in-depth analysis of the transition from chronic inflammation to dysplasia and may help shed light on why some patients maintain active IBD whereas others develop colon cancer. It will be important to expand these studies into investigations of the molecular pathways associated with these three important cancer genes, as well as other pathways of cytokine activation, such as the epidermal growth factor receptor (43,44) and Cox-2 (45), which have been previously studied in colitis models.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Chronic Inflammation Progresses to Dysplasia in a Novel Rat Model of Colitis-Associated Colon Cancer

et al. 2007

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Inflammatory bowel disease (IBD) is a gastrointestinal disorder of unknown etiology or cure. One complication of IBD is an increased risk for development of colon cancer. The aims of this study were to use a previously established rat model of colitis to develop a new model of colitis-associated colon cancer and ascertain the involvement of three cancerrelated genes: K-ras, adenomatous polyposis coli (APC), and p53. Four groups of rats were used: reactivated 1,2-dimethylhydrazine [DMH; trinitrobenzene sulfonic acid (TNBS) was used to induce colitis followed by a weekly s.c. dose of DMH], prolonged reactivation (inflammation was induced with TNBS,

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Section: Discussionmentioning

confidence: 99%

Prolonged Chronic Inflammation Progresses to Dysplasia in a Novel Rat Model of Colitis-Associated Colon Cancer

et al. 2007

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“…Recently, amphiregulin (AREG), a ligand of the epidermal growth factor receptor (EGFR), has emerged as a component of the type 2 inflammatory response (7)(8)(9). In the context of IBD, dysregulated expression of IL-33, EGFR family members, and associated ligands have been reported in patients (10)(11)(12)(13)(14)(15) and in murine models of intestinal inflammation (16,17). Despite these advances, however, the cellular sources and functional significance of specific EGFR ligands during disease remain poorly defined.…”

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confidence: 99%

IL-33 promotes an innate immune pathway of intestinal tissue protection dependent on amphiregulin–EGFR interactions

Monticelli

Osborne

Noti

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

431

423

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The barrier surfaces of the skin, lung, and intestine are constantly exposed to environmental stimuli that can result in inflammation and tissue damage. Interleukin (IL)-33–dependent group 2 innate lymphoid cells (ILC2s) are enriched at barrier surfaces and have been implicated in promoting inflammation; however, the mechanisms underlying the tissue-protective roles of IL-33 or ILC2s at surfaces such as the intestine remain poorly defined. Here we demonstrate that, following activation with IL-33, expression of the growth factor amphiregulin (AREG) is a dominant functional signature of gut-associated ILC2s. In the context of a murine model of intestinal damage and inflammation, the frequency and number of AREG-expressing ILC2s increases following intestinal injury and genetic disruption of the endogenous AREG–epidermal growth factor receptor (EGFR) pathway exacerbated disease. Administration of exogenous AREG limited intestinal inflammation and decreased disease severity in both lymphocyte-sufficient and lymphocyte-deficient mice, revealing a previously unrecognized innate immune mechanism of intestinal tissue protection. Furthermore, treatment with IL-33 or transfer of ILC2s ameliorated intestinal disease severity in an AREG-dependent manner. Collectively, these data reveal a critical feedback loop in which cytokine cues from damaged epithelia activate innate immune cells to express growth factors essential for ILC-dependent restoration of epithelial barrier function and maintenance of tissue homeostasis.

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“…The emergence and maintenance of CC is a complex process characterized by disordered cell division and death and the histological progression occurs in a step-wise fashion: negative, to indefinite dysplasia to dysplasia to cancer [11]. The rate of proliferation and apoptosis is determined by the histologic activity of inflammation [22]. The dysplasia is present in relatively large areas of mucosa (field effect) and areas of dysplasia and cancer are surrounded by mucosa that is less dysplastic.…”

Section: Discussionmentioning

confidence: 99%

Ulcerative colitis and cancer

Kulaylat

Dayton

2010

Journal of Surgical Oncology

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Patients with ulcerative colitis (UC) are at an increased risk for the development of colorectal cancer (CRC). Unlike sporadic CRC, the cancer in UC patients arises from a focal or multifocal dysplastic mucosa in areas of inflammation. The clinical features of UC-associated cancer are similar to those found in patients with hereditary non-polyposis colorectal cancer. As with other varieties of CRC, UC-associated cancer exhibits a variety of genetic and molecular changes/abnormalities. These abnormalities are however clustered in areas of mucosae with histological abnormalities. The magnitude and timing of these changes are however significantly different. Surveillance and identification of patients at risk for cancer are a challenging problem.

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Growth in Epithelial Cell Proliferation and Apoptosis Correlates Specifically to the Inflammation Activity of Inflammatory Bowel Diseases: Ulcerative Colitis Shows Specific p53- and EGFR Expression Alterations

Cited by 54 publications

References 30 publications

Prolonged Chronic Inflammation Progresses to Dysplasia in a Novel Rat Model of Colitis-Associated Colon Cancer

Prolonged Chronic Inflammation Progresses to Dysplasia in a Novel Rat Model of Colitis-Associated Colon Cancer

IL-33 promotes an innate immune pathway of intestinal tissue protection dependent on amphiregulin–EGFR interactions

Ulcerative colitis and cancer

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